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Path Exam 2 > Lungs > Flashcards

Lungs Flashcards

1
Q

contrast atopic vs. non-atopic

A
  • in non-atopic:
    • DON’T see increased IgE,
    • no family history
    • DO see Curschmann spirals, Charcot-Layden crystals and neutrophils
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2
Q

describe complications of the condition shown in the image

A
  • complications:
    • empyema
    • bronchopleural fistula
    • septicemia (meningitis, brain abscess)
    • AA amyloidosis → restrictive cardiomyopathy
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3
Q

describe the image

A

sarcoidosis

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4
Q

describe the paraneoplastic syndromes associated with the condition seen in the image

A
  • SIAD (dilutional hyponaterima): leads to cerebral edema and papilledema
  • gonadotropins
  • Cushing syndrome: buffalo hump, purple striae, moon face d/t bilateral adrenal hyperplasia
  • gastrin releasing peptide: stimulates G cells to secrete acid and hyper-motility of GI
  • antibodies to pre-synaptic Ca2+ channels = Lambert-Eaton syndrome
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5
Q

describe the etiology of the condition seen in the image

A
  • etiology: smoking, radon and asbestos
    • smoking + asbestos = highest risk
    • men > women
    • gene mutations = RB, P16, p53
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6
Q

describe the presentation of the cardiogenic form of the disease shown in the image

A
  • presentation:
    • decreased diffusing capacity, hypoxemia, and shortness of breath
    • increased pulmonary capillary wedge pressure
    • NO hyaline membrane
    • at 2 weeks, hemosiderin layden macrophages/heart failure cells
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7
Q

describe the etiology of the disease seen in the image

A
  • etiology: obligate intracellular bacteria → “walking pneumonia”
    • most common = Mycoplasma pneumoniae (younger people → military recruits/students)
    • chlamydia & Coxiella burnetti (from sheep → farmers/vets)
    • viruses = CMV/influenza
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8
Q

describe complications of the disease seen in the image

A
  • complications:
    • multi-organ problems
    • pulm. failure
    • cor pulmonale
    • contraction atelectasis
    • hypercalcemia → kidney stones
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9
Q

describe the image

A
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10
Q

describe the minor form of the condition seen in the image

A
  • minor = small vessels → asymptomatic
    • if there are a series of recurring minor embolisms → marginate on the walls of the pulm. artery → flow encounters increased resistance → pulm. HTN → RHF WITHOUT LHF
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11
Q

describe the presentation of the disease in the image

A
  • presentation:
    • dry cough with dyspnea (crackles on inspiration)
    • finger clubbing
    • pulm. fibrosis
    • geographic heterogeneity = favors lower lobe first
    • temporal heterogeneity = coexisting of old type I collagen and new fibrosis
    • cobblestone pleural surface → honeycomb lung (pockets of airspaces (cystic spaces) contain mucus and lined by type II pneumocytes)
    • x-ray: bilateral reticulo-nodular shadows mainly lower lobes w/honeycomb lungs
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12
Q

describe why metastatic calcification is seen in the disease shown in the image

A
  • epithelioid cells activate vit. D via 1-alpha hydroxylaseactivity → hypercalcemia → metastatic calcification
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13
Q

describe the histology of the condition seen in the image

A
  • keratin pearls = well differentiated in fxn
  • intercellular bridges
  • individual cell keratinization
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14
Q

describe investigations for atopic asthma

A
  • investigations:
    • sputum cytology = Curschmann spirals (shredding of bronchial epithelial cells + mucus) & Charcot-Layden crystals (MBP & eosinophilic cationic protein)
    • x-ray: hyperinflated lung fields
    • flow meter: decreased peak flow rate
    • blood CBC: lots of eosinophils (eosinophilia)
    • pulm. function tests: decreased FEV1: FVC ratio and increased TLC and RV
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15
Q

describe the pathogenesis of the disease seen in the image

A
  • pathogenesis:
    • alveolar spaces are free/empty, inflammation in alveolar wall (thickened septae) → cough is DRY
      • leukocytes + mononuclear cells (NO PMNs bc no cell death)
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16
Q

describe the pathogenesis of the disease seen in the image

A
  • pathogenesis:
    • bilateral fibrosis of interstitium → severe hypoxia
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17
Q

describe the image

A
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18
Q

describe the cell of origin for the condition seen in the image

A
  • cell of origin = Kulchitsky (neuroendocrine cells)
    • 99% associated with cigarette smoking
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19
Q

describe NSIPF

A
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20
Q

describe the pathogenesis for small cell carcinoma

A
  • myc amplification (most common)
  • p53
  • pRB
  • 3p deletion
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21
Q

who does the disease in the image mainly effect?

A

males over 60; smokers

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22
Q

describe what condition is seen in the image

A

atelectasis

  • lung collapse → decreased O2 → shortness of breath
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23
Q

describe the panacinar form of the disease shown in the image

A
  • panacinar: entire acinus from respiratory bronchioles to the alveolar ducts; lower lobes
    • deficiency of A1AT - PiZZ homozygous recessive on ch. 14 (misfolded protein)
    • A1AT accumulates in the ER
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24
Q

describe how the disease shown in the image occurs in young, immunocompetent patients

A
  • lobar = young immunocompetent
    • streptococcus pneumoniae (95%)
    • COMPLETE RESOLUTION
    • speads via pores of Kohn
      • architecture stays intact
      • confluent consolidation of entire lobe
      • bronchi are NOT involved
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25
Q

name indirect causes of the disease shown in the image

A
  • indirect causes:
    • acute pancreatitis (enzymes causing damage to lung)
    • uremia
    • sepsis
    • burns
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26
Q

the patient can die from ____ in the condition seen in the image

A

patient dies from respiratory failure due to overproduction of mucin

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27
Q

describe the concept of contraction

A
  • contraction = IRREVERSIBLE due to pulm. fibrosis
    • trachea in either direction or central bc both lungs are affected
    • caused by all restrictive lung diseases which lead to fibrosis (irreversible)
    • FEV1:FVC ration is normal but decreased TLC and RV
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28
Q

describe the pathogenesis of the disease seen in the image

A
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29
Q

describe what would be seen on biopsy of the condition seen in the image

A
  • biopsy = malignant glands invading stroma
    • produce lots of mucin → well differentiated in fxn
    • positive for cytokeratin & PAS (diastase resistant bc no glycogen)
    • prominent nucleus & nucleolus and dispersed chromatin
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30
Q

describe complications of the disease seen in the image

A
  • complications:
    • resp. failure early
    • cor pulmonale early
    • cirrhosis/nutmeg liver
    • resorption atelectasis
    • recurrent pneumonia → lung abscess → bronchiectasis
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31
Q

describe what the condition in the image is composed of

A
  • composed of:
    • hyaline cartilage
    • fat cells
    • smooth muscle
    • resp. epi.
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32
Q

describe the presentation of the disease shown in the image

A
  • presentation:
    • skinny (compensating and using accessory muscles)
    • barrel-chested (bc obstructive lung disease)
    • pursed lip breathing
      • “pink puffers” = prolonged expiration through pursed lips → compensating early to prevent cyanosis and hypoxia
    • minimal sputum
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33
Q

describe a massive form of the condition seen in the image

A
  • massive: large saddle embolus straddles the bifurcation of the pulm. artery; caused by DVT
    • sudden obstruction of 60% of pulm. vasculature
    • sudden death & no time to develop infarction, lungs not affected → look normal
      • death due to electromechanical dissociation
    • example: hospitalized patients who get out of bed 1st time dies immediately
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34
Q

describe the image seen

A

asthma

  • top photo:
    • yellow arrow = eosinophils
    • blue arrow = smooth muscle hypertrophy
    • green arrow = goblet cell hyperplasia
    • black arrow = thickened BM
  • bottom photo:
    • Curschmann spirals in a patient with bronchial asthma (shredded bronchial epithelial cells found in sputum)
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35
Q

describe the immunohistochemical stain for the condition seen in the image

A

immunohistochemical stains: TTF-1, cytokeratin 7, napsin-A

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36
Q

describe what is seen in the image

A
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37
Q

describe what is seen in the image

A
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38
Q

describe the pathogenesis of the disease seen in the image

A
  • pathogenesis:
    • type IV hypersensitivity with non-caseating granuloma w/ lymphanetic distribution
    • incidental finding of bilateral hilar lymphadenopathy
      • eventually leads to honeycomb lung w/ pulm. fibrosis
    • Schaumann body (laminated Ca2+ concretions due to metastatic calcification)
    • Asteroid bodies = proteinaceous inclusions in giant cells
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39
Q

describe the major form of the condition seen in the image

A
  • major = multiple medium vessels; presents with dyspnea, pleuritic chest pain & hemoptysis, tachypnea, tachycardia and V/Q mismatch
    • if bronchial arteries are intact → only hemorrhage, no infarction/necrosis
    • if bronchial arteries are compromised OR cardiac failure → red infarct (10% bc of collateral circulation)
      • usually in lower lobes
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40
Q

describe the image

A
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41
Q

describe what is seen in the image

A
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42
Q

describe the prognosis of the condition seen in the image

A
  • worst prognosis since already metastasized
  • cannot be resected → need chemotherapy/radiotherapy
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43
Q

describe the irregular form of the disease seen in the image

A
  • irregular (paracictratrical):
    • only one with fibrosis and contraction atelectasis
    • usually asymptomatic
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44
Q

describe the presentation of the disease seen in the image

A
  • presentation:
    • high spike fevers
    • halitosis
    • productive cough with foul-smelling sputum
    • finger clubbing (due to hypoxia)
    • hemoptysis
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45
Q

describe the pathogenesis of the disease seen in the image

A
  • pathogenesis:
    • bronchus: squamous metaplasia, goblet cell hyperplasia and goblet metaplasia into bronchioles
    • thickened BM
    • hypertrophy of bronchial smooth muscle
    • hypertrophy/hyperplasia of seromucinous glands
  • Reid index (ratio of thickness of submucosal gland:overall bronchial wall) is elevated >50% (normal = 40%)
46
Q

describe the pathogenesis of atopic bronchial asthma

A
  • atopic: extrinsic; genetic/family history
  • pathogenesis:
    • type 1 hypersensitivity
      • 1st exposure = antigen presentation, class switch to IgE
      • 2nd exposure = cross-linking on surface of mast cell → mast cell degranulation → histamine & leukotrienes → edema/exudate/neutrophils/bronchoconstriction (early phase)
      • IL-5 → chemotactic for eosinophils → MBP → damages cells and causes bronchoconstriction (late phase reaction, 4-24 hours)
47
Q

describe complications of the disease seen in the image

A
  • complications:
    • resp. failure
    • pulm. fibrosis
    • contraction atelectasis
    • cor pulmonale
    • nutmeg liver (chronic passive congestion)
48
Q

describe the complications associated with the condition seen in the image

A
  • complications:
    • centrally located = blocks bronchial lumen and no cilia → resorptive atelectasis
    • mucous trapped → recurrent bronchopneumonia → lung abscess → bronchiectasis
    • bilateral hilar lymphadenopathy
    • SVC syndrome
      • edema of face and upper extremities, DJV, cyanosis
    • hoarseness → left recurrent laryngeal n.
49
Q

what is the most common origin and risk factor for the condition seen in the image?

A
  • most common origin = deep leg veins (femoral, popliteal, iliac)
  • most common risk factor = stasis
  • most often clinically silent
50
Q

describe the presentation of atopic asthma

A
  • expiratory wheeze, chest tightness, productive cough, SOB, histamine → edema
    • NO hypertension
51
Q

name complications of neonatal atelectasis

A
  • intraventricular hemorrhage
  • PDA (persistent hypoxemia)
  • necrotizing enterocolitis (intestinal ischemia)
    • bloody diarrhea
  • hypoglycemia (excessive insulin release)
  • O2 therapy → increased ROS formation, can lead to:
    • damage to lungs (bronchopulmonary dysplasia)
    • cataracts/retinal damage (blindness)
52
Q

describe investigations for the disease seen in the image

A
  • investigations:
    • sputum cytology = mixed flora of anaerobes (make it foul smelling) & aerobes
    • high res CT = train track appearance because there is dilatation all the way to pleural surface
53
Q

describe the triad seen in all forms of the disease in the image

A
  • triad:
    • iron def. anemia (d/t blood loss)
    • cough with hemoptysis
    • pulm. infiltrates on x-ray
54
Q

describe Wegener’s granulomatosis (aka granulomatosis with polyangiitis, GPA)

A
  • URT symptoms = naso-mucosal ulceration, sinusitis
  • LRT = necrotizing pneumonia, granulomatous vasculitis that does NOT spare the lung → lung abscess
  • affects kidneys → renal infarcts and affects glomeruli capillaries (glomerular nephritis → crescent shape) → hematuria
55
Q

describe how the condition in the image occurs

A
  • aspiration, complicated pneumonia, obstruction, septic emboli
    • predisposing factors: alcoholics, stroke patients (decreased gag reflex), intubated, seizure, Alzheimer’s or any hospital bedridden patients
    • aspiration = more common on RIGHT side
      • standing = bottom of right lung
      • laying down = top of right lung
56
Q

describe the pathogenesis of the disease seen in the image

A
57
Q

describe the histology of the condition seen in the image

A
  • histology:
    • round, scant cytoplasm, finely granular chromatin
    • frequent mitotic bodies
    • cytology shows nuclear molding (NOT in bronchial carcinoid)
58
Q

describe complications seen in the condition in the image

A
  • cervical sympathetic syndrome
    • ipsilateral Horner syndrome (ptosis, anhydrosis, miosis = PAM)
    • wasting of thenar eminence b/c of brachial plexus compression
    • recurrent laryngeal nerve paralysis & dysphagia (compressed esophagus)
    • SVC syndrome = triad: cyanosis, DJV, edema of face and arms
59
Q

describe the secondary cause of the condition seen in the image

A
  • secondary: endothelial dysfunction due to underlying disorder → loss of vasodilators (NO) or increase in vasoconstrictors (endothelin, serotonin)
    • pulmonary: obstructive and restrictive lung diseases (except bronchial asthma), recurrent minor pulm. embolism
      • high altitude
    • cardiac: L → R shunt (ASD, VSD, PDA), mitral stenosis
      • loud P2: pulmonary valve makes a sound when it closes
60
Q

describe complications of the disease seen in the image

A
  • complications:
    • respiratory failure and cor pulmonale (R heart failure secondary to pulm. hypertension)
      • after 2 weeks → liver cirrhosis/nutmeg liver
      • Pores of Kohn are easier to be spread by → lobar pneumonia is worse if acquired
61
Q

in testing for the condition seen in the image, ____ will be elevated

A

in testing for the condition seen in the image, pulmonary capillary wedge pressures will be elevated (cardiac catheterization measures pressures of heart)

62
Q

describe the paraneoplastic syndrome associated with the condition seen in the image

A

PTH-related peptide → hypercalcemia → can result in metastatic calcification

63
Q

describe who the disease shown in the image mainly affects

A
  • AAs, Danish, Swedish; higher incidence in non-smokers and young females (AA female)
64
Q

describe the presentation of the condition seen in the image

A
  • presentation:
    • dyspnea
    • cachexia (bc of TNF alpha)
    • finger clubbing
    • hemoptysis
65
Q

describe the etiology (cardiogenic) of the disease shown in the image

A
  • etiology (of cardiogenic pulm. edema)
    • LHF
66
Q

describe the presentation of the condition seen in the image

A
  • presentation:
    • productive cough (foul-smelling sputum)
    • halitosis
    • hemoptysis
    • finger clubbing
    • high spiking fever
    • weight loss
  • x-ray: cavity with air-fluid level (liquefactive necrosis due to pyogenic bacteria)
  • sputum: mixed flora
67
Q

describe the diagnosis of the disease seen in the image

A
  • diagnosis:
    • sudden onset
    • ground glass appearance on XR
    • bilateral diffusion interstitial infiltrates
    • pulm. edema with NORMALpulm. capillary wedge pressure (not a heart problem, increased wedge pressure seen in heart problems)
    • refractory hypoxemia (even w/ supplemental O2, cyanosis continues due to hyaline membranes → diffusion barrier)
68
Q

describe the image

A

diffuse pulmonary hemorrhagic syndrome

69
Q

describe the centroacinar form of the disease shown in the image

A
  • centroacinar: respiratory bronchioles & upper lobes
    • have to be a smoker b/c normal levels of A1AT but elastase overwhelms the A1AT
70
Q

describe the organizing (proliferative) phase of the disease seen in the image

A
  • organizing (proliferative) phase = 4 days - 3 weeks
    • proliferation of type II pneumocytes & fibroblasts which lay down collagen → organization of fibrin exudates → fibrosis & alveolar septal thickening
      • chronic inflammation = pulm. fibrosis → contraction atelectasis
      • cor pulmonale = R heart failure secondary to lung disease
71
Q

describe the etiology of non-atopic asthma

A
  • non-atopic: intrinsic; aspirin and viral infxns
    • aspirin: inhibits COX and favors lipooxygenase → increased LTs → bronchoconstriction + bronchospasms
      • aspirin triad = nasal polyps, intrinsic asthma, rhinitis, hives
    • viral: lowers threshold for sub-epithelial vagal receptors to irritants → increased ACh binding → increased PS response → bronchoconstriction
72
Q

name 2 other findings in the disease shown in the image

A
  • polyclonal hypergammaglobulinemia = dysregulation of T cells
  • cutaneous anergy = develop sarcoidosis following TB, use all T cells and epithelioid cells to form non-caseating granulomas → no cells to mount response to PPD →become PPD (-) (even w/ TB)
73
Q

describe the pathogenesis of the condition seen in the image

A
  • pathogenesis: pseudostratified → stratified squamous
    • precursor lesion = squamous dysplasia
    • squamous metaplasia → dysplasia → sq. cell carcinoma in situ → invasive sq. cell carcinoma
74
Q

describe the images

A
75
Q

name direct causes of the disease shown in the image

A
  • direct causes:
    • pulmonary contusion (bruises) due to blunt force trauma to chest
    • near-drowning experiences
    • aspiration pneumonia
76
Q

describe the pathogenesis and location of the condition seen in the image

A
  • cell of origin = bronchioalveolar stem cell/Clara cell
  • precursor lesion = atypical adenomatous hyperplasia
  • located peripherally = coin lesion on x-ray
77
Q

describe the investigations and complications of the disease seen in the image

A
  • investigations:
    • NO dullness on percussion → bc alveolar spaces are empty
    • x-ray = interstitial infiltrates; ground glass opacity
    • serology = IgM, IgG titers = most accurate
  • complications:
    • ARDS → hyaline membranes on autopsy
78
Q

describe Goodpasture’s disease

A
  • pulmonary-renal disorder typically in young men; type II HS
    • proliferative and rapidly progressive glomerulonephritis
    • hemorrhagic interstitial pneumonia
    • antibodies attacking glomerular & pulmonary BM (α3 chain of type IV collagen)
    • triad seen but also affects kidney → glomerular nephritis → hematuria
    • NEVER see URT → no nasal ulceration or sinusitis
79
Q

describe the concept of resorption

A
80
Q

describe the symptoms seen in the disease shown in the image

A
  • sudden onset SOB, tachypnea, tachycardia, cyanosis → resp. acidosis (high CO2)
81
Q

describe the disease shown in the image

A

permanent destruction & dilatation of airways distal to terminal bronchioles without fibrosis (exception: irregular type)

82
Q

describe the presentation of the disease seen in the image

A
  • presentation:
    • mild symptoms in the beginning (dry cough and low grade fever), DAD → hyaline membrane
83
Q

describe the presentation of the condition seen in the image

A
  • presentation: fatigue, syncope, dyspnea upon exertion, chest pain
    • severe resp. insufficiency, cyanosis, death from RHF 2-5 years from diagnosis
    • long standing/chronic severe → plexiform lesions = vasculature channels within the intima → multiple lumina within a small artery at a branch point from a larger artery
    • smaller capillaries can’t take extreme pressure & undergo fibrinoid necrosis, dilations and hemorrhage
      • sign of chronic pulm. HT
84
Q

describe the causes of the disease seen in the image

A
  • cause:
    • # 1 is CF
    • Kartegeners syndrome (sinusitis, bronchiectasis, infertility in males, situs inversus/dextrocardia)
    • chronic bronchitis (mucus plugs)
    • allergic bronchopulmonary aspergillosis
    • TB
    • centrally located tumors
85
Q

describe the presentation of the disease seen in the image

A
  • presentation:
    • blue bloaters bc mucus plugs trap CO2, increase paCO2 and decrease paO2
      • cor pulmonale → ascites and peripheral edema
    • decreased FEV1:FVC ratio and increased TLC and RV
    • x-ray: see pneumonia bc no cilia and resorption atelectasis bc of mucus plugs blocking the bronchial lumen
    • ABG: hypoxia, hypercapnia, resp. acidosis
      • peripheral chemoreceptors detect low O2 but no increased PCO2 → can’t give O2 bc pts stop breathing
86
Q

describe status asthmaticus

A

common in extrinsic/non-atopic asthma

  • do not respond to medications
  • severe and unresponsive to therapy
  • severe mucus plugs → resportive atelectasis
  • require intubation
87
Q

describe complications of the disease seen in the image

A
  • complications:
    • can lead to resp. failure, cor pulmonale
    • decreased FEV1:FVC, increased TLC and RV
    • metastatic abscesses
    • sepsis if travels to blood
    • resorption atelectasis due to obstruction of bronchial lumen
    • AA amyloidosis due to chronic inflam. condition
88
Q

describe the acute phase of the disease seen in the image

A
  • acute phase (exudative phase) = 0-4 days
    • neutrophils, necrotic debris, fibrin
    • heavy and firm lungs, interstitial and intra-alveolar edema/hemorrhage, necrosis and sloughing of alveolar epithelial cells
    • see hyaline membrane → made up of debris and fibrin → diffusion barrier
89
Q

describe the paraneoplastic syndromes associated with the condition seen in the image

A
  • paraneoplastic syndrome = hematological → all due to MUCIN
    • Trousseau’s = thrombus in superficial vein → vein is red, hot, swollen, painful → recurrent and migratory
    • sterile vegetations on heart valves = nonbacterial endocarditis = Marantic endocarditis
      • aortic valve → aortic regurg. → diastolic murmur → pulm. edema
90
Q

describe the presentation of the condition seen in the image

A
  • presents like lobar pneumonia
    • productive cough with a lot of sputum
    • SOB, pleuritic chest pain
    • NO coin lesion
    • consolidation of the lobe on x-ray
91
Q

describe the disease shown in the image

A
92
Q

describe the presentation of the condition seen in the image

A
  • presentation:
    • dyspnea
    • cachexia (b/c of TNF alpha)
    • finger clubbing (all lung cancers)
93
Q

describe the immunohistochemical stain for the condition seen in the image

A

neuroendocrine markers = synaptophysin, chromogranin, CD56

94
Q

describe the cell of origin and markers for staining for the condition seen in the image

A
  • cell of origin = Kulchitsky (neuroendocrine) cells
  • same neuroendocrine markers as small cell = synaptophysin, chromogranin, CD56
95
Q

describe how the disease shown in the image can occur in sick, immunocompromised, elderly patients

A
  • bronchopneumonia: patchy lung; bronchi and bronchioles are damaged
    • Klebsiella → alcoholics, diabetics → aspiration
      • red currant jelly sputum
    • Pseduomonas → CF, ventilators, burns, lung abscesses
    • Klebiella and Pseudomonas both cause necrotizing pneumonia bc they are angio-invasive → endothelial damage
    • S. aureus following viral infxn (influenza)
    • Legionella → contaminated water sources (ACs)
96
Q

what hormone is used to monitor treatment of the disease shown in the image?

A

ACE is elevated in sarcoidosis → used to monitor response to treatment

97
Q

describe the complications of the cardiogenic form of the disease shown in the image

A
  • complication:
    • can lead to pulm. HT → heart failure cells
    • will NOT lead to cor pulmonale bc cardiac problem CAME FIRST
98
Q

describe the pattern of growth of the condition seen in the image

A

there is a lepidic pattern on biopsy (butterfly on fence)

99
Q

describe carcinoid syndrome

A
  • carcinoid syndrome = episodic flushing, wheezing, diarrhea due to increased serotonin
    • look for 5-HIAA in urine
100
Q

describe the pathogenesis of the cardiogenic form of the disease shown in the image

A
  • pathogenesis:
    • <2 weeks = transudate due to increased hydrostatic pressure
    • 2 weeks = alveolar wall fibrosis, heart failure cells
101
Q

describe the septal/distal acinar form of the disease seen in the image

A
  • septal (distal acinar):
    • rupture into pleural space → bullae & pneumothorax → compression atelectasis
102
Q

describe other causes of the condition seen in the image

A
  • other causes of lung abscess: vasculitis
    • lymphomatoid granulomatosis: associated with EBV and necrotizing granulomas
    • Wegener’s granulomatosis → aspergilloma
    • Churg Strauss
103
Q

name the cell of origin and precursor lesion of the condition seen in the image

A

cell of origin = bronchoalveolar stem cells (Clara cells)

precursor lesion = atypical adenomatous hyperplasia

104
Q

describe the primary causes of the condition seen in the image

A
  • primary = mutation in BMPR2
    • BMPR2 normally binds to TGFB and inhibits smooth muscle proliferation
    • mutation causes hyperplasia of smooth muscle and increased vascular resistance
    • common in young females 20-40
105
Q

describe complications of the condition seen in the image

A
  • complications:
    • location makes it easy to cause pleural effusions → compression atelectasis
    • left side → pericardial effusion → pericardial tamponade (hypotension, DJV, distant heart sounds = Beck’s triad)
106
Q

describe the concept of compression

A
  • compression = reversible
    • pneumothorax, hemothorax, pneumohemothorax, chylothorax (lymph), empyema (pus), pleural effusion
    • X-ray: trachea deviates to OPPOSITE SIDE
107
Q

describe diagnosis of the disease seen in the image

A
  • diagnosis:
    • decreased FEV1:FVC ratio, increased TLC and RV
    • ABG: decreased O2, normal pH and normal CO2
      • later stages = pH drops and CO2 increases while O2 decreases
    • x-ray: hyperlucent (air trapping), hyperinflated lungs with flattened domes of diaphragm and narrow mediastinum
      • increased AP diameter (barrel)
108
Q

describe the genetic mutations seen in the condition in the image

A
  • etiology:
    • KRAS = smokers
    • EGFR = women, non-smokers, Asians
    • ALK = signet adenocarcinoma in non-smokers
109
Q

describe the etiology of the non-cardiogenic form of the disease shown in the image

A
  • non-cardiogenic pulmonary edema etiology:
    • ARDS, high altitude, neurogenic, pulm. thromboembolism
110
Q

describe the complications of the condition seen in the image

A
  • complications: RHF → nutmeg liver
    • HEAD: hepatosplenomegaly, peripheral edema, ascites, distended jugular vein
111
Q

describe the disease seen in the image and its etiology

A

productive cough of foul-smelling, purulent sputum for 3 consecutive months for 2 consecutive years

  • etiology: cigarrette smoking, 40-45 years old

Path Exam 2 (4 decks)

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