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CPR Exam 1 > Chapter 15: Part 2 > Flashcards

Chapter 15: Part 2 Flashcards

1
Q

What values on PFT indicate a restrictive disease?

A
  1. Lung compliance: reduced
  2. FVC: decreased
  3. FEV1/FVC: NL
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2
Q

Name the interstitial (restrictive) lung diseases that cause fibrosis.

A
  1. Idiopathic pulmonary fibrosis (IPF)
  2. Non-specific interstitial pneumonia (NSIP)
  3. Cryptogenic organizing pneumonia (COP)
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3
Q

A disease caused by irritiants and toxins that cause waves of inflammation (endothelial activation/injury), causing wound healing and interstitial fibrosis, damaging lung tissue in the alveoli “SCARING LUNG TISSUE”

A

IPF (Interstitial pulmonary fibrosis)

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4
Q

Idiopathic Pulmonary Fibrosis is a disorder where waves of inflammation and injury lead to fibrosis.

What clinical findings will we see in a patient?

A
  1. CXR: Basilar infiltrates that lead to honeycomb lung
  2. SOB (dyspnea)
  3. Velco-like crackles on exam
  4. Restrictive patterns on pulmonary function test (decreased lung volume, DLco and FVC)
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5
Q

Idiopathic Pulmonary Fibrosis (IPF) has no known cause. However, what populations do we see it highest in?

A

1. Increasing age (>50)

2. Smokers

3. Industrial areas

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6
Q

What is the pathogenic mechanism of IPF?

A
  1. Env triggers + genetics damage epithelium.
  2. Injured/activated epithelium release factors => + interstitial fibroblasts.
  3. Interstitial fibroblasts cause abnormal signaling via P13K/AKT.
  4. Fibroblasts deposit collagen => interstitial fibrosis => respiratory failure
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7
Q

Idiopathic pulmonary fibrosis is a disease most common in which age group?

A

>50

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8
Q

Diagnosis of IPF requires what?

A

Classic findings on CT or biopsy of the lungs showing UIP (usual interstitial pneumonia).

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9
Q

On biopsy, what do we see in IPF (Idiopathic Pulmonary Fibrosis)?

A

4 different findings because IPF occurs in a wave:

    1. Normal areas
  • 2. Inflammed areas
  • 3. Fibroblast foci
  • 4. Peripheral honeycombing (cystic spaces of air)
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10
Q

Microscopically, what is the hallmark of Idiopathic Pulmonary Fibrosis; there is coexistence of what?

A
  • Patchy interstitial fibrosis***, which varies in intensity and age
  • Both early fibroblast proliferation(fibroblastic foci) and late (collagenous) lesions, bc inflammation occurss in waves
  • NL tissue
  • Honeycomb fibrosis (cystic spaces)
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11
Q

What is honeycomb fibrosis?

A

Cystic spaces of air that are lined with type 2 pneumocytes or bronchiolar epithelium

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12
Q

What indicates that we have an early lesion formed by IPF?

A

Fibroblastic proliferation (fibroblastic foci)

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13
Q

What is the course of IPF?

A

Progressive. If diagnosis is made, most people die 3-5 years after unless transplant

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14
Q

What are potential treatments to IPF?

A
    1. Lung transplant
    1. Meds that stop fibrosis (tyrosine kinase inhibitors and TGF-B inhibitor)
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15
Q

Why is it important to recognize pt’s with Nonspecific Interstitial Pneumonia?

A

Have much better prognosis than those w/ UIP

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16
Q

What is a major morphological difference between the lesions of Nonspecific Interstitial Pneumonia and Idiopathic Pulmonary Fibrosis?

A
  • In NSIP the inflammation/ pathy fibrosis are SAME stage of development and will be mild-moderate
  • Thus, is NO heterogeneity.
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17
Q

What 4 morphologial findings are does Nonspecific Interstitial Pneumonia NOT have?

A
  1. - NO fibroblastic foci
  2. - NO honeycombing
  3. - NO hyaline membranes
  4. - NO granulomas
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18
Q

What is this?

A

Nonspecific Interstitial Pneumonia (NIP);

Uniform pattern of inflammation; interstitium is thick and has inflammatory cells; all same age

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19
Q

Which population is most likely to be affected by Nonspecific Interstitial Pneumonia?

A
  • Female NON-smokers in their 60s
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20
Q

How do patients with Cryptogenic Organizing Pneumonia (COP) present and what is seen radiographically?

A

1. 50/60s

  1. Pneumomonia like symptoms (cough and SOB)
  2. Patchy SUBpleuralor OR peribronchial areas of airspace consolidation

.

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21
Q

What is the hallmarkhistology seen with Cryprogenic Organizing Pneumonia, inflammation of the small airways (bronchioles)?

A

Intraalveolar fibrosis: plugs of loose, swirly CT (fibroblast foci called Masson bodies in alveoli, alveolar ducts and bronchioles, which is the bodies attempt at fibrosis and scar formation.

Walls will be okay (not harmed)

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22
Q

How do we diagnose COP?

A

Diagnosis of exclusion: make sure not infection, toxins, other CT disorder.

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23
Q

Does honeycombing or interstitial fibrosis occur in COP (crytogenic organizing pneumo)

A

NO

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24
Q

Prognosis and Tx of Cryprogenic Organizing Pneumonia?

A
  • Some recover spontaneously
  • Most need oral steroids x 6 months +for complete recovery
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25
Q

Which 3 autoimmune/CT disease can manifest as interstital lung disease?

A

1. RA

2. Systemic sclerosis

3. SLE

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26
Q

If ILD occurs as a manifestation of RA, SLE, Systemic sclerosis, how are they diagnosed and what is the prognosis?

A

They are not dx as PURE diseases.

Outcome is linked to UNDERLYING (SLE) condition

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27
Q

Which 2 chronic interstitial lung diseases are categorized as granuloma-forming diseases?

A
  • 1. Sarcoidosis
  • 2. Hypersentitivity Pneumonitis
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28
Q

What is this?

A

Granuloma inflammation: nodular collection of epithloid macrophages, giant cells surrounded by a ring of lymphocytes

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29
Q

What is sarcoidosis?

A

Diisease characterized by the growth of tiny collections of inflammatory cells that form non-caseating/non-necrotizing granulomas in any part of your body — most commonly the lungs and lymph nodes.

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30
Q

What is the most common clinical pattern/organs of involvement seen with Sarcoidosis?

A
  • Bilateral hilar LN
  • Lungs

Also occur in eye and skin.

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31
Q

What is the diagnostic feature of Sarcoidosis?

A

Noncauseating granulomas in the tissue

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32
Q

What immune cells are high in patients with Sarcoidosis?

A

CD4+ T cells that secrete TH1 cytokines like IFN-y and IL-2.

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33
Q

Which cytokine found in the bronchoalveolar fluid of pt with Sarcoidosis is a marker of disease activity?

A

TNF, (forms granulomas) in bronchoalveolar fluid => Sarcoidosis

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34
Q

What are the stages of Sarcoidosis?

Which is most common?

Do they go in order?

A
  • Stage 0 (no abnormalities)
  • Stage 1 (hilar lymphandopathy)
  • Stage 2 (hilar lymyphandopathy and lung infiltration)
    • Most common: 25-30% of cases have this.
  • Stage 3 (lung infiltration)
  • Stage 4 (Fibrosis)
  • NO, THEY DO NOT GO IN ORDER.
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35
Q

Is sarcoidosis a progressive disease?

A

no

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36
Q

What is this and how do you know?

A

Sarcoidosis:

Different from other diseases that cause non-causeating granulomas SHARD BORDER between the granuloma and normal tissue

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37
Q

What are 2 characteristic morphological findings within giant cells of pt with Sarcoidosis?

A
    1. Asteroid bodies: stellate inclusions in giant cells
    1. Schaumann bodies: concentration of Ca2+ and proteins in giant cells
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38
Q

What is this?

A

Schaumann bodies (concentrations of Ca2+ and proteins), indicative of Sarcoidosis.

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39
Q

What is this?

A

Asteroid bodies (stellate inclusions), indicative of sarcoidosis.

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40
Q

A biopsy of where is a very good diagnostic source for Sarcoidosis?

A

Bronchial mucosa

ppl have alot of granulomas in the bronchial submucosa

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41
Q

Which LN’s are most frequently affected by Sarcoidosis?

A

Hilar and mediastinal

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42
Q

Which 3 sites other than lungs and LN’s are also commonly affected by Sarcoidosis and what is seen in each?

A
  • Spleen - may be enlarged; granulomas often form small nodules
  • Liver - may be enlarged; scattered granulomas often in portal triad

- Bone marrow - lesions in phalangal bones of hands and feet; small areas of bone resorption within marrow cavity w/ widening of the bony shafts

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43
Q

What 3 types of skin lesions may be encountered in Sarcoidosis?

A
  • Subcutaneous nodules
  • Erythema nodosum
  • Flat, slightly red and scaling, resembling those of SLE
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44
Q

Scattered granulomas associated with Sarcoidosis may be found in the liver, most often where?

A

Portal triads

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45
Q

How are the eyes and glands affected in Sarcoidosis?

A

Eyes: sicca syndrome (dry eyes), iritis, uveitis

Mikulicz syndrome

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46
Q

Elevated serum levels of what enzyme and ion may be seen in Sarcoidosis?

A

- ↑↑↑ ACE

  • ↑ 1ᾳ-hydroxylase –> hypercalcemia
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47
Q

Who does Sarcoidosis most commonly occur in?

A
  1. Young patients below 40
  2. 10-fold more likely in African Americans
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48
Q

What is the recovery of Sarcoidosis; how does death most often occur?

A

60-70% recover

20% have lung disease

Die from cardiac, pulmonary or CNS involvement

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49
Q

What is this?

A

Hypersensitivity Pneumonitis

Different from Sarcoidosis because we see granuloma, but it is NOT surrounded by NL lung tissue.

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50
Q

What is Hypersensitivity Pneumonitis?

A

A spectrum of immunological mediated interstitial diseases caused by inhaled antigens and granulomas formation in airways.

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51
Q

Hypersensitivity pneumonitis affects what structures in the lungs in constrast to asthma?

A

It AFFECTS ALVEOLAR WALLS

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52
Q

Diagnosis of Hypersensitivity Pneumoniitis requires history.

Why is it SO important?

A
  • Disorders such as Pigeon breeder’s lung (rxn to bird shit), Farmers lung (actinomycetic spores in hay) and Hot tub lung (rxn to Mycobacterium avium complex/MAC) are often missed unless a history is taken. -
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53
Q

Presence of noncaseating granulomas in 2/3’s of pt’s with hypersensitivity pneumonitis suggests what type of hypersensitivity rxn?

A

Type 4 T-cell mediated

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54
Q

The histologic changes of hypersensitivity pneumonitis are characteristically centered around which lung structures?

A

Bronchioles

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55
Q

What are 3 histomorphological changes seen with hypersensitivity pneumonitis?

A
  1. Interstitial pneumonitis w/ lymphocytes, plasma cells, and MO
  2. Noncaseating granulomas
  3. Interstital fibrosis w/ fibroblastic foci, honeycombing, and obliterative bronchiolitis (late stages)
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56
Q

What are the 3 Interstitial Lung Diseases that are related to smoking?

A
  1. DSIP (Desquamative Interstitial Pneumonia)

2. RB-ILD (Respiratory Bronchiolitis-Interstitial Lung Disease)

  1. LCH (Langerhans-cell Histiocytes)
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57
Q

What is this?

A

LCH (Langerhan Cell Histiocytosis):

  • 1. Langerhan cells that look like stars, forming lesions
  • 2. Eosinophils
  • 3. Varying fibrosis and cysts
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58
Q

What is this?

A

DSIP (Desquamative Interstitial Pneumonia):

  1. Alveolar spaces are stuffed with brown “smokers MO”
  2. Mild inflammation and little fibrosis
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59
Q

What is this?

How do we know?

A

RB-ILD

  1. MO with a brown tint “smokey” in bronchioles (less than DSIP)
  2. Peribronchiolar metaplasia: ciliated respiratory epitheliid cells move to alveolar septa
  3. If severe, fibrosis
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60
Q

Desquamative interstitial pneumonia is MC in what age group associated w/ what risk factor; what are the sign’s/sx’s?

A
  1. Smokers in between 40-50 YO
  2. Gradual onset of SOB, dry cough that lasts weeks- months and clubbing of fingers
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61
Q

Treatment of DSIP and outcome likelihood?

A

1. Stop smoking and steroids

2. 95% survive

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62
Q

Respiratory bronchiolitis-interstitial lung disease is part of a spectrum with desquamative interstitial pneumonia, except when does it present and what are the sx’s like?

A
  • Presents earlier (30-40 YO)
  • Less symptomatic
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63
Q

In RB-ILD, where are the MO located?

A

1st and 2nd order respiratory bronchioles

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64
Q

Langerhan Cell Histiocytosis is most common in who?

A

Young smokers

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65
Q

Histo in pt w/ Pulmonary Langerhans Cell Histiocytosis will show what?

What is a complication?

A

Stellate shaped nodules that scar => trap air => form a cyst that can pop. If it pops, causes a pneumothorax.

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66
Q

The langerhans cells of Pulmonary Langerhans Cell Histiocytosis will stain positive for what and negative for?

A

Positive: S100 and CD1a

Negative: CD68

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67
Q

Which 2 smoking causing ILD are reversible?

A
  • 1. RB-ILD
  • 2. LCH
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68
Q

What is the unique RLD?

A

PAP (Pulmonary Alveolar Proteinosis)

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69
Q

What is PAP (Pulmonary Alveolar Proteinosis)?

A

Accumulation of surfactant throughout alveoli and airspaces caused by either a :

    1. Defect in GM-CSF (granulocyte MO colongy stimulating factor).
    1. Dysfunction of pulmonary MO
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70
Q

What is the most common cause of PAP?

A

Autoimmune (90%); patient has autoAB againist GM-CSF => dysfunction => alveolar MO cannot break down surfactant properly

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71
Q

Pulmonary Alveolar Proteinosis (PAP) can be treated how if autoimmune vs. secondary?

A
  • Autoimmune = Sub cutaneous injections of GM-CSF
  • Secondary = Tx the underlying disorder
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72
Q

Pulmonary Alveolar Proteinosis (PAP) is characterized by what morphological changes within the alveoli?

A
  1. Proteineosous edema in alveolar spaces with surfactant protein
  2. MINIMAL inflammation
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73
Q

What is found in the alveolar precipitate of Pulmonary Alveolar Proteinosis (PAP) and what does it stain positive for?

A
  • Surfactant protein and cholesterol clefts
  • +PAS (periodic-acid Schiff)
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74
Q

What is the standard of care and provides underlying benefit for pt’s with Pulmonary Alveolar Proteinosis (PAP) regardless of cause?

A

Whole-lung lavage

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75
Q

How do adult pt’s with Pulmonary Alveolar Proteinosis (PAP) present (signs/sx’s)?

A

Cough + shit ton of sputum w/ chunks of jelly material

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76
Q

In what disorder do you see this?

A

PAP (pulmonary alveolar proteinosis): alveoli are filled with protein-lipid edema, but the walls of the alveoli are NL

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77
Q

PAP is most often associated with a mutation in what gene?

A

ABCA3

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78
Q

Fractures of which bone cause a high risk for PE?

A

Hip

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79
Q

How soon can pulmonary infarct be seen on CXR and what is seen?

A
  • 12-36 hours
  • Wedge-shaped d/t the radiating patterns of the vessels
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80
Q

Pulmonary infarction d/t a PE is more likely in who?

A

Ppl without adequate CV functioning

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81
Q

In pt’s w/ adequate CV function, which arterial supply supplies the lung parenchyma following PE; what is seen (hemorrhage/infarction) when a PE is thrown?

A
  • Bronchial arterial supply
  • Ptient will hemorrhage, but NOT INFARCT
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82
Q

How does pulmonary infarction appear morphologically in the early stages and what is seen on the apposed pleural surface?

A
  • Begins hemorrhagic: raised red-blue area.
  • Fibrinous exudate
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83
Q

What occurs 48 hours after pulmonary infarct and what are the morphological changes as time progresses?

A
  • RBC lyse –> infarct becomes paler => red-brown as hemosiderin is produced
  • Over time, fibrosis begins at margins as a gray-white peripheral zone —> contracted scar

SUMMARY: Goes from hemorrhagic => fibrosis

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84
Q

What is the difference in where small and large PE go to?

A
  • Large PE: main pulmonary artery, branches or at the birfurcation of the pulmonary trunk, creating a saddle embolism
  • Small PE: go out more peripherally => cause hemorrhage or infarct.
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85
Q

Which type of emboli are often seen in pt’s who die after chest compressions performed during CPR?

A

Small bone marrow emboli; however, it DOES NOT mean he died BECAUSE of it.

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86
Q

How can we tell if someone died from a clot?

A

Prescence of lines of zahn

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87
Q

PE have what 2 deleterious pathophysiologic consequences?

A

1. Respiratory compromise: area is ventillated, but NOT perfused.

2. Hemodynamic compromise: increased resistance to pulmonary BF

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88
Q

Blood clots that occlude large pulmonary arteries are alsmost always d/t _____ .

What is the usual souce?

A

Emboli

DVT

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89
Q

PE’s usually occur in what people?

A

Ppl with a predisposed condition that makes them more likely to clot.

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90
Q

Majority of infarcts associated w/ PE affect which lobes and occur as (single/multiple) lesions?

A

Lower lobes

Multiple lesions

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91
Q

Besides PE, what else can block a vessel?

A
  1. Blood clot (thromboembolism)
  2. Bone marrow/ fat
  3. Cancer
  4. Septic emboli
  5. Air
  6. Foreign material
  7. Parasites
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92
Q

What is this?

A

Talc embolism are often seen in IV drug users

93
Q

What is this?

A

Septic embolus: Infective materal rom heart valve that causes a local infection, forms an abcess (cyst).

94
Q

In what condition do septic emboli occur?

A

Endocarditis

95
Q

Septic emboli can go to what other places, besides the lung and cause what?

A
  • 1. Skin: janeway lesions
  • 2. Retina: roth spots
  • 3. Nail bed: Splinter hemorrhage
96
Q

If a pulmonary infarct is caused by an infected embolus, there may be intense neutrophilic inflammatory rxn, and these lesions are knowna as what?

A

Septic infarcts

97
Q

Vast majority of PEs are (60-80%) _______

Minority (5%): _______

Remaining _______

A
  • Silent (60-80%)
  • Cause acute cor pulmonale, shock, death d/t saddle
  • Pulmonary infarction
98
Q

How is PE usually DX?

A

Spiral CT angiography

99
Q

Pulmonary HTN is defined as mean pulmonary artery pressure ≥______mmHg at rest

A

greater than 25 mmgHg at rest (cannot measure with BP cuff)

100
Q

What are the 5 classification of pulmonary HTN as classified by the WHO?

A

1. Pulmonary arterial HTN - primarily vascular disease ***

  1. pHTN d/t left-heart failure
  2. pHTN d/t chronic pulmonary parenchymal disease or hypoxemia ***
  3. pHTN d/t to thromboembolic pulmonary HTN
  4. Multifactorial

***Most common

101
Q

Mutation of _____ is indicated in primary pulmonary HTN.

A

BMPR2 mutation on Chr2q33 => endothelial cell and vascular SM proliferation => thickening and occlusion of pulmonary vasculature.

102
Q

All forms of pulmonary HTN are associated with what 3 things?

A
  1. Hypertrophy of medial SM layer in pulmonary and elastic arteries
  2. Atherosclerosis in pulmonary a.
  3. RV hypertrophy
103
Q

Pulmonary HTN affects which BVs?

A

Arterioles and small arteries, causing medial hypertrophy and intimal fibrosis

104
Q

What is this?

A

Plexiform lesions, tangled knot of BVs that is VERY characteristic of long-standing, severe pulmonary HTN

105
Q

What are the 3 pulmonary hemorrhage syndromes?

A
  • 1. Goodpasture
  • 2. Granulomatosis with polyangiitis (Wegners)
  • 3. Idiopathic pulomonary hemosiderosis
106
Q

What finding in patients is common in all pulmonary hemorragic syndromes?

A

Pts will have bright red hemoptosis bc hemorrhaging though lungs. All will have hemosiderin laden MO.

107
Q

What is Goodpasterues syndrome?

A

Disorder where autoAB against noncollagenous domain of collagen 4 destroy BM in glomerulus and aveoli.

108
Q

In Goodpasture Syndrome autoantibodies destroy the glomerular BM in renal glomeruli and pulmonary alveoli giving rise to what disease in each system?

A

- Rapidly progressive glomerulonephritis (RPGN)

- Necrotizing hemorrhagic interstitial pneumonitis

109
Q

Which sex and age group is most often affected by Goodpasture Syndrome?

A
  • Males in teens or 20 who are active smokers
110
Q

What is unique about immunofluorescene of lung in Goodpatures?

A

Linear pattern of deopsition on BM of lung d/t anti-BM AB with RBC present

111
Q

What is the histology of the damage to alveolar walls in Goodpasture Syndrome?

A
  1. Focal necrosis
  2. Intraalveolar hemorrhage
  3. hemosiderin-laden macrophages
112
Q

What type of hypersensitivity reaction is Good Pastures?

113
Q

What are the diagnostically important features of Polyangiitis w/ Granulomatosis (Wegener), in contrast to Sarcoidosis?

A
  • GPA (Wegners): Capillaritis and poorly formed granulomas
  • Sarcoidosis: Rounded, well defined granulomas
114
Q

What is this?

A

GPA: white is inflammed lung and in the middle is coagulated blood; capilartitis and poorly formed granulomas

Lungs are more prone to bleed.

115
Q

Which biopsy technique may provide the only tissue necessary for diagnosis of Polyangiitis w/ Granulomatosis (Wegener)?

A

Transbronchial biopsy

116
Q

What is pneumonia?

A

Pneumonia is any infection to the lung parenchyma/

117
Q

lHow can we classify pneumonia, a pulmonary infection.

A

1. Clinical setting

  1. Anatomic distribution (broncopneumonia or lobar pneumonia)
118
Q

Community-Acquired Pneumonia can be due to what 2 things?

A

1. Bacterial

2. Viral

119
Q

What patterns can bacterial pneumonia produce

A

1. Bronchopneumonia: patchy consolidation

2. Lobar pneumonia: consolidated (air fluid level in cystic space)

120
Q

Lobar pneumonia has an acute progression.

Name the staqes.

121
Q

What are the 4 stages of the inflammatory response for lobar pneumonia?

A

1) Congestion: Lung is boggy and red d/t vascular engorgement and intra-alveolar fluid with neutrophils
2) Red hepatization: Congestion with massive oozing of alveolar spaces w/ lots of neutrophils; RBCS, fibrin => lung is red, firm and airless lk liver
3) Gray hepatization: RBC distengrate, leaving fibrin + inflamm cells
4) Resolution: fibrosis and macrophage clean-up

122
Q

What is a complication of lobar pneumonia?

A

1. Abcess/cyst, walling itself off.

2. Emphyma (pleural space filled with blood)

3. Bacteremia.

123
Q

What bacteria cause typical pneumonia?

A
  1. 1. S. pneumo
  2. 2. H. influenza
  3. 3. S. aereus
  4. 4. K. pneumoniae
  5. 5. P. aeruginosa
124
Q

What are 2 acute phase markers made in the liver that are specific for bacterial infection and can be useful in dx community-acquired bacterial pneumonia?

A

- CRP

- Procalcitonin

125
Q

What is this?

A

Lobar pneumonia

126
Q

How do we clinically diagnose someone with lobar pneumonia?

127
Q

What is the most common cause of community-acquired pneumonia?

A

Strep. pneumoniae

128
Q

How do we dx someone with community-acquired bacterial pneumonia d.t Streptococcus pneumoniae?

A

Sputum culture that shows neutrophils w gram (+) lacet-shaped diplococci

129
Q

What is this?

A

CABP due to Strep pneumo: Gram + lancet shaped diplococci in pairs and chains

130
Q

Vaccination for Strep Pnemo is recommeded for who?

A
  1. Infants
  2. Patients over 65 YO
  3. Pts with Resp disease/smokers
131
Q

What is a cause of common cause of DANGEROUS/VIRULENT pneumonia in children?

What is recommended?

A

H. Influenza

Vaccinate kid 5 years or younger for H. Influenza type B

132
Q

Pneumonia caused by what bacteria is a pediatric emergency due risk of acute epiglottitis w/ high mortality rate?

A

H. influenzae

133
Q

What is the pulmonary consolidation associated w/ H. influenzae typically like?

A

Lobular and Patchy

134
Q

Which patient population is especially susceptible to bacterial pneumonia by Moraxella Catarrhalis?

135
Q

What is the most common cause of gram-negative bacterial pneumonia and who does it most commonly affect?

A
  • Klebsiella pneumoniae
  • Debilitated and malnourished people, particularly chronic alcoholics
136
Q

What type of sputum is characteristic of Community Acquired Klebsiella pneumoniae?

A

Thick, sputum w alot of mucus and blood (currant jelly sputum)

137
Q

Pseudomonas aeruginosa is a common cause of pneumonia in whom and in what setting?

A
  • -Hostpital acquired
  • -Cystic Fibrosis and immunocompromised
138
Q

What bacteria cause atypical (“walking) pneumonia?

A
  • 1. Mycoplasma pneumoniae
  • 2. Legionella pneumopila
  • 3. Chlamydia pneumonia
  • 4. Chlamydia psittaci
139
Q

What is the difference between typical and atypical pneumonia?

  • Onset:
  • Symptoms:
  • CXR:
  • Age group:
A

Typical pneumonia:

  • Onset: Abrupt
  • Symptoms: Mainly respiratory
  • CXR: Consolidated (not patchy)
  • Age group: Young children or older adults

Atypical pneumonia

  • Onset: Slower onset
  • Symptoms: Systemic sx (may not have resp sx)
  • CXR: Patchy infiltrates
  • Age group: Older children - teens- young adults
140
Q

Which is atypical pneumonia and which is typical?

A

Left is typical bc it is consolidated

Right is atypical bc it is patchy and has lines

141
Q

Which bacteria cause of pneumonia live in warm freshwater (i.e., AC units, misters, hot tubs); what does it live inside?

A

- Legionella pneumophila

- Lives in amoebas

142
Q

What type of pneumonia affected more than 1 person at once at the American LEgion because they were drinking FRESHWATER

A

Legionella pneumophila induced pneumonia

143
Q

What are the 2 common modes of transmission for Legionella pneumophilia?

A

1. Airborne

2. Drink contaminated water

144
Q

What is the gram stain and morphology of Legionella pneumophila?

A

Gram NEGATIVE bacillus

145
Q

Mycoplasma pneumoniae infections are common in which age groups and occur most often how?

A

- Children and young adults

  • Sporadically or as local epidemics (i.e., schools, military camps, prisons)
146
Q

What is unique about Mycoplasma pneumonia?

A

ISmallest free-living organism and has NO CELL WALL so it is EASILY TREATED

147
Q

Which pattern of bacterial pneumonia is often multilobular and frequently bilateral and basal?

A

bronchopneumonia

148
Q

What are causes of community-acquired viral pneumonia?

A
  • 1. Influenza (H1N1)
  • 2. SARS
  • 3. RSV (respiratory syncytial virus)
149
Q

Tissue destruction and abscess formation as a complication of pneumonia are most common associated w/ what 3 organisms?

A
  1. - Type 3 pneumococci
  2. - Klebsiella
  3. - S. aureus
150
Q

What are the 2 virulence factors of H. Influenza virus, allowing it to cause infections; function of each?

A
    • Hemagglutinin: allows for attachment to cells; via sialic acid residues
    • Neuraminidase (NA): allows release of replicated virus from cells by cleaving sialic acid residues on hemagglutinin
151
Q

What is the action of Tamiflu?

A

Tamiflu prevents the spread of H. influenzae by blocking neuraminidase, preventing cleaving of sialic acid residues => prevents virus from being able to infect other cells.

153
Q

What is the difference between antigenic drift and antigenic shift in regards to H. Influenza?

Which causes epidemic and pandemic?

A

Antigenic drift: point mutations to HA/NA antigens => virus is slightly altered => spread increases => epidemic but is similar enough to the original virus to allow for some immunity

Ex. seasonal flu

Antigenic shifts: antigenic RNA segments of HA/NA switch between species through recmobination => forming a new virus that no one is immune to => pandemic

154
Q

If influenza virus gains entry into pneumocytes what are the cytopathic changes that it can elicit which contribute to its pathogenesis?

A
  • Inhibits Na+ channels –> electrolyte + H2O shifts = fluid accumulation in alveolar lumen
  • Inhibits host mRNA translation and activates caspases –> cell death via apoptosis
155
Q

What was the last pandemic we had?

A

H1N1 swine flu in 2009 in MX: bird flu + human => swine flu in pigs.

Transmitted from pigs => humans via inhalation

156
Q

Which bacteria is most commonly found as cause of superimposed bacterial infection on a viral pneumonia?

157
Q

Which family of viruses does SARS, outbreak that began in ChInA belong to?

A

Coronavirus

158
Q

Why is SARS a distinct coronavirus in terms of infection?

A

Coronavirus causes many URI, however, SARS is a LRI that can spread t/o body.

159
Q

What are the most common cause of PNEUMONIA in NEONATES?

A

Bacterial pneumonias from mom

  • 1. Group B strep
  • 2. Gram (-) bacilli
  • 3. Listerialis
160
Q

What are 5 major viral causes of pneumonia in children >1 month?

A
  • RSV**
  • Parainfluenza virus, Influenza A and B, Adenovirus, Rhinovirus
161
Q

What are 4 major bacterial causes of pneumonia in children >1 month?

A
  • - S. pneumoniae
  • - M. catarrhalis
  • - H. influenzae
  • - S. aureus
162
Q

In older children and adloscesncents, how do causes of pneumonia change?

A
  1. Less likihood of RSV
  2. Also consider M. pneumoniae and C. pneumonia (a.trpical)
163
Q

Respiratory syncytial virus (RSV) belongs to what family of viruses?

A

Paramyxoviruses

164
Q

What are the sx of RSV in infants?

A

1. Rhinorrhea and wheezing, scarycough

2. Wheezing, SOB and fast breathing

3. Cyanosis bc mucus builup and bb cant breath

165
Q

How does respiratory syncytial virus (RSV) spread from the nasopharynx to lower respiratory tract; what is the effect of viral replication on this process?

A
    1. RSV virus attaches and infects epithelial ells in the nose.
    1. Cells slough off and carry the virus to the LRT.
    1. Viral replication causes epithelial cells to slough off, invasion by inflamm cells, increase mucus production and damage to cilia, causing mucus to build up.
166
Q

Which family of viruses does _Human Metapneumovirus (MPV) b_elong to?

A

Paramyxovirus

Cause pneumo in very young, very old and immunocompromised

167
Q

ALL VIRAL INFECTIONS = SIMILAR MORPHO CHANGES

What are the 3 major morphological changes seen in upper respiratory viral infections?

A

1. Mucosal hyperemia (too much blood in vessels)

  1. Infiltration of submucosa w lymphocytes and plasma cells
  2. Make too much mucus
168
Q

How does the inflammatory rxn (location and immune cells) differ between bacterial vs. viral causes of pneumonia?

A
  • Bacterial = Neutrophillic inflammation INSIDE alveoli
  • Viral = Lymphocytic inflammation in interstitiam (WALLS of alveoli)
169
Q

When viral pneumonia is complicated by ARDS what is seen lining the alveolar walls?

A

Pink hyaline membranes

170
Q

Patient comes in with pneumonia. How do we determine if viral or bacterial?

What is the onset, fever, and infiltration seen on CXR like for bacterial vs. viral causes of pneumonia?

A

Bacteria: abrupt onset with high fever, lobar/considated

Viral: gradual onset with no/low fever and diffuse infiltrates on XR

171
Q

In _________ pneumonia, epidemics are common.

What are the exceptions?

A

Viral= common.

Bacterial pneumo is not assx w epidemics e_xcept Legionells and pertussis_

172
Q

What do you hear on lung exam in Bacterial vs. Viral pneumo?

involve pleura?

A
  • Bacterial: crackles (d/t parenchyma involvement)
    • ​may involve pleura
  • Viral: Wheezes (d/t airway involvement)
    • ​will not involve pleura
173
Q

Bacterial pneumo is/isnt assx with bacteremia

Viral pneumo is/isnt assx with viremia

A

Bacteria: may

Viral: not

174
Q

Which is bacterial pneumo and which is viral pnemo?

A

L: bacteria bc intraalveolar neutrophil inflammation

R: viral bec interstitial lymphocytic inflamm

175
Q

What is this?

A

RSV, a paramyxovirus (they all look the same on histo): collection (syncitium) of nuclei

176
Q

Bacterial causes of pneumonia are not typically associated w/ epidemics, except those caused by what 2 types?

A

- Legionella

- Pertussis

177
Q

A red, flat to slightly bumpy (maculopapular) rash that starts on the forehead and spreads to the face, neck, torso, and finally the feet is associated with what virus?

A

Measles (paramyxovirus)

178
Q

What is the gram stain and shape of Bordatella pertussis?

A

Gram negative bacillus

179
Q

What are the 4 major virulence factors of Bordetella pertussis?

A
  • - Pertussis toxin: activates G proteins –> ↑cAMP
    • Extracytoplasmic adenylate cyclase: “weakens” immune cells
    • Filamentous hemagglutinin: binding to ciliated epithelial cells
    • Tracheal cytotoxin: kills ciliated epithelial cells
180
Q

While working the pediatric ED, you see a child with a sore throat and fever. There is a dark exudate on the child’s pharynx, which appears darker and thicker than that of strep throat; which bacteria is most likely responsible and what its gram stain/shape?

A

- Corynebacterium diptheriae

  • Gram + rods - very pleomorphic and club-shaped
181
Q

If Corynebacterium diptheriae is suspected why must you NOT scrape the pseudomembranes formed on the pharynx; may lead to what?

A
  • May bleed and systemic absorption of lethal EXOTOXIN will increase
  • Can cause: myocarditis and neural involvement( peripheral nerve palsies, Guillan Barre-like syndrome, and palatal paralysis/cranial neuropathies
182
Q

Who gets lung abcesses?

A

-Complication of pneumonia d/t S. aureus and K. pneumoniae (both cause lobar pneumo)

-Ppl who aspirate: Chronic alcoholics, elderly ppl who have had strokes, anaerobic bacteria

183
Q

Aspiration pneumonia occurs most frequently in whom; what are the risk factors?

A
  1. D_ebilitated pts (elderly w stroke),_ u_nconscious pts,_ chronic alcoholics who aspirate gastric contents/repeated vomitting.

Often times will have a lung abcess

184
Q

What type of damage is seen with a_spiration pneumonia_ and what is its typical course?

A

Often necrotizing and pursues sudden clinical course

  • Frequent cause of death
185
Q

In those who survive aspiration pneumonia what is a frequent complication that arises?

A

Lung abscesses

186
Q

What are the 4 anaerobic oral bacteria commonly recovered in the culture of pt with aspiration pneumonia?

A

- Bacteroides

- Prevotella

- Fusobacterium

- Peptostreptococcus

187
Q

Lung abscesses due to aspiration are more common on which side of the lung and are most often (single/mutliple)?

A

Right side of lung; most often single

188
Q

What is the cardinal histologic change in all lung abscesses?

A

Suppurative destruction of the lung parenchyma within the central area of cavitation

189
Q

Which pattern of tuberculosis arises in a nonimmune host vs. previously sensitized host?

A
  • Non-immune = primary TB
  • Previously sensitized = secondary TB

Primary infection can create a primary complex (localized caseation) that can heal or become latent. Upon reactivation, pt developes secondary TB.

190
Q

Secondary pulmonary tuberculosis classically involves which area of the lungs?

A

APEX of one or both lungs

191
Q

What is this?

A

TB: caseating granuloma “dust” necrosis surrounded by giant cells

192
Q

Which chronic lung disease puts people at a particularly high risk for tuberculosis?

193
Q

Ghon complex seen in primary TB is a combination of what?

A

Parenchymal lung lesion (Ghon focus- center undergoes caseous necrosis) + LN involvement

194
Q

What type of pneumonia is most often a localized lesion in the immunocompetent pt, with or without LN involvement; typically featuring a granulomatous inflammatory rxn?

A

Chronic pneumonia

195
Q

What funguses cause Chronic pneumonia?

A
  • 1. Histoplasma
  • 2. Blastomycosis
  • 3. Coccidiomycosis

Which tend to be endemic in diff areas.

196
Q

Histoplasma capsulatum infection is acquired via inhalation of what?

A

Dust or soil contaminated with bird or bat shit, which has small spores in it (microconidia)

197
Q

Histoplasma capsulatum is endemic where?

A
  • Endemic –> Midwest (Ohio/Mississippi Rivers) and Caribbean
198
Q

Histoplasma capsulatum typically causes what type of infection with what type of immune response; what is seen on CXR?

A

Subclinical infection that forms granulomas w/ coagulative necrosis => coalesce by fibrosis and calcify. On XR looks like coin lesions/calcifications

199
Q

What is the morphology (aka shape) of the yeast forms seen with Histoplasma capsulatum?

A

Thin-walled yeast w/ “pumpkin seed” morphology

200
Q

Granulomas in the lungs associated with Histoplasma capsulatum may liquefy and form cavities in pt’s with what underlying disease?

201
Q

How is the morphology of the disease caused by Histoplasma capsulatum different in immunosuppressed individuals?

A
  • Causes fulminant disseminated histoplasmosis
  • Granulomas do NOT form
  • Instead there are focal accumulations of phagocytes FILLED w/ yeasts throughout the body
202
Q

Blastomyces dermatitidis is a soil-inhabiting dimorphic fungi that is endemic where in the US

A
  • Central (Ohio and Mississippi river valleys) and SE United States
203
Q

How do the lung lesions of Blastomyces dermatitidis appear morphologically in a normal host?

A

- Suppurative granulomas

  • MO find it hard to kill, so yeast persists, leading to increase in neutrophiles
204
Q

What does Blastomyces dermatitidis yeast look like that distinguishes it from other fungi?

A
  • Round w/ BROAD-BASED BUDDING
  • THICK, double-contoured cell-wall
205
Q

What parts of the body does Blastomyces Dermatitidis affect?

A

Skin and larynx, RARELY spreading

Epithelial hyperplasia

206
Q

Where is Coccidioides immitis endemic and in the lungs what does the infection cause?

A
  • Endemic in SW United States and Mexico
  • Formation of granulomas w eosinophils

thick wall, dont bud, filled w endospores

207
Q

What are the signs/sx’s of pulmonary and cutaneous infection with Coccidioides immitis?

A

Sx are often subclinical and self-limited. Can disseminate, esp in immunocom

  • Fever + cough + pleuritic chest pain
  • Erythema nodosum or erythema multiforme (the San Joaquin Valley fever complex)
208
Q

Which pt population and ethnic groups are at the highest risk for the rare disseminated infection caused by Coccidioides immitis?

What type of lesions dominate in the disseminated disease?

A

- Filipino and African Americans

- Immunosuppressed

- Purulent lesions dominate

209
Q

A pt with known lung disease presents with recurrent hemoptysis, a tissue sample from the lungs shows this; what is the diagnosis and how do you know?

A
  • Aspergillosis

- Septate hyphae w/ acute-angle branching (40 degrees)

210
Q

A tissue biopsy of a pt with granulomatous lung disease shows this; what oganism is this most consistent with?

A

Coccidioides immitis

211
Q

Opportunistic infections rarely cause infections in NL hosts, but can cause lifethreatening pneo im immunocompromised.

List 3 common causes of diffuse pulmonary infiltrates that can cause pneumonia in an immunocompromised person?

A
  • CMV

- Pneumocystis jiroveci

  • Drug rxn
212
Q

Opportunistic infections rarely cause infections in NL hosts, but can cause lifethreatening pneumo im immunocompromised.

List 5 common causes of focal pulmonary infiltrates that can cause pneumonia in an immunocompromised person?

A
  1. - Gram-_negative_ bacterial infections
  2. - S. aureus
  3. - Aspergillus
  4. - Candida
  5. - Malignancy
213
Q

Which chronic lung disease puts people at a particularly high risk for tuberculosis?

214
Q

Which critical mediator released from TH1 cells both in LN’s and the lung enables macrophages to contain M. tuberculosis infection?

Which immune cells form the granulomas and caseous necrosis seen in M. tuberculosis infection?

Macrophages activated by IFN-γ in M. tuberculosisinfection differentiate into what?

A

IFN-y

Th1

Epitheliod histiocytes that aggregate to form granulomas; some may aggregate to form giant cells

215
Q

Pt’s with RA treated with what type of drugs are at an increased risk for tuberculosis reactivation?

A

TNF antagonist

216
Q

Secondary pulmonary tuberculosis classically involves which area of the lungs?

A

APEX of one or both lungs

217
Q

TB is inhaled. Once infected, TB resides and proliferates in MO.

VF: mycolic cell wall, cord factor (protect bacteria from being destryoed by forming granulomas by releasing TNF-a => activate other MO. How does this protect? Walls off bacteria in granuloma, created by newly activated MO).

Sulfatides prevent phagocyte=lysosome fusion, allowing the TB to survive in granuloma.

Infected => primary infection. 3 different outcomes: healed latent infection, systemic infection (milary TB) or reactivate and become secondary TB later in life.

Primary pneumo will form a small caseating granuloma in the lower or middle lobes. After the lesion heals, becomes fibrotic and calcifies, forming a Ghon complex (calficiation of hilar LN and caseating granuloma in lung parenchyma). Most cases will heal and form a fibrotic scar.

TB can become progressive primary TB => become bactermic and become milary TB (affects several organs like liver and spleen).

Or if latent TB reactivates => secondary TB d/t immunosupression by downregulating TNF-a release. TNF-a keeps the inflammation contained. Bc gone=> reactivation. What happens if to give a pt a TNF-a inhibitor? IF GIVING ANY1 a TNF-a inhibtor (Inflixomab), DO A PPD SKIN TEST. Reactivation will affect the UPPER LOBES and form caseating granumolas (also affecting kidney). Sx of rx: skin, hemoptysis and night sweat, cachexia.

What is the disosrder called in TB infects bones? Potts disease

Granulomas are formed to wall off infection (activated MO).

218
Q

tx TB?

A

RIPE

  1. Rifampin
  2. Isoniazid
  3. Pyrazinamide
  4. Ethambutol
219
Q

Primary tuberculosis almost always begins in which organ and what is seen morphologically as sensitization develops?

A

Lower part of upper lobe, middle lobe or lower lobe

Ghon complex formation: calficiation and caseous necrosis of granuloma and hilar LN

220
Q

What is this?

A

Caseating granuloma seen in TB

221
Q

What is the most common opportunistic infection of AIDS patients, which causes pulmonary problems?

A

Pneumocystis jiroveci

222
Q

As a general rule of thumb which organisms causing pulmonary infections in HIV pt’s are more likely with a CD4 count >200, 50-200, and <50?

A
  • >200 = bacterial and TB infections
  • 50-200= Pneumocystis jiroveci (carinii)
  • <50 = CMV, fungus, and Mycobacterium avium complex (MAC
223
Q

What is most likely seen on CXR of pt with HIV infected with Pneumocystis jiroveci?

A

Diffuse BILATERAL interstitial infiltrates

  • Can also be focal or show nothing!
224
Q

What is the characteristic morphology of the yeast, Pneumocystis jiroveci?

A

Cup-shaped yeast forms

225
Q

What is the hallmark finding of MAC infections in patients with immunosuppressed (i.e., HIV, elderly, transplant); morphology of the organism?

A
  • Abundant ACID-FAST bacilli INSIDE macrophages
  • Thin mycobacteria seen as slender red forms
226
Q

Which type of organism is the most common cause of pulmonary infection in the early post-transplant period (first few weeks)?

227
Q

Since acute rejection following a lung transplant has a similar picture to infections, diagnosis relies on what?

A

Transbronchial biopsy

228
Q

What does acute rejection of a lung transplant look like on histo?

A

Mononuclear infiltrates around small vessels, submucosa of airways or both

CPR Exam 1 (19 decks)

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