Otitis Externa

Otitis Externa:

1) Definition

2) Give examples of the following predisposing factors:

-1 mechanical trauma

-1 concomitant skin disease

-1 Seasonal factor

-1 Irritant

-1 Occupation

3) What are 4 possible pathologic organisms:

-state morphology and stain

-*which have affinity for moisture?

-*which seen in immunocompromised pts?

1) Infection of the external auditory canal

2)

-mechanical trauma= ear cleaning

-concomitant skin disease=seborrhea

-Season=water exposure in summer months

-Irritants=hair spray/dye

-Occupation=professional swimmer?

3) Gram neg rods: Pseudomonas, E. coli (proteus). *Gram neg rods have affinity for moisture*.

Gram positive coccus: Staph aureus

Fungal (immunocompromised)

Pt presents with ear pruritis, exudate, decr hearing (due to debris), and pain after you pulled on the helix and pressed on the tragus.  TM is red but motile.

...In the external ear canal there is visible debris/discharge...name the pathogen....

a) if there is copious green exudate

b) if there is yellow crusting

c) if there is scaling, cracked, weeping skin

d) if there is a fluffy, breadlike mold

Otitis Externa due to the following pathogens:

1) pseudomonas

2) staph aureus

3) eczema

4) fungus

What is the tx for otitis externa?

Care, topicals (3), systemics for bacterial and fungal (2).

Care:

Remove debris and avoid further trauma/moisture.

Topical antimicrobials (eardrops):

Neomycin/polymixin B/hydrocortisone (Cortisporin Otic)

cipro+cortizone (Cipro HC Otic)

ofloxacin otic

Systemic:

antibiotics in severe cases.

Fluconazole for fungal infections.

1) Mastoiditis: tender over mastoid

2) Malignant Otitis Externa: osteitis of bone underlying external auditory canal, most commonly seen in DM or immunocompromised pts.  Common Pathogen: Pseudomonas aeruginosa.

 An otitis externa complication that occurs in patients who are immunocompromised or in those who have received radiotherapy to the skull base. In this condition, bacteria invade the deep soft tissues and cause osteomyelitis of the temporal bone. This is a life-threatening disorder with an overall mortality rate that approached 50% historically.

Sx: fever, severe pain, friable granulation

 Malignant Otitis Externa - usual pathogen is P. aeruginosa

Tx: Hospitalization/IV ABX

[image]Figure 1: CT scan showing the soft tissue obliterating left external auditory canal left mastoid, infra-temporal fossa, skull base and involving the left TMJ.

Acute Otitis Media

1) Define

2) Usually secondary to...

3) Effected Population, Highest incidence age group...

4) Pathology

5) Etiology (5 pathogens)

6) risk factors (6)

1) Bacterial infection of middle ear

2) 2º to viral URI

3) Under 8 yrs, highest incidence 6mos-3 yrs, children with lots of colds.

4) Neg middle ear pressure causes eustachian tube to collapse (cutting off middle ear ventilation & increasing neg pressure)-->accumulate fluid and mucus that become secondarily infected.

5) S. pneumoniae, H. influenzae, M. catarrhalis, GAS (S. pyogenes), viruses

6) URI, nasal allergies, male, day care, passive smoke exposure.

3 y/o child presents with fever, earache, & unilateral hearing loss.  Mother reports the kid had a cold that seemed to be getting better and then, kid got a fever and earache.

PE:

TM with erythema, injection, bulging, immobile.

conductive hearing loss.

mastoid tender to palpation.

**If, there were a sudden relief of pain and shit started draining out of ear, what would this be?**

Acute Otitis Media.

** Occasionally tympanic membrane ruptures….sudden relief of pain and shit drains out. Common.  Heals well.**

Acute, suppurative proccess in the middle ear creating pain and fever.  TM immobile to pneumatic testing and often red and bulging.  Commonly follows URI.

**For this to be classified as recurrent, what are requirements?

Acute Otitis Media

Recurrent Otitis Media: 3 times in 3 months OR >4 times per year WITH resolution btwn episodes.

Amber fluid within the middle ear WITHOUT evidence of acute infection.  TM immobile.  Common in children.  Usually don´t treat.

**When would you treat these cases?...Requirements, 2 treatments options.

Serous Otitis Media (Otitis Media with effusion)

*Persistance Otitis Media with Effusion: effusion persists for 4-6 months (could be due to angle of eustachian tubes).  Kids may not be talking b/c decr hearing.  May have nasopharyngeal obstruction/allergies. 

Tx with drainage tubes or prophylactic ABX.

Purulent middle ear infection.  Perforation of TM present.  Chronic otorrhea.  Hearing loss.  Pain uncommon except during acute exacerbations.

1) What is this?

2) As a result of...

3) Pathogens...

4) Tx

1) Chronic Otitis Media

2) Not common.  As a result of trauma or recurrent otitis media.

3) Staph aureus, Pseudomonas, proteus species (like e. coli).

4) Tx: long term ABX or surgery to repain TM

Tx for acute otitis media.

*contraindication

-Oral Antipyretics and analgesics (*NO ASPIRIN for children with coexisting viral illnesses...Reye's)

Usually treat all cases with ABX (always when there is pain) to prevent 2º infections: meningitis and mastoiditis.  Begin with 1º ABX, switch to alt if no response in 48-72hrs. If still no response: tympanocentisis to culture bacteria or provide immediate pain relief.

1º ABX: Amox or Amoxicillin/clavulanate x 10d

Alternatives: 3rd gen cephalosporins (cefdinir, ceftriaxone) or azithromycin

Invagination of the tympanic membrane that becomes pulled into the middle ear space because of  negative pressure effect of eustachian tube dysfunction.   Pockets initially self cleansing, although neck of pocket may narrow and trap squamous cells with keratin accumulation and retention; proliferation = expansion and ____(answer)______ formation. The _(answer)_______ sac is associated with enzymatic bony destruction due to cytokine-induced inflammatory changes, with activation of osteoclasts and lysozymes (osteomyilitis of temporal bone), destruction of the ossicles causing a conductive hearing loss, destruction of the semicircular canals (vertigo), cochlea (sensorineural hearing loss), and facial canal (facial palsy).

what is this?

what is this a complication of?

Cholesteatoma

a complication of acute otitis media.

acute otitis media

*FYI: Labryrinthitis: An inflammatory condition, caused by bacteria or viruses, that affects the labyrinth in the cochlea and vestibular system of the inner ear. Typically, it presents with sensorineural hearing loss, vertigo, and disequilibrium (problems with balance) and may affect one or both ears. It may be further classified as suppurative or serous. Suppurative (bacterial) labyrinthitis follows direct microbial invasion of the inner ear and usually presents with severe to profound hearing loss and vertigo. Serous (viral) labyrinthitis results from inflammation of the labyrinth only and usually presents with less severe hearing loss and vertigo than suppurative labyrinthitis, and the hearing loss often recovers.

Inflammation of the nasal mucosa...

1) Name

2) due to...(2 + 5 less comon causes)

Rhinitis due to...

1. viral (common cold), allergy, chronic bacterial sinusitis, polyposis, deviated septum, tumor, foreign body

Pt has stuffy/runny nose, mucosal edema, sneezing, PND, cough, sore throat. Pt is a smoker.

What is your dx and tx?

Dx: Viral rhinitis

Tx: stop smoking, liquids, vit C, salt water gargle, cough preps & decongestants (sprays no more than 3 days because of rebound congestion, switch to oral).

Sneezing, nasal congestion, pruritis of nose/eyes/soft palate, dry mouth, decr smell/taste.   Possible headache, lassitude, fatigue.

PE: mucosal edema, boggy/pale mucosa, allergic shiners, eye irritation.

1) what is the dx (state the types).

2) management: 3 parts

1) Allergic Rhinitis:

a) Seasonal: Sx occur at same time every year.  Common onset btwn ages 10-20 and continues throughout life.

b) Perennial: Sx occur throughout year and can be induced by dust, dander, mold.  Seasons may exacerbate.  May have positive family Hx.

2) Management

a) avoidance

b) drug therapy:

Mild Sx: antihistamines (Benadryl, Claritin)

Mod Sx: intranasal corticosteroids, Singulair (leukotrine receptor antagonist)

Severe Sx: oral corticosteroids (3-5 days at a time)

c) Immunotherapy: Sx>1mnth or through many seasons even with meds.  Req: + skin test, correlation to allergen, takes alot of meds.

Acute Bacterial Sinusitis:

1) Pathogens in healthy vs. immunocompromised pts

2) May be a complication of....(4)

3) Which sinus most commonly affected?

4) Dx studies

5) Management

6) 4 complications

1) S. pneumoniae, H. influenzae, M. catarrhalis, GABHS, viruses.

Immunocomp: fungal

2) Allergic rhinitis, polyps, anatomical abnormality, NG tubes.

3) Maxillary

4) CT and culture

5) Keep hydrated (steam, liquids), stop smoking, amox, AM-CL, cephalosporins, resp-FQs (fluroquinolones), azithromycin x 10-14 d.  Decongestants, antihistamines, analgesics.  **Pretty much the same as otitis media.

6) Cellulitis, Osteomyelitis, Cavernous venous thrombosis, meningitis

Pt presents with fever, perinasal swelling, tenderness upon palpation to maxillary sinuses.  Posterior pharyngeal wall has fluid discharge drip. 

Pt c/o Fever, congestion, PND, upper teeth pain, cough that worsens at night.

What is this and do you treat it?

Acute Bacterial Sinusitis.

tx with ABX x 10-14 d (less treated in kids)

Pt presents with PND, nasal cavity pain, nasal congestion, dental pain, chronic cough, facial discomfort, headache for more than 12wks.

3 Dx studies and Dx?

Tx?

Chronic Sinusitis

*determine that pt has inflamm of paranasal sinuses vs. nasal passages.

Dx by CT, MRI (complex cases), nasal endoscopy.

tx: decongestants, intranasal corticosteroids, nasal irrigation, ABX?, ENT referrel for endoscopic surgery.

What is one of the most common complainst seen in clinical practice?

What is primary task of practitioner with this complaint?

Pharyngitis.

ID and tread GABHS or see if there is association of serious systemic illness.

Viral pharyngitis is caused by what 2 viruses?

This is commonly know as...

May cause pharyngitis alone (herpangina) or a syndrome of pharyngeal vesicles and ulcers acoompanied by a vesicuopapular rash on hands and feet (hand foot and mouth disease)

Assoc anorexia, vomitting, diarrhea.

School age child presents in winter or spring with fever, sore throat (exudative), tender anterior cervical nodes.  No cough or nasal congestion.  Possible assoc Sx of headache, malaise, rash, abdominal pain, and vomiting.

Diagnostic tests?

Def Dx?

Tx?

Complications?

GABHS: Bacterial pharyngitis

dx by throat culture (gold standard) or rapid antigen (90% specificity).

TREAT (within 9 days of onset to prevent RF/PSGN) if rapid antigen is pos (& awaiting culture) or if neg with high clinical suspician.

tx ABX:

1 time IM Pen G (painful!)

PO: pen v, amox, erythro, azithro, cephalos, clindamycin.

Complications: peritonsilar abcess, retropharyngeal abcess.

1) Rheumatic fever with damage to heart valves.

2) Post-strep glomerulonephirits (PSGN) with acute renal failure.

1) N. gonorrhoeae: tx with ceftriazone IM + doxy x 10 days (chlamydia tx)

2) Corynebacterium diphtheriae...pseudomembrane and have toxic clinical appearance.  Foreign born pt.

Gingivitis:

caused by bacterial plaque, reversible, red/puffy/bleeding gingiva

Pt presents with chronic gingival inflamm, pocket formation, bone-loss, tooth mobility, and pathological migration of teeth.   Irreversible.

State disease and management.

What progresses the disease rapidly?

Periodontitis:

Deep cleanings q 3-4 months with maintenance.

Arestin (Minocycline) in pockets.

Smoking progresses disease.

What are 6 dental disease that you should refer to appropriate dental professional?

CADET PEDS

Caries: root canal if decay has infected the nerve.  You are not born with the bacteria that causes caries: S. mutans.  Depends on bacteria + carbs= acid by product = caries. ¨baby bottle caries¨

Dental Abcess: accumulation of inflamm cells at apex of non vital tooth. Infection travels down nerve and into bone...EMERGENCY.  Can also travel to skin (cellulitis) where tissue becomes hard and warm...

Trauma

Pericoronitis: inflamm lesions around partially developed tooth, most common mandibular 3rd molars. There is pain and bad taste. Tx: peridex/saline lavage

Dry Socket: post-op 3-4 days, no infection, dull radiating pain.  tx: iododorm gauze soaked in eugenol.

Subperiosteal Infection: post op 1-2 months, infection, fever over 100º

Luwig's Angina.

A medical emergency caused by a dental abcess that spread to bone than soft tissue (cellulitis).

Upper tooth infetion spreads to cause preorbital enlargment with involvement of eyelids and conjuctiva.  Infection can spread to brain.

Pt has fever, headache, chills, sweating.

Cavernous Sinus thrombosis.

A medical emergency caused by a dental abcess that spread to bone then soft tissue (cellulitis).

chronic cheek biting on anterior buccal mucosa

Man presents with lethery wrinkled white gums found in mandibular vestibule without pain or ulceration.

Dx and Tx

Smokeles Tobacco/Snuff Pouch Keratosis

Tx: quit, f/u in 6wks, if doesn´t go away or see little red dots...suspect CA and get biopsy.

Intraoral carcinoma arising from preexisting leukoplakis or erythroplakia.  Irregular, pebbled appearance. Hx: heavy drinker, smoker.

What is it, 2 most commonly found sites, and danger?

Squamous Cell Carcinoma

1st: tongue, 2nd: floor of mouth

Can spread easily to neck and throat through cervical lymphs.

[image][image]

SPUTUM COLLECTION

1) Indications

2) 4 methods

3) Adequate specimen?  2 things to look for. #squamous/LPF* for satisfactory and rejected.

1) productive cough, fever, CXR

2) cough into sterile container (induce with inhalation of mist/hypertonic saline), via ET tube, fiberoptic bronchoscopy, tracheal aspiration (needle through cricothyroid membrane)

3) Look for PMN and inflamm cells.

<10 squams/LPF (low power field)=good.

>25 squams/LPF= rejected

Atypical Sputum Examinations: what prep/stain do you use for the following...

1) Legionella

2) Mycobacteria (2)

3) Fungal

4) Histoplasmosis

1) Legionella: immunoflorescent stain

[image]

2) Mycobacteria (2): Ziel-Nihlson (flourescent) & acid-fast (more sensitive & quicker.  MTb=blue)

[image][image]

3) Fungal: KOH prep

[image]Candida vulvovaginitis

4) Histoplasmosis: Wright Stain

[image]

A gross sputum examination reveals the following characteristics...what conditions/diseases do you see these characteristics in?

1) gray, white, viscous, worse in the morning.  *with infection, what color does it become?

2) purulent, rust colored

3) copious yellow/green

4) purulent with foul odor

1) gray, white, viscous, worse in the morning= Chronic Bronchitis.  *with infection, becomes yellow or green

2) purulent, rust colored=pneumococcus (S. pneumoniae)

3) copious yellow/green=bronchiectasis (chronic COPD, CF pts)

4) purulent with foul odor= lung abcess (anaerobic bacteria)

PPD for TB

1) read within...

2) measure what area?

3) % of pts that have active disease and neg PPD?

4) positive PPD indicates...

5) Requierments for +PPD @ 5mm, 10mm, 15mm

1) read within 48-72 hrs

2) measure INDURATED area (not erythema)

3) % of pts that have active disease and neg PPD= 25%

4) positive PPD indicates exposure to TB, not necessarily active...TREAT and get CXR.

5) Requierments for +PPD @

5mm: recent exposure, abnml CXR, immunosuppressed pts

10mm:foreign born, underserved, IV drug users, long term facility residents, medical staff.

15mm: no known risk factors.

Scan performed by inhalation of a radioactive gas or nebulized aerosol of radioactive particles.  Then scan performed by injecting radiolabeled particles into blood which become lodged in pulm capillary bed in normal regions.

What test is this?  Indications? What is abnml?  Not sufficient in what pts?

Ventilation/Perfusion Scan (V/Q) scan.

Evaluate for PE or Pre-op lung function studies.

If blockage, certain areas in lung don't pick up radiolabelled particles (PE blood clot)= V/Q mismatch.

Not sufficient in pts with scarring of lung tissue (COPD) b/c there may be perfusion defect and abnml ventilation.

4 types of pleural effusions:

1) white, milky-chylothorax, malignancy, emphysema.  From lymphatics.  *What is pseudo?*

2) from trauma, malignancy, PE (>100K RBC/mm³). *Hematocrit % Requirement?*

3) CHF, cirrhosis, renal failure, PE.  *Tx?*

4) infectious, malignancy, PE.  Most dangerous.  Dark, turbid fluid.

1) Chylous: white, milky-chylothorax, malignancy, emphysema.  From lymphatics.  *pseudo: RA with crystals.

2) Hemorrhagic: from trauma, malignancy, PE (>100K RBC/mm³). *Requires more than 50% hemtocrit in fluid (to make sure it is not just a tint of blood).

3) Transudative: CHF, cirrhosis, renal failure, PE.  *Tx: drain and forget about it.

4) Exudative: infectious, malignancy, PE.  Most dangerous.  Dark, turbid fluid.

meet AT LEAST ONE of the following criteria:

PLeural Fluid Dx:

1) If WBC >1,000, suggests...

2) If WBC >10,000, suggests...

3) >50% lymphocytes, 2 differentials...

4) When would your differential include acute inflammation (PE, TB, pneumonia)?

5) When would your differential include pneumonia, TB, malignancy, rheumatoid effusion.

6) A right side pleural effusion and  elevated pleural fluid amylase, what 2 suspects?

7) a pH<7.2 or pos gram stain indicates what?  requires what?

1) Exudative Effusion: WBC >1,000 ?

2) Infection: WBC >10,000

3) TB, Malignancy >50% lymphocytes (B, T cells)

4) PMN predominance (neutrophils, esinophils, basophils)= acute inflammation (PE, TB, pneumonia)

5) Glucose<60= pneumonia, TB, malignancy, rheumatoid effusion.

Glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis.

6) Pancreatitis, Esophageal Rupture= A right side pleural effusion and  pleural fluid amylase>serum

Pleural fluid amylase is elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer.

7) Empyema** requiring chest tube drainage: pH<7.2 or pos gram stain

Pleural fluid pH is low in empyema (<7.2) and may be low in cancer.

**FYI: An empyema is a collection of pus within a naturally existing anatomical cavity, such as the lung pleura. It must be differentiated from an abscess, which is a collection of pus in a newly formed cavity.Usually an empyema starts with pneumonia, followed by a parapneumonic effusion. This effusion, which starts out sterile, then becomes infected. As the infection progresses, the thickness of the fluid increases, going from a broth type consistency to concrete. When the fluid is still free flowing, it can be treated with a thoracentesis or a chest drain. When it thickens, it can usually be treated with thoracoscopy

What test would you use to ID cause of dyspnea, measure effect of disease or med like Albuterol, follow course of disease process?

What is required for adequate interpretation?

PFT (pulmonary function tests)

PFT is adequate for interpretation ONLY if pt  exhales for 6 seconds

PFTs:

1) largest volume measured on complete exhalation after full inspiration

2) #1 above, but slowly. *What can this demonstrate?

3) #1 above, but with max force.  *In what diseases is this low?

4) Volume of gas exhaled over 1st second during #3.

5) FEV-1%=

6) Average rate of flow during middle half of volume expire during FVC. *This is dependent on what?

7) Max flow obtained during FVC maneuver.

1) Vital Capacity (VC): largest volume measured on complete exhalation after full inspiration

2) Slow vital capacity (SVC): #1 above, but slowly. *Can demonstrate possible obstruction*

3) Forced Vital Capacity (FVC): #1 above, but with max force.  *lower in obstructive diseases*

4) FEV-1: Volume of gas exhaled over 1st second during #3.

5) FEV-1%= (FEV-1/FVC) x100

6) FEF 25-75%: Average rate of flow during middle half of volume expire during FVC. *This is dependent on pt's size.

7) Peak Flow: Max flow obtained during FVC maneuver.

obstruction vs restriction (as per Dr. Maouelainin)

1) FEV-1.....incr/decr/nml

2) FVC........incr/decr/nml

3) FEV-1%...%/incr/decr/nml

4) TLC.........incr/decr/nml

5) FRC.........incr/decr/nml

6) Lung elasticity..........nml/elastic/stiff

7) Elastic Recoil............nml/low/high

8) Airway resistance......nml/low/high

9) Expiratory Flow rate...low/high

[image]

Lung Volumes:

1) volume inspired with each breath.  Based on body weight.  Normal is about 5 ml/kg of ideal body wt

2) :  volume of gas remaining after a maximal expiration

3) :  maximum volume of gas that can be inhaled above an inhaled tidal volume

4) maximum volume of gas that can be exhaled below Functional Residual Capacity

5) :  Maximum volume inspired from resting volume.  Give formula

6) maximum volume of gas that can be exhaled after a maximal inspiration. (give formula)

7) :  maximum volume of gas that the lungs can contain. *What do you need to obtain this?  Give 2 formulas

Tidal volume (TV):  volume inspired with each breath.  Based on body weight.  Normal is about 5 ml/kg of ideal body wt

Residual volume (RV):  volume of gas remaining after a maximal expiration

Inspiratory reserve volume (IRV):  maximum volume of gas that can be inhaled above an inhaled tidal volume

Expiratory reserve volume (ERV):  maximum volume of gas that can be exhaled below FRC

Inspiratory capacity (IC):  Maximum volume inspired from resting volume

IC = TV +IRV

Vital Capacity (VC):  maximum volume of gas that can be exhaled after a maximal inspiration.

VC = IRV + TV + ERV

Functional residual capacity (FRC): volume of gas remaining in the lung after a normal expired tidal volume

FRC = RV + ERV

Total lung capacity (TLC):  maximum volume of gas that the lungs can contain. Need this number given or need body box to measure.

TLC = VC +RV

TLC = FRC + IC

Volume where the inward elastic recoil forces of the lungs are exactly equal to the outward forces of the chest wall.

¨Resting position¨

What is this?

What occurs here?

Functional Residual Capacity

Volume where gas exchange occurs.

[image]

A Bronchodilator response from an asthma attack defined as meeting what 3 criteria?

Bronchodilator response defined as:

•  12% improvement in FEV-1 AND at least 200cc improvement

OR

• 12% improvement in FVC AND at least 200cc improvement.

OR

• 30-40%* improvement in FEF 25-75%

*Note: Dr. Schullman said 30%, Dr. Mauelaninin said 40%.

Pulmonary Diseases that cause impaired gas diffusion:

1) loss of surface area for gas exchange (3)

2) thickening of aveolar/capillary membrane (2)

1) emphysema, pulm fibrosis, lung resection*

2) pulm fibrosis, edema fluid

*A lung resection is a surgical procedure to remove a portion of the lung or the whole lung.

Acute Bronchitis

1) Etiology in pts without underlying lung disease

2) Etiology in smokers or pts with underlying lung disease

1) Virus in 80% of cases or mycoplasma or chlamydia

2) Bacterial agents: S. pneumonia, H. influenza, M. catarrhalis, B. pertussis

Pt has dry hacking cough with little sputum that later became copious, purulent, or blood streaked.  Pt had a URI a couple weeks ago, felt better, and then there was a gradual onset of this cough.

Assoc Sx: fever, chills, low sternal chest pain, cough, SOB, wheezing, runny nose, scratchy throat.

Pulse=norm/elev

Resp=norm/elev

URT sx may be present: conjunctival & mucosa injection

Accessory muscle use, nasal flaring, bulge/retract of IC spaces.

Fremitus=norm

Resp/diaphragmatic expansion=norm.

Percuss=resonance

Auscult=bronchovesicular pattern, ronchi, possible wheeze, no egophony.

Acute Bronchitis

Fever=elevated HR

Respirations could be elevated b/c of bronchospasm.

BP incr if pt is hypoxic during bronchospasm

Pt has cough, low grade fever, predominante mucous membrane involvement, malaise, aches, pains.  

Lung exam reveals ronchi, and nothing else notable.

What is condition and etiology?

Pt is smoker and has chronic lung disease. Pt Has cough, high fever, productive mucopurulent cough, chest pain.

Lung exam reveals ronchi, and nothing else notable.

What is condition and etiology?

Managment of Acute Bronchitis:

1) Avoid use of what?

2) what can you recommend at night?

3) What can help alleviate bronchiole inflammation?

4) ABX?

1) avoid antihistamine: they will dry pt up.

2) cough suppressants at night: DXM ,codeine sulfate.

3) steroidal inhaler.

4) ABX rarely indicated: depends on pt age, PMH, and clinical picture.

Stay hydrated, get rest, stop smoking.

What are the 3 major mechanisms that microbes gain entry to cause pneumonia?

What is the most common pathogen of pneumonia?

What are the 2 classifications of pneumonia?

#1) Aspiration of oropharyngeal secretions 

2) Aerosol inhalation (TB, fungal)

3) hematogenous spread (IV drug abuser or stab wounds)

S. pneumonia (CAP) most common pathogen in pneumonia.

2 classifications: CAP & nosocomial

S. pneumoniae:

1) most common cause of...

2) morphology/gram stain

3) typically follows...

4) seen in pts with what disease...

1) CAP pneumonia

2) gram positive diplococci

3) follows URI

4) chronic cardiopulmonary disease.

These organsisms are mixed oral flora associated with periodontal disease and aspiration.  They cause both CAP and nosocomial pneumonia with pts on ventilators.

The pneumonia is often more severe. 

These are the 3rd most common cause of pneumonia.  Usually Seen in epidemic outbreaks (not sporadic) and spread by droplets.  No gram stain.

Give two examples.

Mycoplasma (M. pneumoniae)

No gram stain b/c no cell wall.

Nosocomial Pneumonia

1) When do symptoms occur?

2) Freq seen in what pts (2)?

3) Common organisms (6) EPPSSK

1) >48 hrs after admission

2) ICU and mechanical ventilation pt

3) S. aureus, E. coli, P.aeruginosa, Klebsilla, Proteus, Serratia.

Important Historical Data and Pneumonia:

1) Age: what etiology is more common in young vs. old?

2) Season: what is seen throughout (1), summer/fall (3), winter/spring (1)

3) What vaccines are important to ask about (what are their durations)

4) Social Hx: southwest, mississippi border, cruises

5) Occupation:

contruction/HVAC guys, hunters/farmers, bird handlers

1) young=viral & mycoplasma

old=bacterial

2) throughout: S. pneumonia

summer/fall: Mycoplasma, Legionella, viruses

winter/spring: influenza

3) Pneumococcal (Pneumovax)= 6 yr duration.

Influenza: give annually

4) 

southwest: coccidiomycosis

MI border: histoplasmosis

Cruise: legionella

5) 

Construction/HVAC=legionella

Hunter/farmer= Q fever*

Bird handlers=Psittacosis*

*Q fever is a worldwide, zoonotic (cattle, sheep, goats) disease caused by the gram-negative, obligate, intracellular bacterium Coxiella burnetii. The disease presents in 2 forms: acute infection (a self-limiting febrile illness with varying degrees of pneumonia and hepatitis) and chronic infection (mainly endocarditis).

*Chlamydophila psittaci is both a respiratory and an ocular pathogen acquired from domesticated or commercially raised birds, mammals, exotic imported birds, and feral animals.

Sudden onset of high fever, tachycardia, hypotensive, 1 set of shaking chills, cough productive of purulent sputum, rust-colored.

Pt may have or have had URI.

1) What is this?

2) prodromal sx?

3) CXR

4) Lung exam:

inspection

resp expansion

tactile frem

percussion

Auscultation: what is the hallmark sound?  What sounds are less diagnostic (30% cases)?

5) IF...

Trachea displaced to contralat side.  

Bacterial Pneumonia= pneumococcal

2) uncommon to get prodromal sx

3) lobar consolidation on CXR

4) Lung exam:

inspection=resp distress

resp expansion=norm/decr (splinting)

tactile frem=incr over consolidation

percuss=dull over consolidation

Auscultaton= bronchial sounds over consolidation, rales/wet crackles (80% cases), broncho/ego/WP (<30%).

5) with pleural effusion.

Onset insidious and slow with classic prodromal sx of headache, myalgia, arthralgia, malaise, photophobia.

Typically follow URI.

Low grade/absent fever

cough with scanty mucus production

Minimal dyspnea

rare pleuretic chest pain

CXR with patchy/diffuse infiltrates

Rales/crackles on lung exam

Pneumonia Pathogens:

Gross inspection of sputum:

1) thick, yellow, foul smelling

2) thick, purulent, minimal odor

3) scanty, clear, mucopurulent

4) rust color

5) thick currant jelly

6) grossly bloody

1) thick, yellow, foul smelling= anaerobes

2) thick, purulent, minimal odor=bacterial

3) scanty, clear, mucopurulent=viral/atyp

4) rust color=pneumococcal

5) thick currant jelly=Klebsiella

6) grossly bloody=TB

Pharma tx of pneumonia

1) youth with mycoplasma

2) 2 other ABXs

1) macrolides/erythromycen

2) doxy or fluroquinolones (leviquin)

38 y/o female with sudden onset of SOB, cough productive of thick rust color sputum, high fever, shaking chills x 1-day.

PE: fits of coughing, fever, resp 24, HR 100 regular, B/P 128/78. Skin warm, dry, rapid turgor.  HEENT unremarkable.

Lung Exam: tact frem incr, dullness to percussion, and bronchial breath sounds with crackles and egophony in RLL.

1) Clin dx & etiological agent

2) labs to order (4) and results

3) Tx

1) bacterial pneumonia (pneumococcal or s. pneumonia) in RLL.

2) CXR=lobar consolidation

sputum culture/stain=gram positive diplococci

CBC=leukocytosis with left shift (younger)

Blood Culture=negative

3) f/u 24 hrs.  ABX: macrolide/b-lactamase inhibitor: AM-CL or cephalosporin cefuroxime axetil, supportive care.

1) Heart Disease

2) CA

3) Stroke

4) COPD

Disease characterized by airflow limitation.

Sx: cough, dyspnea, sputum production.

1) What is the disease

2) List spirometry values for classification of mild and moderate.

3) #1 risk factor

4) genetic factor

1) COPD

2) mild: FEV-1% <70% & FEV1>80%

moderate: FEV-1% <70% & FEV1<80%

3) smoking

4) a1-antitrypsin deficiency=leads to destruction of airways.

COPD

Smoking habits and aging population=increase in prevalance.

chronic inflammatory disorder of the airways with episodic or chronic airway obstruction.

Sx: wheezing, SOB, cough, chest tightness

Influenza

1) Types

2) Resevior

3) Transmission

4) incubation

5) Time of year most prevalent

6) Sx and recovery time

7) people at risk for complications

1) A,B,C viruses

2) humans, swine, birds

3) airborne

4) incubation 3-7 days

5) Winter/Spring occurence

6) fever, headache, myalgia, soar throat, cough with recovery in 2-7 days

7)6mos-3yrs, >65yrs, pregnancy, immunocompromised people, chronic diseases

Pneumococcal Pneumonia

1) Pathogen

2) Resevior

3) Transmission

4) incubation

5) Occurence season

6) sx

7) other illnesses that the pathogen causes

8) ethnic populations at risk

9) immunization and booster recommendations: for geriatrics, adults with chronic disease, children, alaskan natives/nat americans

1) S. pneumoniae

2) Humans - upper resp tract

3) Droplet, direct oral, indirect by touching soiled articles with resp discharge.

4) 1-3 days

5) winter/spring

6) fever, chills, dyspnea, productive cough, pleuretic chest pain.

7) URIs, otitis media, sinusitis, meningitis, bacteremia, pneumonia

8) Af Amer, Alaskan natives, native americans

9) immunization: (pneumococcal polysacchride vaccine PPV):

>65yrs, no booster needed

adults w/ chronic condition every 5yrs.

al natives/nat americans>2y/o.

children 2-23 mnths

COPD:

1) Anatomic definition

&

2) Clinical Definition

1) Anatomic definition= Emphysema: permanent enlargement of gas-exchanging units in assoc with destruction of aveolar walls and without obvious fibrosis

&

2) Clinical Definition=Chronic bronchitis: condition assoc with excessive mucous sufficient to cause cough > 3mnths/yr for 2 cnsecutive years, excluding other causes.  Think cigarettes

Obstructive or restrictive?

1) FEV1%<70%

2) Decreased TLC

1) Obstructive

2) Restrictive

Emphysema

anatamical definition of COPD

condition assoc with excessive mucous sufficient to cause cough > 3mnths/yr for 2 cnsecutive years, excluding other causes.  Think cigarettes

State and Justify FEV-1%, FVC, and FEV-1 in obstructive lung disease as defined by Dr. Schulman.

State three obstructive lung diseases.

FVC=normal, in more severe cases it is reduced

the person can get the air out, it just takes longer, but FVC doesn´t measure time, just volume, so it is normal.

FEV-1= reduced (<80% predicted)

the person cannot get as much air out in the 1st second of the test.

FEV-1%<70%

Since FEV-1% is the ratio of FEV-1:FVC, if FVC remains the same, but FEV-1 decreases, then the ration will decrease.

Asthma, Emphysema*, Chronic Bronchitis*

*Emphysema and Chronic Bronchitis are SUBTYPES of COPD*

Centrianicar: initial dilation of respiratory bronchioles.

Panacinar: initial distention of peripheral structures (aveolus and associated duct).

[image]

[image]

Lg Airways:

Increase in the size/# of mucous glands, goblet cells, smooth muscle, focal squamous metaplasia.

Ciliary abnormalities.

Partial destruction of bronchial cartilage.

Incr in neutrophils (inflamm).

Small airways:

lumen occlusion by mucus and inflamm cells

fibrosis in walls

Emphysema vs Chronic Bronchitis

1) Major sx

2) appearance

3) PO2

4) PCO2

5) Elastic Recoil of Lung

6) Diffusing capacity

7) Hematocrit

8) Cor pulmonale

Cough is frequently the 1st sx of this disease.  Cough and sputum may precede development of airflow limitation for many years.

Dyspnea

FEV1 post bronchodilator<80% predicted in combination with FEV-1%<70%

The condition results from an imbalance between proteinases and antiproteinases in favor of proteinases.

What condition?

What inhibits proteolytic enzymes in the lung?

Emphysema

Alpha-1-antitripsin

COPD

1) FEV-1% (%)

2) FEV1, FVC, Residual Volume, TLC, Funct Res capacity, DLCO incr/dec

3) ABGs (explain CO2 narcosis)

1) FEV-1%<70%

2) decr FEV1, FVC, DLCO (CO2 Diffusing Capacity).

incr RV, TLC, FRC

3) decr pO2, incr pCO2.

CO2 narcosis= with pCO2>70%, CO2 acts like a narcotic and you fall asleep and die...you must do something quickly! - give pt Albuterol and recheck with spirometry after 15 min.  

COPD Therapy

1) smoking

2) Bronchodilators:compare b2 agonists and anticholinergics (state 2 drugs)

*combo of the two

1) quit smoking

2) 

b2 agonists: short and long acting

anticholinergics:

ipratroprium bromide (4-6hrs) and

tiotropium bromide=Spareeva (1 inhalation=24 hrs).

min adv rxns.

Slower onset and longer duration that b2 agonists.

*Combination=20-40% additional bronchodilation.

Theophylline

*dosage and usage.

Long acting bronchodilator and anti-inflammatory for COPD.

Keep dose low at 5-8ug/mL so that drug interactions don't raise it above 20 ug/mL.

Tiotropium

1) class

2) duration

3) administration

4) tx for...

COPD Therapy

New generation anticholinergic.  Long duration (24 hrs).  Inhaled as dry powder.  Tx for COPD maintenance stages II-IV

Managemnt of COPD: All Stages

1) Avoid noxious agents (name 3) 

2) Vaccinations (name 2)

1) Avoid cigs, air pollution, occupational exposures

2) Influenza and Pneumococcal Vaccine

Management of COPD:

For the following stages, state the FEV-1%, FEV-1, and Sx.  Also state recommended tx

1) Stg I: Mild COPD

2) Stg II: Moderate COPD

3) Stg III: Severe COPD

4) Stg IV: Very Sever COPD

1) FEV-1%<70%

FEV-1 >80%

W or w/o Sx

Tx: short-acting bronchodilators as needed.

2) FEV-1%<70%

50%<FEV-1 <80%

W or w/o Sx

Tx: Prn short-acting bronchodilators, reg tx with long acting bronchodilators, rehab

3) FEV-1%<70%

30%< FEV-1 <50%

W or w/o Sx

Tx: PRN short-acting bronchodilators, reg tx with long acting BDs, inhaled glucocorticosteroids if repeated exacerbations. 

4)FEV-1%<70%

FEV-1 <30%

Presence of resp failure or RHF

Tx: see stg III + long-term O2 therapy if resp failure, surgical tx.

ABX for acute exacerbations of COPD (*will not eliminate organisms)

1st line

2nd line

1º: amox, cefaclor, bactrim

2º: azithro, clarithro, fluoroquinolones

What is the most common pathogen for TB in the US?

State its shape, motility, living arrangement, incubation pd, growth time, and staining procedure

Mycobacterium tuberculosis

Non-motile rod, intracellular aerobe, 3-18wk incubation, slow generation time, ACID-FAST

[image]

What are the key differences between TB infection and disease?

Describe the pathogenesis of TB.

Make sure to talk about how no infection results, primary TB, latent TB, reactivation, and progressive primary TB.  State which stages are symptomatic.

**Which phase is biggest problem in USA??

Droplet pass mucocillary clearance and carried into lung...ingested by aveolar macrophages...

...opt 1: macrophages kill bacilli & NO INFECTION results.

...opt 2: PRIMARY TB: bacilli multiply and escape macrophages.  Some remain local, others disseminate via blood/lymphatics.  PPD prob negative/asymptomatic at this point....can go 2 ways

#1....LATENT TB=infection: in immunocopetent pts, bacilli encased, forming granulomas.  May have radiographic findings. POsitive PPD. Asymptomatic

....reactivation of LATENT TB: when immune system wanes as pt ages or develops DM.  Granulomas breakdown.  Bacilli in lungs migrate to apex (high O2).  Sx: cough, nightsweat, fever.

#2...PROGRESSIVE PRIMARY TB=disease: in immunocompromised pts.  Symptomatic

**Reactivation is biggest issue in USA.

Insidious onset with rapid progression.  Sx: fever, anorexia, weight loss, wasting, night sweats, chronic cough, dyspnea, hemoptysis.

What is this condition?

When and what do you hear upon lung auscultation?

What do you see in lung inspection?

CXR signs?

TB.

Postussive apical rales

Signs of resp distress

POssible consolidation.

Describe the Mantoux test and reading in FULL:

What are 2 causes of false positives?

=TB skin test...

-0.1mL purified protein derivative (PPD)

injected intradermally injection via tuberculin synringe/27 gauge on volar surface of forarm.

-Read in 48-72 hrs areas on INDURATION (not erythema)

+PPD 5mm: recent exposure, radiographic evidence of old TB, HIV+, organ transplants, immunosuppressed, PREDNISONE>1mnth.

10mm: immigration from endemic area<5yrs, IV druggies, hospital workers, institutionals, DM, Chronic Renal Failure, Silicosis, Gastrectomy, lymphomas/leukemia, CA of ENT/lung, weight loss >10% body weight.

15mm: no risk factors.

False positive PPD: BCG (Bacillus Calmette-Guérin) Vaccine or Non-TB mycobacteria (MAC, M. Kansasii)

What would be a positive PPD for....

1) Organ transplant pt

2) Hospital Worker

3) a person who just lost more than 10% of their ideal body weight.

4) Silicosis*

5) HIV

6) Hx of old TB

7)Immigrant from endemic area that moved here 4 yrs ago

8) hospital workers

9) Lymphoma, Leukemia, ENT, Lung Cancers

10) jailed up

11) heroin addict

12) Person on prednisone* for 2 months

13) DM

1) Organ transplant pt= 5mm

2) Hospital Worker=10mm

3) a person who just lost more than 10% of their ideal body weight=10mm

4) Silicosis*=5mm

5) HIV+=5mm

6) Hx of old TB=5mm

7)Immigrant from endemic area that moved here 4 yrs ago=10mm

8) hospital workers=10mm

9) Lymphoma, Leukemia, ENT, Lung Cancers=10mm

10) jailed up=10mm

11) heroin addict=10mm

12) Person on prednisone* for 2 months=5mm

13) DM=10mm

*Silicosis: Chronic lung diseases caused by exposure to a mineral dust or a metal. The major pneumoconioses include asbestosis, silicosis, coal workers' pneumoconiosis (black lung disease), and chronic beryllium disease.

*Prednisone is a synthetic corticosteroid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. It is used to treat certain inflammatory diseases and (at higher doses) cancers, but has significant adverse effects.

What is the standard method of TB testing for healthcare workers?

Describe the 3 possible results.

What is a true conversion?

2-step testing.

PPD planted than replanted in 1-3 wks.

(-)(-)=(-)

(+)=(+)

(-)(+)= booster phenomenon awoke immune system, not a recent converter.

True converter= incr in >/=10mm induration within 2 year pd.

CXR for TB.  What TB stage are the following findings?

1) Infiltrates, nodules, cavitary disease, miliary lesions

2) Cavitation

3) Inflitrate in middle or lower lobes, possible hilar/paratracheal adenopathy, segmental atelectasis, pleural effusion

4) Ghon (calcified primary focus) & Ranke (calcified hilar lymph node) complexes

1)REACTIVATION: Infiltrates, nodules, cavitary disease, miliary lesions

2) PROGRESSIVE PRIMARY: Cavitation

3) PRIMARY TB: Inflitrate in middle or lower lobes, possible hilar/paratracheal adenopathy, segmental atelectasis, pleural effusion

4) LATENT TB: Ghon (calcified primary focus) & Ranke (calcified hilar lymph node) complexes

[image]

1=ghon focus

2=hilar lymph node infected with TB

[image]this arrow shows a cavity of TB

**MILIARY: Its name comes from a distinctive pattern seen on a chest X-ray of many tiny spots distributed throughout the lung fields with the appearance similar to millet seeds, thus the term "miliary" tuberculosis. Miliary TB may infect any number of organs including the lungs, liver, and spleen. It is a complication of 1-3% of all TB cases

In the dx of TB, what % of cases have positive sputum smears for AFB?  What does a positive sputum smear mean for infectivity?

What is used for a DEFINITIVE Dx of M.tb? (Give percent sensitivity).  What is the problem with this method (and an alternative to the problem).

Only 50% of TB cases have positive sputum smears for AFB.  Positive smears=more infectivity.

Sputum Culture used for def dx and is positive in 80% of cases.  BUT, it can take days to weeks, depending on growth medium.  Nucleic acid amplification is faster.

Tx of latent TB in immunocompetent and immunocompromised hosts.

When do you do LFTs?

Immunocompetent:

Isoniazid (INH) + Pyridoxine (Vit B6) x 9mnths

*LFTs if HIV, preggers, liver disease, alcohol.

Immunocompromised (or can't do 9 mnths):

Rifampin (10mg/kg to max 600mg) x

4mnths

OR

Rifampin or rifabutin with pyrazinamide (PZA) x 2mnths.

*check LFT baseline, and at 2,4,6 weeks

start with 4 drug therapy in areas with greater than 4% drug resistance

Isolate pt or N95 respiratory masks. Discontinue if recieved meds for 10-14d, not coughing, or AFB smears neg

a chronic inflammatory disorder of the airways due to increased hyperresponsiveness.

Sx: recurrent wheezing, coughing, SOB.

Often reversible spontaneously or with tx.

FEV-1% reduced

Name 3 asthmatic PREFORMED inflammatory mediators and 2 effects.

What is airway remodelling? (Cause and reversibility)

Histamine, Serotonin, Proteolytic Enzymes

Effects: direct bronchoconstriction (smooth muscle stimulation) and disruption of epithelial layer (swelling, edema)

Airway remodelling caused by inadequate tx of asthma with solely bronchodilators...you need to tx with anti-inflammatories as well.  THis is irreversible!

Pt presents with acute episode of wheezing, SOB, chest tightness, chest pain, sputum production, and cough (which may be present without wheezing)

Name triggers of asthma

environmental

infections

drugs

diseases

allergens, sdtress, changes in weather, exercise, cold air, strong emotion

viral infections, chemicals, drugs (b-blockers, NSAIDS), additives (sulfites), GERD, endocrine (pregnancy)

Laryngeal Asthma

(vocal cords should open with inspiration/expiration)

*this is not really asthma: just a misnomer*

Dx of Asthma

1) Hx

2) Physical Exam:

2a) Lung Inspection, Percussion, Auscultation (*what does it mean if nothing heard during attack?)

2b) RR, HR, speech

3) PFTs:

3a) During attack, FEV-1%=?.  What does this qualify as? When does it improve?

3b) 3 bronchodilator responses

3c) Peak flow variability for dx.

3d) 3 Bronchoprovovation Tests

hx: reccurrent attacks triggerred by asthma triggers with return of functions betwn episodes.  Helpful if FH of asthma.

2) Phys Exam:

a) Airtrapping (incr AP diam), accessory muscles, hyperress on percussion, Wheezing. *No wheezing during attack=large mucous plug)

b) tachypnea, tachycardia, speech fragmented

3) PFT-

3a) FEV-1%<75%=obstructive lung disease. Improves with bronchodilators.

3b)Meet 1 of 3

*12%  in FEV-1 AND >200cc improvement

*12% in FVC AND >200cc improvement

*30% FEF 25-75% improvement

3c) Peak flow meter (cheaper than spirometry) >20% variatiability.

3d) Nonspecific (methacholine, histamine, carbachol), cold air challenge, exercise challenge.

Corticosteroids: Inhaled -

-most common

-don´t cross into blood= high potency but low absorption = less adv rxns.

-Block production of arachidonic acid metabolites (no PGD2, no leukotrienes) by blocking phospholipase A2 enzyme...prevents inflamm cell influx and activation in airway.

Which 2 asthma drugs (1class) prevent the degranulation and release of mast cell mediators and therebye prevent airway inflammation?

Used more commonly in what age group and why?

What are 2 negatives about these drugs?

Mast cell inhibitors: Cromolyn, Nedocromil

Used more commonly in children to avoid inhaled steroid use which is shown to slow, not stunt, growth.

Cause cough and tastes bad.

What anti-inflammatory agent would you use to treat an asthmatic with RA?

What do you need to monitor while pt is on this drug?

Zileuton: prevents production of all leukotrienes

*RA: can't give steroidal.

**This drug can cause liver function impairment...monitor LFTs**

What is the most potent class of bronchodilators for asthma tx and preferrred administration route?

What is a commonly used inhaled anticholinergic agent to cause bronchodilation (relaxion of smooth muscle) in asthmatics?

-When/how is it most useful?

-What disease is it more useful in treating?

Ipratropium Bromide

-Most useful as additive withe B2-agonist in severe acute asthma attack

-More useful in treating COPD

Asthma Summary:

A 57 y.o. smoker presents with progressive dyspnea on exertion and dry cough over 6 months. He has worked as an accountant all his life, has no pets and denies known occupational exposures.

Physical exam:

fine bilateral inspiratory crackles

+1 digital clubbing,

ABG:    pH = 7.42, PO2 = 57 mmHg, PCO2 = 39 mmHg

Lab Tests:   Unremarkable ANA and RF both positive at 1:40 titer.

PFT’s:   

FVC 64% predicted

FEV1 62% predicted,

FEV1/FVC 80%

TLC 60% predicted,

DLCO 38% predicted

Idiopathic Pulmonary Fibrosis-

-insidious onset on Sx in middle aged and older pts

-associated with tobacco (75%)

-HRCT (high res CT): peripheral/subplueral abnmlities

-CV seroligies (ANA, RF) low titer and non-specific

-Surgical lung biopsy for Dx

In the following collagen vascular diseases (state the full name), which lung diseases do you see (can choose more than 1).

Collagen Vascular Diseases

1) SLE

2) RA

3) PSS

4) SS

5) PM/DM

6) MCTD

Choices of Lung Diseases

a) pleural disease

b) insterstitial pneumonia

c) atelectasis

d) parenchymal nodules

Collagen Vascular Diseases:

1) SLE (lupus): Pleural Disease, Atelectasis, ISpneumonia

2) RA (rheuma arth): IS pneumo, Pleural disease, parenchymal nodules

3) PSS (progressive systemic sclerosis): IS pneumonia

4) SS (sickle cell): IS pneumo

5) PM/DM (polymyositis/Diabetes): atelectasis, IS pneumo

6) MCTD ( mixed connective tissue disease): IS pneumonia

Choices of Lung Diseases

a) pleural disease

b) insterstitial pneumonia

c) atelectasis

d) parenchymal nodules

A 32 y.o. female presents with one week of raised, red, tender skin lesion on her legs, knee and ankle pain (anthralgias), and dry cough. 

PE: temperature is 100ºF; lungs are clear to auscultation.  

CXR displays bilat hilar adenopathy (BHA).

What is the dx?  (*What is the rash?)

Sarcoidosis with Lofgrens Syndrome

Characterised by:

*Erythema Nodosum

Anthralgias

Bilat hilar adenopathy
Fever

This disease is characterized by development of non-caseating granulomas in 1 or more organs.

Unknown etiology, tho may be hypersensitivity rxn.

Onset in young adults, females>males, blacks>whites (in US).

Labs reveal hypercalcemia, elevated LFTs, elevated ACE (angiotensin-converting enzyme)*.

What is this?  What is the most common organ involved in 90% of cases? What is a good Dx method?

Sarcoidosis:

Can involve any organ, but resp system most common (90%)

Dx by biopsy, for lung=bronchoscopy.

ACE* Angiotensin-Converting Enzyme: ACE is ordered when you have sx such as granulomas, chronic cough or SOB, red watery eyes, and/or joint pain that may be due to sarcoidosis or to another disorder. This is especially true if you are between 20 and 40 years of age, when sarcoidosis is most frequently seen.

This disease appears more frequently in white smokers. 

Presentation of dyspnea, cough, spontaneous PTX.

CXR: upper/middle lobe ILD, no costophrenic angle involvement.

CT scan: upper lobe cysts w/ small peribronchial stellate nodules.

What is the Dx?

What is the pathology? (state cells, granules, and antigen stain)

What is the Tx

Pulmonary Langerhans' Cell Histiocytosis

Pathology: Langerhan's cells with Birbeck granules and positive staining for CD1a antigen.

Tx: d/c cigs, ¿corticosteroids?

Interstitial lung disease with onset 20+ years after exposure (often occupational exposure: miners, insulators, boiler workers, ship yard workers, pipe fitters, sheet metal workers, and spouses of stated occupations).

What is this and what are 4 other manifestations (2 benign, 2 malignant) of this exposure?

Asbetosis.

Other manifestations of asbestos:

1) Pleural Plaques - benign pleural thickening; marker of asbestos exposure.

2) Benign asbestos pleural effusion

3) Lung CA

4) Mesothelioma: highly fatal malignancy 30-40 years after exposure onset.  No therapy.  Unrelated to pleural plaques.

Rare disorder of surfactant metabolism resulting in accumulation of abnorml lipids and proteins in aveolar spaces.

2º cases (10%) causes: hematologic malignancies, acute silica exposure.

CXR: bilat peripheral airspace disease (batwint/butterfly) resembling pulm edema.

HRCT: crazy paving= patchy ground-glass and interstitial opacities.

BAL (bronchoaveolar lavage): milky white, PAS(?) positive, lipid macrophages.

What is the DX and TX?

Dx: Pulmonary Aveolar Proteinosis

Tx: Whole lung lavage via ET tube

New GM-CSF (granulocyte-macrophage colony stimulating factor)

A 47 y.o. male presents with acute onset of dyspnea, dry cough, fever and myalgias.  

PE: T=101°, bilateral inspiratory crackles

CXR: Bilateral fine reticular markings greatest in the mid lung fields.

PMH:

-2 hospitalizations for pneumonia within the last year, with complete response to a course of azithromycin. 

SH: 40 pack-year of smoking history and works as a laborer on a local farm

LAB:

-Stains and cultures of sputum and bronchoalveolar lavage specimen = clear. 

-Transbronchial biopsy shows loosely formed granulomas.

Hypersensitivity Pneumonitis

Immunologic disease of the lung due to repeated or prolonged exposure to variety of organic dusts in suseptible individual.

Pathology=mononuclear cell infiltration and loosely formed granulomas.  Biopsy not req for Dx.

Reticulo-nodular CXR infiltrates may normalize btwn acute episodes.

**WHAT IS THIS?**

What are 2 common antigens?

Therapy?

Hypersensitivity Pneumonitis

acute - repeate acute ¨pneumonia¨

subacute- slow onset, less systemic sx

chronic- slowly progressive w/ chronic interstitial abmlties

Common antigens: Farmer's lung, bird-fancier's lung

Therapy: avoidance, corticosteroids prn.

Pt presents with recent history of flu-like symptoms which progressed to dyspnea and dry cough.

CXR: patchy infiltrates

You knew what this was and confirmed your dx with surgical lung biopsy.

You treated with corticosteroids for 6-12mnth.  Pt has recovered.

Causes:  80% idiopathic, 20% collagen vasc disorders, viral infections, drugs, transplant, radiation therapy.

What is it?

Pt presents with hemoptysis as well as lower and upper airway sx. 

Glomerulonephritis involved.

CXR: multiple nodules, masses, infiltrates, cavitation.

Dx confirmed by c-ANCA presence.

Tx: cyclophosphamise + corticosteroids.

Pt presents with hemoptysis and renal dysfunction.

CXR: diffuse aveolar hemorrhage.

Dx by prescence of Anti-GBM antibody.

Tx: plasmapheresis + corticosteroids + cyclophosphamide.

What is it?