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CPR II Exam 2 > Chapter 15: Pulmonary Pathology (Singh) > Flashcards

Chapter 15: Pulmonary Pathology (Singh) Flashcards

1
Q

What are the two major requirements for normal fetal lung development to occur?

A
  1. space in the thoracic cavity
  2. ability to inhale
    • chest wall needs to move
    • need enough material to be present (amniotic fluid)
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2
Q

What is the difference between type 1 and type 2 pneumocytes?

What are Alveolar pores of Kohn?

A

Type 1: facilitate gas exchange
Type 2: produce surfactant, create new Type 1 cells

APK: allow air to move between alveoli but can allow bacteria/cells/exudate to travel between as well

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3
Q

Pulmonary Hypoplasia

What are two main causes of disease (RS/II) and when does immediate death occur?

A
  1. Reduced space in thoracic cavity
    • diaphragmatic hernia (lungs cannot push solid organs)
  2. Impaired Inhalation
    • Oligohydramnios = not enough amniotic fluid
    • airway malformation (tracheal stenosis)
    • chest wall motion disorder

immediate death occurs in neonatal period if LUNG WEIGHT < 40%

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4
Q

What is Potter Sequence and what is it associated with?

A 
P - pulmonary hypoplasia
O - oligohydramnios (trigger)
T - twisted face
T - twisted skin
E - extremity defects
R - renal agenesis (renal failure)

associated with pulmonary hypoplasia due to dec. production of amniotic fluid

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5
Q

Foregut Cysts

What are they and how can you differentiate a respiratory/esophageal/gastroenteric cyst?

What are their 3 main complications (R/I/C) and how are they cured?

A
  • detached outpouchings of foregut seen along hilum and mediastinum

R - lined by respiratory epithelium
E - lined by squamous tissue
G - lined by glandular tissue

C: rupture, infection, airway compression
- EXCISION is curative

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6
Q

Congenital Pulmonary Adenomatoid Malformation (CPAM)

What is it, how does it interact with the tracheobronchial tree, and what are complications of development?

A
  • arrested development of pulmonary tissue with formation of intrapulmonary cystic masses (would produce tissue mass of level of differentiation)
  • DOES communicate with tracheobronchial tree
  • can be detected with Fetal US and is DEADLY due to hydrops or pulmonary hypoplasia (also gets infected)
    • CAN REMOVE in utero to help save lung function
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7
Q

Pulmonary Sequestrations

What are they and where do they most commonly occur at?

What are their two major characterizations? (NC/IA)

A
  • nonfunctioning lung tissue that forms an abberrant accessory lung bud (usually LEFT LOWER LOBE)

C: does NOT communicate with tracheobronchial tree and has independent arterial supply

  • can be either intralobar or extralobar
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8
Q

What is the difference between Intralobar vs Extralobar Pulmonary Sequestrations? (ILS vs ELS)

Which one presents with congenital anomalies?

A

ILS: presents in older children/adults

  • lack of airway perfusion = abscess formation
  • infection due to under oxygenation

ELS: presents after birth with CONGENITAL anomalies

  • has its own PLEURAL LINING
  • seen as mass lesions in chest/abdomen
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9
Q

What is Atelectasis and what is the difference between Resorption, Compression, and Contraction types?

A
  • acquired failure of expansion of lung parenchyma

Re: airway obstruction with resorption of air reducing lung expansion

Com: accumulated material in pleural cavity compresses the lung parenchyma

Con: fibrotic/innate restrictive process in pleura restricting lung expansion

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10
Q

What is the most common cause of Pulmonary Edema and what does it look like histologically?

A

MCC: left-sided heart failure

Histo: PINK interstitial fluid in alveolar spaces

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11
Q

What are examples of these causes of Pulmonary Edema:

  1. “Pushing Out” of fluid (HF/VO/PVO)
  2. “Leaking Out” of fluid (HA/NS/LD)
  3. Alveolar Wall injury (P/S/S/A)
  4. Unsure mechanisms (N/A)
A
  1. left-sided HF, volume overload, pulmonary V. obstruction
  2. hypoalbuminemia, nephrotic syndrome, liver disease
  3. bacterial pneumonia, sepsis, smoking, aspiration
  4. neurogenic, high altitudes
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12
Q

What are “heart failure cells” and what are they associated with?

A
  • scattered hemosiderin-laden macrophages that accumulate in the alveoli
  • associated with congestive heart failure that backs up and causes pulmonary edema in the lungs (microhemorrhages)
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13
Q

What are the 4 criteria you must have in order to have a CLINICAL DIAGNOSIS of Acute Respiratory Distress Syndrome? (AO/H/BI/NC)

A
  1. abrupt onset of symptoms
    • can be in hospital or as out-patient
  2. hypoxemia (PaO2/FiO2 < 200; ALI only < 300)
  3. bilateral infiltrates
  4. non-cardiac in nature
    • basically make sure that heart failure is NOT the cause
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14
Q

How does Acute Respiratory Distress Syndrome (ARDS) tend to develop?

What is disrupted in its early stages?

What does it lead to the development of and what does it look like histologically?

A
  • begins in the BLOOD VESSELS = inc. capillary permeability allowing fluid to leak into alveoli (edema)
    • due to DISRUPTED VE-cadherin bonds
  • endothelium becomes activated, allowing neutrophils to accumulate in alveoli along with fluid, leading to the development of HYALINE MEMBRANES
    • requires edema + fibrin + cell debris
    • hyper-pink outline around alveolar membrane
    • causes DECREASED AERATION = hypoxemia
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15
Q

What is PaO2 and FiO2?

A

P = partial pressure of oxygen
- measure with arterial blood gas

F = calculate based on what patient is breathing
- normal room air is = 21%

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16
Q

What are the 3 major stages of ARDS (E/P/F) and how are they characterized?

What are the two possible resolutions of ARDS?

A
  1. Exudative - edema, hyaline membrane, neutrophils
    • 40% of patients die in this phase
  2. Proliferative - fibroblasts, early fibrosis, organizing pneumonia
  3. Fibrotic - extensive fibrosis, loss of normal alveolar architecture

Resolution: either restoration of normal structure and function or DESTRUCTION/DISTORTION that is IRREVERSIBLE

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17
Q

How is ARDS pathologically diagnosed and what is the name for this condition?

A
  • called DIFFUSE ALVEOLAR DAMAGE (DAD)

- requires hyaline membranes, interstitial edema, and epithelial necrosis

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18
Q

What is the difference between Restrictive and Obstructive Lung diseases?

How do FEV1, FVC, and TLC change in both of these diseases?

A

Restrictive = restriction of overall volume of lung(s)

  • also called INTERSTITIAL LUNG DISEASE
  • due to fibrosis of alveolar walls
  • normal FEV1/FVC, dec. TLC and FVC

Obstructive = hyper-expanded lungs

  • dec. flow
  • low FEV1/FVC, dec. FEV1, inc. TLC
  • dec. ratio is MOST RELIABLE statistic
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19
Q

What are 3 common examples of Obstructive Lung Disease? (B/E/A)

Which ones are most often caused by smoking?

A

chronic Bronchitis, Emphysema, and Asthma

bronchitis and emphysema (COPD) are most often caused by smoking

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20
Q

Chronic Bronchitis

How does it develop, what is used to make the diagnosis, and what does it look like histologically?

A

D: mucus hypersecretion in response to smoking causes inflammation and damaged cilia, which can then be infected (thick muscle wall with mucus dec. lumen size)

Dx: pt. with PERSISTENT cough with sputum production of 3 months out of 2 consecutive years

H: mucous gland hyperplasia with damaged airway epithelium

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21
Q

Chronic Bronchitis

What are its 3 major complications? (C/B/D)

A
  1. carcinoma (from squamous metaplasia that becomes dysplastic)
  2. bronchiectasis
  3. death from respiratory infection
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22
Q

Emphysema

How is it generated, how does it present clinically, and where does it occur at?

A
  • caused when chronic bronchitis reaches terminal bronchiole, causing alveolar sac to collapse

CP: enlarged lungs on CXR (super black) with flattened diaphragm and “barrel chest” with inc. AP diameter

  • diminished breath sounds, prolonged exp. wheeze
  • PFTs show obstructive pattern (looks like a CHAIR)

emphysema is an IRREVERSIBLE airspace enlargement occurring DISTAL to terminal bronchiole

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23
Q

How does a Chronic Bronchitis pt. differ in presentation compared to an Emphysema pt.?

A

CB = BLUE BLOATERS (clinical diagnosis)

  • overweight and cyanotic
  • elevated hemoglobin lvls (trying to compensate)
  • peripheral edema and rhonchi/wheezing

E = PINK PUFFERS (pathological diagnosis)

  • permanent enlargement/destruction of airspaces
  • older/thin with severe dyspnea
  • dec. breath sounds
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24
Q

Alpha-1 Antitrypsin Deficiency

What is it and how does it develop, what kind of emphysema does it cause, and where is this condition seen in lungs?

What genetics are associated with this disease and how can it be screened? What is the classic pt. presentation?

A
  • lack of a1-antitrypsin due to mutations trapping them in liver (liver damage), unable to prevent Neutrophil Elastase from damaging alveoli = PANACINAR EMPHYSEMA (panacinar enlargement)
    • panacinar because alveoli are soaked in elastase
  • seen in LOWER lung due to gravity (more prominent at the base of the lung)

G: pts. homozygous for PiZZ (Pi on C 14, Z allele associated with dec. circulating a1-AT)
- serum test for a1-AT is primary means of diagnosis

pt: young 30 yo smoker with obstructive lung disease

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25
Q

Emphysema

What are its 4 major complications? (RF/CAD/HF/P)

A
  1. respiratory failure
  2. coronary artery disease
  3. RIGHT HEART FAILURE (Cor pulmonale)
  4. pneumothorax with lung collapse
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26
Q

Asthma

What are its 3 main components?

A
  1. recurrent airway obstruction with REVERSIBLE component
  2. airway HYPER-responsiveness
  3. airway inflammation due to responsiveness
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27
Q

Asthma

What is the difference between Atopic and Non-Atopic asthma?

A

A = extrinsic

  • 2/3 of all patients, usually in childhood
  • family history of asthma
  • elevated IgE lvls (inc. eosinophils, mast cells, lymph)

NA = intrinsic

  • 1/3 of all patients, usually older age
  • NORMAL IgE lvls (neutrophils and T-lymphocytes)
  • triggers = cold, exercise, and infection
  • prolonged coughing, wheezing w/infection
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28
Q

Asthma

What is the main mediator for bronchoconstriction, mucus secretion, and inc. vascular permeability in disease?

A

Leukotrienes C4-D4-E4

interleukins recruit inflammatory cells

histamine, PGD2, ACh also cause bronchoconstrict

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29
Q

What is Status Asthmaticus?

What are two diagnostic histological findings of this disease? (CS/CLC)

A
  • unremitting, potentially fatal asthma attack due to bronchial occlusion by thick mucus plug
  1. Curschmann Spirals (coiled mucus plugs)
    • MORE diagnostic
  2. Charcot Leyden Crystals (eosinophil breakdown)
    • crystals from eosinophil breakdown
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30
Q

What is Aspirin-Sensitive Asthma?

What is Samter’s Triad? (NP/RR/AS)

A
  • aspirin causes inc. production of leukotrienes C4-D4-E4
  • leads to development of Samter’s Triad
    • nasal polyps, recurrent rhinitis, and aspirin sensitivity
  • cross-reacts with other NSAIDs
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31
Q

What is Bronchiectasis and what are 4 entities that can cause it? (ABPA/CF/TB/PCD)

A
  • necrotizing inflammatory response that is an end-stage process of multiple processes
  • can be caused by:
    1. Allergic Bronchopulmonary Aspergillosis
    2. Cystic Fibrosis
    3. Chronic infection (TB)
    4. Primary Ciliary Dyskinesia
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32
Q

Kartagener’s Syndrome (Primary Ciliary Dyskinesia)

What is it, what is its triad (S/B/SI), and what is a reproductive complication it can cause?

A
  • due to dysfunction of dynein arm of microtubules

Triad: sinusitis, bronchiectasis, situs inversus
- SI = heart faces the wrong way (apex on right)

  • can often occur with MALE INFERTILITY (disrupted microtubules in pts. SPERM FLAGELLA = no swimming)
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33
Q

Allergic Bronchopulmonary Aspergillosis (ABPA)

What is it, what test is positive identification, and what does its sputum look like?

A
  • exaggerated hypersensitivity response to Aspergillus infection overlying chronic lung disease (no invasion, just sits in the lumen)
    • requires background of Asthma or Cystic Fibrosis
    • can cause severe bronchiectasis

Testing: skin test (+), inc. IgE on serum testing

Sputum: thick dark mucus in bronchi with fungal hyphae (characteristic of Aspergillus)
- use Silver Stain to visualize Aspergillus

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34
Q

Idiopathic Pulmonary Fibrosis (Usual Interstitial Pneumonia)

What does diagnosis require on CT, what are 3 factors that contribute to development (E/G/A), and how does it present clinically?

What is seen on chest XRay?

A
  • diagnosis requires classic findings on CT or pulmonary biopsy (normal areas, inflammation, fibroblast foci, peripheral honeycombing)
  • inc. with smoking (environment), genetics, or > 50 yo

CP: dyspnea (most prominent symptom) and VELCRO-sounding chest crackles on ausculation

Xray = basilar infiltrates that progress to “honeycomb” lung

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35
Q

Idiopathic Pulmonary Fibrosis (UIP)

What is the outlook for pts and what are two potential therapies for treatment of disease? (LT/MAF)

A
  • progressive course = most pts. die from respiratory disease 3-5 yrs after diagnosis (massive fibrosis or Cor Pulmonale)
  1. Lung transplantation
  2. Medication to arrest fibrosis
    • tyrosine kinase inhibitors, TGF-b inhibitors
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36
Q

Non-specific Interstitial Pneumonia (NSIP)

What is it and what does it look like histologically?

What is its prognosis compared to UIP?

A
  • idiopathic fibrosis that has uniform infiltrates and fibrosis (DIFFUSE) but no heterogeneity, fibroblast foci, or granulomata) –> BETTER prognosis that UIP

Histo: uniform inflammation/fibrosis with chronic inflammatory cells

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37
Q

Cryptogenic Organizing Pneumonia (COP)

When does it occur, when does it present, and what histology is seen in it (MB)?

How is it diagnosed and what is its prognosis?

A
  • occurs superimposed on a PRIOR infection or inflammatory process that presents with pneumonia-like consolidation during 5th-6th decade

Histo: MASSON BODIES (fibroblast foci) = organized plugs of connective tissue

Dx: diagnosis of EXCLUSION

Prognosis: good, full recovery with ORAL STEROIDS

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38
Q

What are 3 autoimmune diseases that can present as Interstitial Lung diseases, like IPF, NSIP, or Organizing Pneumonia?

A

Rheumatoid Arthritis, Systemic Sclerosis, Lupus Erythematous

  • ILD occurring as a manifestation of one of these diseases is NOT a pure disease
  • prognosis is linked to treatment of the underlying condition
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39
Q

Sarcoidosis

What is it, how does it present initially, what does it look like on histology (AB/SB), and what serum finding corresponds to the amount of Sarcoidosis in the pt?

A
  • systemic disease showing NON-CASEATING granulomata in various organs; presents either incidentally or with dyspnea

CP: pts usually < 40 yo, 10x inc. in African Americans, commonly involves LUNGs

Histo: well-defined with histiocytes, Asteroid Bodies, and Schaumann Bodies (while under polarized light)

  • elevated serum ANGIOTENSIN CONVERTING ENZYME (ACE lvls)
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40
Q

What is seen at each stage of Sarcoidosis on Chest X-Ray:

Stage 0
Stage 1
Stage 2
Stage 3
Stage 4
A

0 = no abnormalities

1 = lymphadenopathy (50%)

2 = lymphadenopathy + pulmonary infiltrates (25%)

3 = pulmonary infiltrates

4 = fibrosis

41
Q

Hypersensitivity Pneumonitis

What is it, what does it look like on histology, and who does it commonly affect?

What is absolutely required for diagnosis?

A
  • immune reaction to inhaled antigens causing AIRWAY-centered granulomata with lymphocytes; is NOT well-demarcated and is NOT caseating
  • commonly occurs in pigeon-breeders (bird poop), farmers (actinomyces), and from hot tub use (MAC)

Dx: HISTORY is required

42
Q

What are the two granulomatous Interstitial Lung Diseases?

A

sarcoidosis and hypersensitivity pneumonia

43
Q

What are three smoking-related Interstitial Lung Diseases? (D/R/L)

A

DSIP = Desquamative Interstitial Pneumonia

RB-ILD = Respiratory Bronchiolitis Lung Disease

LCH = Langerhans Cell Histiocytosis

idiopathic pulmonary fibrosis fits in this category too

44
Q

Desquamative Interstitial Pneumonia (DSIP)

Who does it affect and when, what is seen on histology, and what is its prognosis/treatment?

A
  • occurs in smokers with SOB during their 4th-5th decades (restrictive disease presentation)

Histo: alveoli spaces “stuffed” with macrophages

Prognosis: good, 95% survival at 5 years
- treat with corticosteroids and NO SMOKING

45
Q

Respiratory Bronchiolitis-Interstitial Lung Disease (RB-ILD)

Who does it affect and when, what are its 3 major histological findings, and what is its prognosis?

A
  • earliest form of interstitial lung disease that affects smokers in their 3rd-4th decades (on spectrum with DSIP but less symptomatic)

Histo: alveolar macrophages (less than DSIP), peribronchiolar metaplasia (cilia cells in alveoli), and fibrosis (if advanced case)

Prognosis: often reversible with smoking cessation if caught early

46
Q

Langerhans Cell Histiocytosis (LCH)

Who does it affect, what is seen on histology, what can it lead to the development of, and what stain is it (+) for?

A
  • affects young smokers causing STELLATE LUNG LESION, with progressive scaring leading to CYSTS of trapped air that can rupture = PNEUMOTHORAX
    • can be reversed with smoking cessation

Histo: eosinophils, langerhans cells, cysts/fibrosis

(+) staining for CD1a (and S-100) in setting of abundant eosinophils

47
Q

Pulmonary Alveolar Proteinosis

What is it and what is it caused by, how is it treated, and what does it look like histologically?

A
  • impaired surfactant metabolism due to loss of GM-SCF most commonly due to autoimmunity; causes accumulation of surfactant proteins in alveoli and airways
  • treat with steroids (autoimmune), subQ GM-CSF, and lavage (removes copious milky-looking fluid)

Histo: proteinaceous collections in alveolar spaces

48
Q

What is Pneumoconiosis?

What 3 situations make this disease process worse (RE/SP/S)

What are 3 common types of this disease?

A
  • reaction of lungs to inhaled MINERAL or ORGANIC dust/vapors usually due to occupational exposure or air pollution
  • can be made worse with repetitive exposure, small particles (1-5 um allow alveoli passage), and SMOKING

Types: coal workers pneumoconiosis, silicosis, asbestosis

49
Q

Coal Worker Pneumoconiosis

What is it caused by and what is seen on histology?

A
  • disease due to inhaled COAL DUST, with spectrum of anthracosis, coal nodules, and progressive massive fibrosis (most pts. will NOT have progressive disease)

Histo: anthracosis (dark pigment), coal nodules (dark accumulations)

50
Q

Silicosis

What is it caused by, what is seen on histology, and what is seen on radiographic imaging (EC)?

What is its prognosis?

A
  • disease from inhaled SILICON DUST seen in mining/quarry work and concrete repair/demolition

Histo: dense collagenous nodules
Radio: EGGSHELL CALCIFICATIONS (hilar LNs)

Prognosis: can progress to massive pulmonary fibrosis and has 2x risk of developing cancer

51
Q

Asbestosis

What is it caused by, what does it affect, which fiber is most dangerous, and what does it look like histologically (AB/CD)?

What is a serious complication of this disease?

A
  • disease from inhaled ASBESTOS fibers seen in insulation workers, shipyard workers, paper mill/oil refinery workers that affects lungs and PLEURA
  • Amphibole fiber is MOST DANGERIOUS since it can be inhaled deeper into lung than Serpentine

Histo: ASBESTOS BODIES or Ferruginous Bodies (golden dumbbell with iron debris on ends) and “Candlewax drippings” on pleura (hyalinized collagen)

Comp: can cause MESOTHELIOMA

52
Q

What does a pulmonary infarct look like on radiography?

What is a characteristic finding in ANTEMORTEM clots that helps identify them as such?

A

WEDGE-SHAPED LESION

  • begins as hemorrhagic, then fibrosis sets in

AC: have “Lines of Zahn” which show alternating areas of fibrin and RBCs in structure of clot = clot was present while pt was ALIVE

53
Q

What is a Talc Embolism. who is it commonly seen in and what is the physical exam finding that should prompt investigation?

What does a Talc embolus look like histologically?

A
  • embolus usually seen in IV drug users or those that crush pills
  • see Track Marks on pts skin

Histo: REFLECTIVE substances in embolus that are shiny

54
Q

Septic Emboli

What are caused by and what are 3 common physical exam findings in pts? (JL/RS/SH)

A
  • bloodborne infective material that can occur in endocarditis = valve vegetations break off and manifest in other sites

PE: Janeway Lesions (skin microemboli), Roth Spots (retinal microemboli), and Splinter Hemorrhage (vascular damage in nail bed)

**tricuspid valve vegetations can break off and become lodged in the lung, causing abscesses to form)

55
Q

What is Pulmonary Hypertension and what are its 5 types?

What are two common histological findings in pts. with Pulmonary Hypertension (PL/MH)

A
  • pulmonary artery pressure greater than 25 mmHg

Types:

  1. PAH - primary vascular disease
  2. 2nd to Left Heart Failure
  3. 2nd to Chronic Pulmonary Parenchymal disease
  4. 2nd to Thromboembolic Pulmonary Disease
  5. Multifactorial

Histo: Plexiform Lesion (tangled web of vessels) and Medial Hypertrophy (SM in small arteries)

56
Q

What are 3 examples of Pulmonary Hemorrhage Syndromes? (GS/GP/IPH)

A
  1. Goodpasture Syndrome
  2. Granulomatous w/Polyangiitis
  3. Idiopathic Pulmonary Hemosiderosis
57
Q

Goodpasture Syndrome

Who is it seen in and what is seen on imaging?

What two locations are findings commonly seen in?

A
  • seen in young male patients (2-3 decade) with Pulmonary Hemorrhage (Type 2 Hypersensitivity)

Imaging: immunofluorescence showing LINEAR deposition due to anti-BASEMENT MEMBRANE Abs
- Abs against subunit of collagen IV

  • seen in the lungs and KIDNEY
58
Q

What is the difference between Bronchopneumonia and Lobar Pneumonia?

A

BP = patchy appearance

LP = confluent and consolidated

59
Q

What are the 4 stages of Lobar Pneumonia (C/RH/GH/R)?

What are 3 complications of development? (A/E/B)

A
  1. Congestion = vascular engorgement
  2. Red Hepatization = red cells/inflammation
  3. Gray Hepatization = debris/inflammation
  4. Resolution = fibrosis, macrophage clean-up

Comp: abscesses, empyema, bacteremia
- almost ALWAYS caused by bacteria

60
Q

What are 7 organisms that cause Community-Acquired Bacterial Pneumonia? (SP/HI/SA/KP/PA/LP/MP)

A
  1. Streptococcus pneumoniae
  2. H. influenzae
  3. Staph Aureus
  4. K. pneumoniae
  5. P. aeruginosa
  6. L. pneumophilia
  7. M. pneumoniae
61
Q

Streptococcus Pneumoniae and CAP

What does it look like, what is it the most common cause of, and who is vaccination recommended in?

A
  • LANCET-shaped gram (+) DIPLOCOCCI (pairs and chains)
  • MOST COMMON CAUSE OF CAP
  • vaccination for infants, pts >65 yo, and in respiratory disease/smoking
62
Q

How do Haemophilus influenzae, Staphylococcus aureus, and Klebsiella pneumoniae present in pts. with Community Acquired Pneumoniae?

A

HI: gram (-) coccobacillus causing virulent pneumonia in children
- superinfection in pts. with flu

SA: gram (+) with round shape
- abscess formation, especially in IV DRUG USERS

KP: gram (-) rod

  • currant jelly sputum in ALCOHOLICS
  • extremely hemorrhagic
63
Q

Pseudomonas aeruginosa and CAP

Which pt. population is it commonly seen in, what else is it associated with, and what does it look like?

A
  • seen often in CYSTIC FIBROSIS pts. or as an opportunistic infection (associated with hospital-acquired infections)
  • looks green when plated and in tissue
  • gram (-) encapsulated rod
64
Q

What is the difference between Typical Pneumonia and Walking Pneumonia?

A

TP: more abrupt onset (older adults, young kids)

  • respiratory symptoms mainly
  • consolidation on CXR

WP: slower onset (young adults, teens, older kids)

  • SYSTEMIC symptoms mainly
  • PATCHY infiltrate on CXR
65
Q

What are 4 common causes of Community-Acquired Walking Pneumonia? (MP/LP/CP/CP)

A
  1. Mycoplasma pneumoniae
    • MOST COMMON cause of walking pneumonia
  2. Legionella pneumophilia
  3. Chlamydia pneumonia
  4. Chlamydia psittaci
66
Q

What are the presentations of Mycoplasma pneumoniae and Legionella pneumophilia?

A

MP: smallest free-living, self-replicating microorganism
- NO CELL WALL (is neither gram (-) or gram (+))

LP: gram (-) bacillus that grows in warm FRESHWATER

  • commonly infects air conditioners, misters, hot tubs
  • is an AIRBORNE disease
67
Q

What are the 4 common causes of Community-Acquired VIRAL Pneumonia? (I/S/C/RSV)

A
  1. Influenza (H1N1)
  2. SARS
  3. COVID-19
  4. Respiratory Syncytial Virus
68
Q

Influenza Virus and CAP

What two proteins does it possess (H/N) and how does it present clinically?

A
  1. Hemagglutin - attaches virus to cell
  2. Neuraminidase - allows release of replicated virus from cells
    • cleaves hemagglutin tether
    • TAMIFLU can block neuraminidase

CP: abrupt onset with fever of 3-4 days, severe aches, chills, fatigue/weakness; headaches are common

69
Q

What is the difference between Antigenic DRIFT and Antigenic SHIFT?

A

Drift: causes EPIDEMICS

  • minor changes to antigens on virus = inc. spread
  • similar to original virus, allow some immunity

Shift: causes PANDEMICS

  • genomic alteration w/major protein changes
  • naive immunity for almost all people
  • usually due to recombination with animal flu strains
70
Q

SARS-CoV-2 and CAP

What is it and what does it target, why should D-Dimer be checked, and what cell type can be identified in circulation?

A

COVID-19 = positive sense ssRNA virus

  • targets ACE receptors, spread via respiratory droplet
  • causes cytokine storm that leads to ARDS
  • also caused coagulopathy
  • check D-Dimer –> correlates with POORER outcome in COVID patients due to thrombotic complications
  • can see MEGAKARYOCYTES in circulation of COVID-19 pts.
71
Q

Respiratory Syncytial Virus and CAP

What is it, how does it present, and how does it affect the airways?

A
  • paramyxovirus that commonly causes viral pneumonia in children > 1 month

CP: rhinorrhea, cough, wheezing/dyspnea, tachypnea, cyanosis

  • virus infects epithelial cells, leading to sloughing and inflammation as it progresses further down airway; leads to dec. aeration due to mucus/inflammatory blockage
72
Q

What are differences in presentation of Bacterial and Viral pneumonias?

A

B: abrupt onset with HIGH GRADE fevers

  • lobar/consolidated appearance
  • crackles on lung exam

V: gradual onset with low grade or no fevers

  • diffuse infiltrate appearance
  • wheezes on lung exam
  • associated with EPIDEMICS
73
Q

Which two bacteria often present with lobar pneumonia with ABSCESS formation?

Where do aspirations tend to occur at in the lungs and what are 3 groups aspiration is seen with? (CA/EP/AB)

A

S. aureus and K. pneumoniae

  • aspiration tends to follow gravity into right mainstream bronchus
  • aspiration seen with chronic alcoholics, elderly stoke pts, and anaerobic bacteria
74
Q

What are two findings of Tuberculosis infection? (CG/GC)

A
  1. Caseating Granulomas
  2. Ghon Complex = parenchymal and hilar LN lesions (calcify over time)

miliary TB occurs when tuberculosis has massive hematogenous dissemination

75
Q

What are 3 fungal causes of Chronic Pneumonia?

A

Histoplasma, Blastomycosis, Coccidiomycosis

76
Q

Histoplasma capsulatum and Chronic Pneumonia

Where is it found, what does it look like, and what budding does it have?

A
  • endemic in MIDWEST and Caribbean that runs aggressive course in immunocompromised pts
  • usually subclinical infection with GRANULOMATOUS response, creating COIN LESION (calcifications) on CXR

Budding: NARROW-BASED budding

77
Q

Blastomyces dermatitides and Chronic Pneumonia

Where is it found, what does it look like, and what budding does it have?

A
  • endemic in CENTRAL and SE United States that can also infect the skin
  • infection causes granulomatous response; looks like MARBELS on histological imaging

Budding: BROAD-BASED budding

78
Q

Coccidiodes immitis and Chronic Pneumonia

Where is it found, what does it look like, and what is seen on histology?

A
  • endemic in SW United States and Mexico and can produce disseminated infection in immunocompromised pts.
  • causes granulomatous response with EOSINOPHILS

Histo: contained in ENDOSPORE (small balls within a larger ball)

79
Q

Pneumocystis jiroveci

What is it, who is it most commonly seen in, and what does it look like?

A
  • opportunistic FUNGAL infection that is an AIDS-defining illness (Immunocompromised pneumonia)
  • has a “cup-shaped” yeast form that is characteristic
  • is notorious for looking like any kind of pneumonia on an X-Ray
80
Q

Mycobacterium Avium Complex (MAC)

Who does it commonly affect and what does it look like on what stain?

A
  • seen in immunocompromised or elderly patients (immunocompromised pneumonia)
  • thin mycobacteria seen as slender red forms on acid-fast staining
81
Q

What is seen on biopsy of a patient with lung transplant rejection, and what are two infections that commonly target lung transplant patients?

A

Rejection = mononuclear infiltrates around vessels
- due to NOT ENOUGH rejection

Opportunistic Infections: zygomycosis and CMV
- due to TOO MUCH rejection

82
Q

What two lung carcinomas is smoking classically associated with?

A

Squamous Cell Carcinoma and Small Cell Carcinoma

83
Q

Adenocarcinoma Progression

What is Atypical Adenomatous Hyperplasia (AAH) and Adenocarcinoma in Situ (AIS)?

A

AAH: < 5mm

  • dysplastic pneumocytes present along alveoli
  • some interstitial fibrosis

AIS: < 3mm

  • dysplastic pneumocytes confluently growing along alveoli
  • aka “Bronchioloalveolar carcinoma”
84
Q

Pulmonary Adenocarcinoma

What is it, what stain is it (+) for, and how does mucinous adenocarcinoma progress?

A
  • most common lung malignancy in smokers AND non-smokers (malignant glands invading lung tissue)
  • stains (+) for TTF-1 (thyroid transcription factor-1)
  • mucinous adenocarcinoma shows mucinous epithelium growing along alveoli with bilateral pulmonary infiltrates that MIMIC PNEUMONIA
85
Q

Pulmonary Squamous Carcinoma

Who does it affect and where does it occur, what is seen on histology and what is seen on cytology?

A
  • more common in males that smoke, and is often found more centrally (damage is required to turn normal bronchial epithelium into squamous metaplasia)

Histo: KERATIN PEARLS

Cyto: ORANGLE CYTOPLASM (keratin)

86
Q

Small Cell Neuroendocrine Carcinoma

What does it look like, what is it associated with, and what are treatment options?

A
  • smalls cells with fine blue nuclear chromatin, scant cytoplasm, and necrosis (HIGH rate of metastasis usually by time of diagnosis)
  • associated with SMOKING
  • surgical excision not recommended if metastatic, chemo-radiation responsive but high rate of reoccurrence
87
Q

What Paraneoplastic Syndrome(s) are related to Squamous Carcinoma and Small Cell Carcinoma?

A

SC: Hypercalcemia due to PTH-related peptide

SCC: SIADH (inappropriate ADH secretion) and Cushing’s Syndrome (ACTH secretion)

88
Q

What is Horner’s Syndrome and how does it present (E/P/M/A)?

A
  • compression of sympathetic trunk by cancer growing at apex of lung that can have related ARM PAIN due to nerve compression (helps localize to thoracic outlet)
  • OCULOSYMPATHETIC PALSY

CP: enophthalmos (sunken eyeball), ptosis (droopy eyelid), miosis (persistent small pupil), anhidrosis (no sweating on that side of face)

89
Q

Neuroendocrine Tumors of the Lung

What is the difference between DIPNECH and Carcinoid Tumor?

A

D = diffuse interstitial pulmonary neuroendocrine cell hyperplasia (NOT MALIGNANT)

  • PRECURSOR lesion, detect nodule with CT scan
  • very small, less than 5 mm (tumorlets)

C = 5 mm or LARGER that can METASTASIZE

  • indolent
  • also called neuroendocrine carcinoma GRADE 1
90
Q

Neuroendocrine Tumors of the Lung

What is an Atypical Carcinoid Tumor?

A
  • aka neuroendocrine carcinoma GRADE 2
  • has inc. mitotic activity, NECROSIS, and disordered growth
  • inc. rate of metastasis and a lower survival probability (but better than small cell carcinoma)
91
Q

What syndrome is associated with Carcinoid, Atypical Carcinoid, and Small Cell Neuroendocrine tumors?

A

CARCINOID SYNDROME

  • flushing, diarrhea, and cyanosis
  • usually seen with metastasis
92
Q

What is a “Cannonball” Tumor and what two things is it associated with?

A
  • metastatic malignancy that causes large tumors in the lungs
  • associated with testicular cancer and melanoma
93
Q

Pulmonary Hamartoma

What are they and what is seen on CT?

A
  • completely benign well-circumscribed fibrous tissue mass with benign glandular epithelium around hyaline cartilage
  • produced a “coin sign” lesion in CT
94
Q

Pulmonary Lympangioleiomyomatosis (LAM)

What are they, what marker do they have, what is it associated with, and how does it present? (P)

What cell type is seen in these cystic spaces (PEC)?

A
  • proliferation of cells creating cystic spaces that are positive for HMB-45; perivascular epithelioid cells mostly seen in YOUNG WOMEN
  • associated with loss of Tumor Suppressor TSC2
  • may present with PNEUMOTHORAX
95
Q

How can the cause of a pleural effusion be determined?

A
  • can identify cause by tapping the fluid

Transudate = heart failure (clear serous fluid)
Exudate = infection (pus)
Malignancy (usually see blood)

96
Q

What is an Empyema?

A
  • inflammatory exudate with accumulation of pus in the pleural space, typically caused by a bacterial infection (Pneumonia)
  • notorious for creating LOCULATIONS = web-like traps for fluid (fluid is thick, yellow, and smears show neutrophils/bacteria)
97
Q

What is a Pneumothorax?

What is the difference between Primary and Tension Pneumothoraxes?

A
  • injury to chest wall that results in a one-way valve allowing air INTO the pleural space but not OUT OF the pleural space (air is pulled in from wherever its easiest)

Primary: pleural cavity is < atmospheric pressure
- punctured lung
Tension: pleural cavity is > atmospheric pressure
- puncture of chest wall

can decompress with needed

98
Q

Solitary Fibrous Tumor

What does it look like on histology (SV)?

A
  • benign when small and pedunculated (larger ones can behave like sarcomas)

Histo: spindle cell lesions with “staghorn” vessels

  • circumscribed pleural-based mass that becomes pedunculated from excision from neighboring lung tissue
99
Q

Mesothelioma

What is seen on histology (FB) and what staining can be done for it (C)?

A
  • associated with Asbestos exposure and can occur decades after exposure; most common type is epithelioid
  • stain for CALRETININ helps differentiate this from adenocarcinoma, also has Ferruginous bodies present
  • difficult to treat since it cannot be excised surgically and has limited responsiveness to radiation/chemotherapy
  • most pts. do NOT survive past 2 years after diagnosis

CPR II Exam 2 (10 decks)

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