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CPR II Exam #1 > Pulmonary Pathology II > Flashcards

Pulmonary Pathology II Flashcards

1
Q

Clinical findings of IPF

A

Basilar infiltrates, leading to honeycombing
Dyspnea
Velcro rales
Restrictive pattern on PFT (dec. DLco, FVC)

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2
Q

Contributing factors to development of IPF

A

Environment - industrialized places, smoking.

Genetics

Age >50 y/o

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3
Q

How is IPF DX?

A

High-res CT or pulmonary BX.

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4
Q

What will a pulmonary BX show in IPF?

A

Usual interstitial pneumonia

  • normal areas
  • inflammation
  • fibroblast foci
  • peripheral honeycombing
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5
Q

How long do patients die after receiving DX of IPF?

A

Approx 3-5 years from respiratory DZ

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6
Q

What are some therapies to treat IPF? (2)

A

Lung transplant

Meds to arrest fibrosis (tyrosine kinase inhibitors and TGF-beta inhibitors)

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7
Q

Non-specific interstitial pneumonia (NSIP) develops how?

What is its histology?

What is the prognosis?

A

Idiopathic.

Has unique histology:

  • uniform infiltrates (uniform inflammation/fibrosis)
  • no hetergeneity
  • no fibroblast foci
  • no granulomata

Better than usual interstitial pneumonia (UIP).

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8
Q

Cryptogenic organizing pneumonia (COP or BOOP) presentation:

What is seen on histology?

How is it DX?

What is the prognosis?

A

Pneumonia-like consolidation. 5th/6th decades of life.

Fibroblast foci (Masson bodies) - organizing plugs of CT.

DX of exclusion - not infections, drug or toxin induced or related to CT DOs.

Prognosis is good, and pts. tend to fully recover w/ steroids.

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9
Q

Which Autoimmune or CT DZs can manifest as ILD? (3)

Which ILDs? (3)

A

RA, Systemic sclerosis, SLE

UIP, NSIP, Organizing pneumonia (BOOP)

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10
Q

What determines the prognosis of an autoimmune-related cause of ILD?

A

The underlying AI DZ.

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11
Q

Sarcoidosis def:

Clinical presentation:

A

Systemic DZ manifesting non-caseating (non-necrotizing) granulomata.

Presentation is usually incidental on CXR or dyspnea.

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12
Q

What is seen on histology in a patient w/ sarcoidosis?

A

Granuloma inclusions including:

  • asteroid bodies
  • Schaumann bodies
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13
Q

What is the demographic for pts. w/ Sarcoidosis?

What is the COD?

A

<40 y/o
10x many in AA

COD may be from pulmonary, cardiac or neurologic involvement.

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14
Q

What enzyme is elevated in a pt. w/ Sarcoidosis?

A

ACE

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15
Q

Hypersensitivity pneumonitis may mean prior exposure to: (3)

A

Immune reaction to inhaled Ag

  • Pigeon-feeder’s lung
  • Farmer’s lung: Actinomycetic spore in hay
  • Hot-tub lung: reaction to mycobacterium avium complex (MAC)
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16
Q

What typically exists in a patient w/ Hypersensitivity pneumonitis?

DX of HP requires:

A

Airway-centered granulomata w/ associated lymphocytes

Hx

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17
Q

Desqaumative interstitial pneumonia (DSIP) presents in what age/patient?

What kind of lung DZ is it?

What does histology show?

What is the prognosis?

Tx?

A

Smokers in 4th-5th decades.

Restrictive lung DZ.

Histology shows characteristic “stuffed” alveolar spaces full of Mo.

Good prognosis, >95% survival at 5 yrs.

Smoking cessation, corticosteroids.

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18
Q

Respiratory Bronchiolitis-Interstitial Lung DZ (RB-ILD):

What age/patient does it present in?

How is DX made?

A

Part of a spectrum w/ DSIP, but less symptomatic and earlier presentation.

Smokers in 3rd-4th decades.

CXR abnormalities prompt BX for DX.

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19
Q

What 3 features exist in the histology of RB-ILD?

Is it reversible?

A

Mo present to lesser extent than DSIP.

Peribronchiolar metaplasia (abnormally located ciliated cells).

Possible fibrosis in advanced stage.

Can be reversible w/ smoking cessation if caught early enough.

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20
Q

Langerhans cell histiocytosis presents in what patient population?

What is the pathologic progression?

What exists on histology?

Reversible?

A

Young smoker w/ stellate lung lesions

Progressive scarring leads to cysts. Cysts may rupture and present w/ PTX.

Eosinophils, Langerhans cells, varying fibrosis and cysts.

Possible w/ smoking cessation

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21
Q

Pulmonary alveolar proteinosis def:

What accumulates?

Tx?

A

Impairment of surfactant metabolism due to defect in granulocyte-macrophage colony stimulating factor (GM-CSF). Can be AI (most common), secondary or hereditary (rare).

Surfactant accumulates throughout alveoli and airspaces.

Tx w/ subQ GM-CSF.

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22
Q

Pulmonary infarct gross appearance

A

Wedge-shaped lesions. Begins as hemorrhagic, then fibrosis sets in.

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23
Q

What setting can cause a bone marrow embolism?

A

Trauma

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24
Q

What patients do talc embolism occur?

A

IV drug users

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25
Q

How can IE lead to embolism?

A

A vegetation from a valve can break off and get lodged in the pulmonary vasculature

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26
Q

What is the definition of pulmonary HTN?

A

Pulmonary artery pressure greater than 25 mmHg

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27
Q

What are the WHO subgroups of pulmonary HTN? (5)

A

Pulm. arterial HTN (PAH) - primary vascular DZ

Secondary to LHF

Secondary to chronic pulm parenchymal DZ or hypoxia

Secondary to thromboembolic pulm DZ

Multifactorial

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28
Q

2 major histological features of pulmonary HTN

A

Plexiform lesions

Medial hypertrophy (SM in small arteries)

29
Q

Goodpasture syndrome tends to occur in what patients?

What is the pathogenesis?

What is the clinical DZ a result of?

A

Males in their 2nd-3rd decades.

Abs against non-collagenous subunit of collagen IV.

Clinical DZ results from AB-mediated damage to basement membranes in lung and kidney.

30
Q

What type of hypersensitivity is Goodpasture syndrome?

A

Type 2

31
Q

What is the leading COD in children >5 y/o?

A

Pneumonia

32
Q

Pneumonia is the most common cause of:

A

Sepsis and septic shock (50%)

33
Q

4 stages of lobar pneumonia

A
  1. Congestion: vascular engorgement.
  2. Red hepatization: red cells and inflammation.
  3. Grey hepatization: inflammation and debris.
  4. Resolution: fibrosis, Mo clean-up.
34
Q

What are some complications of lobar pneumonia?

A

Abscess
Empyema
Bacteremia

35
Q

Community-acquired bacterial pneumonia can be from what pathogens?

A 
S. pneumoniae
H. influenzae
S. aureus
K. pneumoniae
P. aeruginosa
L. pneumophilia
M. pneumoniae
36
Q

Most common cause of commuity-acquired bacterial pneumonia is:

What do these bacteria look like?

What is the vaccine recommendation?

A

S. pneumoniae

Lancet-shaped G+ diplococci

Vaccination recommended for infants, pts. >65 y/o and in respiratory DZ/smoking Hx.

37
Q

H. influenzae is more prevalent among:

Vaccine recommendation?

A

Most prevalent amongst kids.

Vaccine recommended for type B for kids <5 y/o.

38
Q

S. aureas can cause ______ formation.

What patients is it seen in most?

A

Abscess formation.

Mostly seen in IV drug users.

39
Q

K. pneumoniae is seen most in what patients?

What does the sputum look like?

A

Alcoholics.

Currant jelly sputum.

40
Q

P. aeruginosa is seen in tandem w/ what DZ?

A

CF

41
Q

Typical pneumonia

Onset:
SX:
On CXR:
Pt. pop:

A

Onset: abrupt
SX: respiratory predominate
On CXR: consolidation
Pt. pop: older adults or young kids

42
Q

“Atypical” or Walking Pneumonia

Onset:
SX:
On CXR:
Pt. pop:

A

Onset: slower
SX: systemic SX predominate
On CXR: patchy infiltrates
Pt. pop: young adults, teens, older kids

43
Q

Common causes of atypical “walking” pneumonia

A

Mycoplasm pneumoniae
Legionella
Chlamydia pneumonia
Chlamydia psittaci

44
Q

What is unique about Mycoplasma pneumoniae?

A

Smallest free-living, self-replicating microorganisms known.

No cell wall.

45
Q

Legionella Gram stain:

Where is it found?

A

G+ bacillus

Warm freshwater, or airborne

46
Q

Hemagglutinin

Neuramidase

A

Protein that attaches to cells.

Allows release of replicated virus from cells.

47
Q

Antigenic drift

A

Epidemics.

Minor changes to proteins (Ags) on virus allowing increased spread.

Can be similar enough to other viruses to allow for some immunity.

48
Q

Antigenic shift

A

Pandemics.

Genomic alterations w/ major protein changes.

No immunity for almost everyone.

49
Q

Severe acute respiratory syndrome (SARS) is from what virus?

Where did it originate?

When was the outbreak?

A

Coronavirus

China

Worldwide outbreak from 2002-2004

50
Q

3 most common causes of bacterial neonatal pneumonia

A

Grp B Strep
G- bacillus
Listeria

51
Q

What are the most common causes of viral pneumonia in children > 1 mo?

A 
RSV*
Parainfluenze virus
Influenze A/B
Adenovirus
Rhinovirus
52
Q

What are the most common causes of bacterial pneumonia in children > 1 mo?

A

S. pneumoniae
H. influenzae
M. catarrhalis
S. aureus

53
Q

RSV is caused by:

SX?

A

Paramyxovirus

Rhinorrhea, cough, wheezing, dyspnea, tachypnea, cyanosis.

54
Q

Histologically, where do bacteria invade in pneumonia vs. viruses?

A

Bacteria invade in the alveolar spaces.

Viruses invade the interstitium.

55
Q

With which 2 pneumonias can lung abscesses occur?

A

S. aureus

K. pneumoniae

56
Q

What 3 scenarios might an aspiration pneumonia occur?

Can aspiration pneumonia lead to lung abscesses?

A

Chronic alcoholics
Elderly pts. (stroke)
Anaerobic bacteria

Yes

57
Q

When was the Swine Flu epidemic?

What country?

Death count?

A

2009

Mexico

> 200K

58
Q

How do bacterial vs. viral infections differ on CXR?

A

Bacterial: lobar or consolidated appearance.

Viral: diffuse infiltrates.

59
Q

In what type of infection are epidemics more common?

A

Viral

60
Q

3 fungi common in chronic pneumonia

A

Histoplasma
Blastomycosis
Coccidiomycosis

61
Q

Histoplasma capsulatum is endemic in which areas?

What is the course of the infection generally?

What is the unique fungal characteristic seen on morphology?

Can it ever be more aggressive?

A

Midwest and Caribbean.

Usually subclinical infection w/ granulomatous response (calcifications or coin lesions on CXR).

Yeast forms “pumpkin seed” morphology.

It can have a more aggressive course in the immunocompromised.

62
Q

Blastomyces dermatitides is endemic in which areas?

What does the infection cause?

What is the unique yeast form on morphology?

Where else (besides) lungs can it infect?

A

Central and SE US.

Granulomatous response.

Broad-based budding.

Skin, but rarely becomes disseminated infection.

63
Q

Coccidiodes immitis is endemic in which areas?

What kind of infection does it cause?

What is the course?

Can it ever become disseminated?

A

SW US and Mexico.

Granulomatous infection w/ eosinophils.

Usually subclinical and self-limited.

Can be disseminated in the immunocompromised.

64
Q

Pneumocystis jiroveci (carinii) features:

Characteristic morphology:

How does it look on CXR?

A

Opportunistic fungal infection. AIDS-defining illness.

Cup-shaped yeast forms.

Can be diffuse or focal or anything else.

65
Q

Mycobacterium avium complex (MAC) is found mostly in what patients?

What does it look like on histology?

A

Immunocompromised elderly pts.

Thin mycobacterium look slender red on acid-fast stain.

66
Q

What most impacts the differential for the cause of a pneumonia infection?

A

Setting/method of acquisition

67
Q

In lung transplant patients, rejection shows which features on histology?

A

Mononuclear infiltrates around vessels.

68
Q

What is the unique cell marker for Langerhan’s cell Histiocytosis?

What cell type is abundant on histology?

A

CD1a

Eosinophils clump

CPR II Exam #1 (30 decks)

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