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Step 1 Complete > Respiratory Path USMLE > Flashcards

Respiratory Path USMLE Flashcards

1
Q

What is the difference between oxygen saturation (SaO2) and partial pressure of oxygen (PaO2)?

A

SaO2: oxygen in the red blood cell attached to the Hb.

PaO2: oxygen dissolved in plasma. If PaO2 is decreased, SaO2 has to be decreased.

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2
Q

How could you determine if hypoxemia is due to a pulmonary cause or an extrapulmonary cause?

A

Hypoxemia due to a pulmonary cause will cause an increase in the A-a gradient. Extrapulmonary cause will have a normal A-a gradient.

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3
Q

What are the causes of hypoxemia?

A

Increased A-a gradient: ventilation defects, perfusion defects, diffusion defects, R-L shunts.
Normal A-a gradient: depression of respiratory center in the medulla, upper airway obstruction, chest bellows dysfunction.

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4
Q

If a patient is anemic, do they have hypoxemia?

A

No. The patient will have normal respiration, normal PaO2 and normal SaO2.

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5
Q

What are the SaO2 and PaO2 values in a patient with carbon monoxide poisoning?

A

CO competes with O2 for binding sites on Hb, which decreases SaO2 without affecting PaO2.

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6
Q

What three ways does CO cause hypoxia?

A

CO competes with O2 for binding sites.
Inhibits cytochrome oxidase in the ETC.
Causes a left shift in the O2-binding curve.

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7
Q

Patient who lives in a cabin presents with cherry-red discoloration of skin and blood. They have a headache initially, but after you give 100% O2, the symptoms subside. What did you treat?

A

CO poisoning.

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8
Q

Patient presents with cyanosis, a normal PaO2 and a decreased SaO2. 100% oxygen doesn’t improve the cyanosis. How would you treat this patient?

A

Patient will also have chocolate colored blood. Methemoglobin (metHb) is Hb with Fe3+ and cannot bind O2. MetHb reductase normally converts Fe3+ to Fe2+. Treatment: IV methylene blue (activates metHb reductase) and ascorbic acid.

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9
Q

Name some causes of metHb.

A

Nitrite or sulfur-containing drugs (dapsone).

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10
Q

A newborn turns cyanotic when breast-feeding. Crying causes the child to pink up again. Diagnosis?

A

Choanal atresia: unilateral or bilateral bony septum between the nose and the pharynx.

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11
Q

What causes nasal polyps?

A

Nasal polyps develop as a response to chronic inflammation. They are non-neoplastic and consist of an edematous mucus and loose stroma. Allergies and NSAIDs are the most common cause. CF in child must be considered.

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12
Q

What ABG’s would you find in a patient in an episode of sleep apnea?

A

Decreased PO2 and O2 saturation and increased PCO2 (respiratory acidosis).

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13
Q

Name the most common pathogens in sinusitis.

A

Streptococcus pneumoniae (most common).
Chronic sinusitis: rhinoviruses, anaerobes.
Systemic fungi: mucor (diabetics) or aspergillus.

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14
Q

What are the most common sinuses involved in sinusitis?

A

Maxillary: adults.
Ethmoid: children.

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15
Q

Define atelectasis. What are the three types of acquired atelectasis?

A

Loss of lung volume due to inadequate expansion of the airspaces (collapse).

Resorption (obstruction), compression, contraction (fibrosis).

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16
Q

Explain the pathophysiology of resorption atelectasis.

A

Resorption: airway obstruction prevents air from reaching aveoli. Pores of Kohn drain pre-existing air from aveoli causing collapse. Mediastinum shifts toward effect lung.

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17
Q

Explain the pathophysiology of compression atelectasis.

A

Compression atelectasis occurs whenever the pleural cavity is filled by exudate, tumor, blood or air (tension pneumothorax). The pressure causes collapse of small airways beneath the pleura. Mediastinum will shift away from the effected lung.

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18
Q

What week of fetal life does surfactant synthesis begin? What hormones increase surfactant production? What decreases surfactant production?

A

28th.
Increases: cortisol and thyroxine.
Decreases: insulin.

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19
Q

What are some causes of respiratory distress syndrome in newborns?

A

Prematurity, maternal diabetes (fetal hyperglycemia increases insulin), and Cesarean section (lack stress = lack of cortisol release).

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20
Q

This is a slide of neonatal respiratory distress syndrome. What is the arrow pointing at?

A

Dilated alveolar ducts are lined with a fibrin-rich membrane (hyaline membrane). Subjacent alveoli are collapsed.

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21
Q

What complications can arise from treating neonatal RDS with O2 therapy?

A

Superoxdie free radical damage can cause blindness and permanent damage to small airways (bronchopulmonary dysplasia).

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22
Q

What are the pathological causes of pulmonary edema?

A

Alteration in Starling pressure (transudate): hemodynamic disturbances - LHF, volume overload, mitral stenosis. Decreased oncotic pressure (less common) - nephrotic syndrome, cirrhosis.

Microvascular or alveolar injury(exudate): sepsis, aspiration (drowning, gastric contents), drugs, shock, trauma, high altitude.

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23
Q

Define acute respiratory distress syndrome. What is the histological manifestation of ARDS?

A

Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage. DAD - diffuse alveolar damage is the histological manifestation.

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24
Q

What are the top 4 causes of ARDS?

A

Gram-negative sepsis (40%)
Gastric aspiration (30%)
Severe trauma with shock (10%)
Diffuse pulmonary infections, heroin, smoke inhalation.

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25
Q

What is the morphological changes of alveoli in ARDS? Acute and chronic changes?

A

Alveolar walls become lined with waxy hyaline membranes due to a protein-rich exudate. Pneumocytes (both I and II) are also damaged leading to a decrease in surfactant and atelectasis. Late features of ARDS: progressive interstitial fibrosis.

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26
Q

Define acute interstitial pneumonia.

A

Same clinical course as ARDS but etiology is unknown.

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27
Q

Broadly define pneumonia. In what clinical setting does pneumonia commonly occur?

A

Pneumonia can be defined as any infection of the lung parenchyma. It can result whenever the defense mechanisms of the lung are impaired or whenever the resistance of the host in general is lowered.

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28
Q

How can the clearing mechanisms of the lung be interfered?

A

Suppression of cough reflex (coma, anesthesia, drugs, etc.).
Injury to the mucociliary apparatus (viral infection, smoking, etc.)
Interference with the phagocytic or bactericidal action of alveolar macrophages.
Pulmonary congestion/edema.
Accumulation of secretions (e.g. CF).

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29
Q

What is the most common cause of death in viral influenze epidemics?

A

Bacterial pneumonia. This highlights the point that one type of pneumonia (viral) often predisposes to another type, especially in debilitated patients.

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30
Q

What are some typical community-acquired pneumonia?

A

Most are bacterial pathogens. Most often it is due to Streptococcus pneumoniae. Other: Haemophilus influenzae, Moraxella catarrhalis, Legionella pneumophilia (gram -), Klebsiella pneumoniae

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31
Q

What does this sputum stain show?

A

Numerous lancet-shaped diplococci. Streptococcus pneumoniae.

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32
Q

Explain the findings on this lung specimen.

A

Cross section of lung showing patchy areas of consolidation consistent with bronchopneumonia.

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33
Q

What are the four stages of the inflammatory response in lobar pneumonia?

A

Congestion: intra-alveolar fluid + bacteria
Red hepatization: massive exudation + fibrin, red
Gray hepatization: fibrinosuppurative exudate, dry/gray
Resolution

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34
Q

What are of the lung does bronchopneumonia usually involve?

A

Lower lobes or right middle lobe.

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35
Q

Many of the clinical features of typical pneumonia is due to _______. What are the clinical features?

A

Consolidation (inflammatory exudate causing solidification of pulmonary tissue). Clinical features: high fever, productive cough, consolidation: dullness to percussion, increased vocal fremitus, inspiratory crackles, whisper pectoriloquy, egophony.

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36
Q

What are the atypical community-acquired pneumonias?

A

Mycoplasma pneumoniae, Chlamydia pneumoniae (TWAR agent), Chlamydia trachomatis (newborns), viruses: RSV, influenza, adenovirus.

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37
Q

A child presents with an ear infection an pneumonia. The causative agent is worrisome in young children because it can lead to meningitis. This bacteria also cause purulent conjunctivitis. What is it?

A

Purulent conjunctivitis (pinkeye). Haemophilus influenzae.

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38
Q

An alcoholic presents to the ER with a productive cough, thick/gelatinous sputum and a CXR showing patchy consolidations. What is the most likely pathogen?

A

Klebsiella pneumoniae often effects alcoholics and malnourished people. Thick and gelatinous sputum is very characteristic.

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39
Q

What water-loving bacteria causes Pontiac fever (self-limiting URT infection) and pneumonia?

A

Legionella pneumophila

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40
Q

What does the atypical stand for in atypical pneumonia?

A

Atypical denotes the moderate amount of sputum, no physical findings of consolidation, moderate elevation of WBC, and lack of alveolar exudate. Atypical pneumonia also has an insiduous onset, a low-grade fever, and a non-productive cough.

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41
Q

What pathogens cause nosocomial pneumonia?

A

Gram-negative bacteria: Pseudomonas aeruginosa (respirators), Escherichia coli
Gram-positive bacteria: Staph aureus

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42
Q

What pathogens cause pneumonia in immunocompromised hosts?

A

CMV, Pneumocystis jiroveci, Aspergillus fumigatus.

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43
Q

What portion of the lung does Primary TB commonly infect? How about reactivation TB?

A

Primary: upper part of the lower lobes or lower part of the upper lobes.

Reactivation: involves apices in upper lobes.

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44
Q

This silver-impregnated cytologic smear of bronchial tissue shows what fungi?

A

AIDS patient with Pneumocystis jiroveci pneumonia.

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45
Q

Lung biopsy stained with Gomori methenamine-silver showing septated hyphae. The inset shows a fruiting body. Fungi?

A

Aspergillus fumigatus.

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46
Q

Narrow-based bud. This fungus was contracted by a pigeon carer.

A

Crytococcus neoformans.

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47
Q

This lung biopsy shows a spherule containg endospores. What fungi?

A

Coccidiodes immitis.

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48
Q

This yeast has been phagocytosed by macrophages.

A

Histoplasma capsulatum.

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49
Q

Broad-based bud. Fungi?

A

Blastomyces dermatidis.

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50
Q

What clinically distinct sign will a newborn present with it contracts Chlamydia trachomatis from its mother?

A

Staccato cough.

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51
Q

What is the bacteria that cause Q-fever? Who most commonly acquires atypical-pneumonia via this bacteria?

A

Coxiella burnetii. Contracted by dairy farmers, veterinarians.

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52
Q

What is a lung abscess? What is the most common cause of lung abscesses?

A

A pulmonary abscess describes a local suppurative process within the lung, characterized by necrosis of lung tissue. Aspiration of oropharyngeal material is the most common cause.

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53
Q

Which bacterial pneumonia can lead to a lung abscess?

A

Staph aureus, Klebsiella, an type 3 pneumococcus.

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54
Q

Which of these pathogens does NOT cause granulomatous inflammation with caseous necrosis:
Histoplasma, Coccidioides, TB, Blastomyces, Cryptococcus, Sarcoidosis

A

Sarcoidosis (noncaseating)

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55
Q

What is empyema?

A

Pus in the pleural cavity.

56
Q

A patient presents to you with a spiking fever, a productive cough, and copious amounts of foul-smelling purulent or sanguineous sputum. The patient also has a history of IV drug abuse. What do you suspect, but what must you rule out?

A

This patient has a lung abscess due to a septic embolism from infective endocarditis. 10-15% of abscesses are due to an underlying carcinoma.

57
Q

What is the most common site of aspiration in the lung?

A

Superior segment of right lower lobe.

58
Q

Name the fungi associated with the region:
Ohio/Mississippi river:
Central/SE US:
Southwest US:

A

Histoplasma
Blastomyces
Coccidioides

59
Q

Where do most pulmonary thromboemboli originate from?

Where do most pulmonary thromboembolisms occur in the lung?

A

Femoral vein (DVT’s of the calf must propogate to the femoral vein to have the potential to be embolic).

Majority are located in the lower lobes where perfusion is greater.

60
Q

Three days after undergoing hip surgery, a patient has a sudden bout of dyspnea and tachypnea. What is the most likely cause?

A

Pulmonary thromboemboli from the femoral vein. Virchow’s triad: stasis, hypercoagulability and endothelial injury (less important in venous thrombi).

61
Q

What is the cause of primary pulmonary hypertension? What are the main causes of secondary pulmonary hypertension?

A

Primary: W>M. Vascular hyperactivity with proliferation of SMCs.

Secondary: respiratory acidosis and/or hypoxemia leading to hyperplasia/hypertrophy of SMCs

62
Q

How does emphysema cause pulmonary hypertension?

A

Loss of pulmonary vasculature increases the workload for remaining vessels.

63
Q

Smoker presents with dysnpea, accentuated P2, and a left parasternal heave. Diagnosis?

A

Pulmonary hypertension. Patient CXR may also show tapering of the pulmonary arteries. Left parasternal heave is a sign of RVH which can lead to RHF due to cor pulmonale.

64
Q

What are the classical physiological features of the restrictive lung diseases?

How is FVC, FEV1 effected? How about RV?

A

Reduced carbon monoxide diffusing capacity, decreased lung volume, and decreased compliance (increase elasticity).

FEV1 is normal to decreased. FVC is severely decreased. RV is also decreased.

65
Q

List some causes of restrictive lung disease:

A

Chest wall disorders: kyphoscoliosis, pleural disease, obesity
Acute interstitial lung disease: ARDS
Chronic interstitial lung disease: fibrosing disorders (e.g. pneumoconiosis, IPF), granulomatous disease (sarcoidosis).

66
Q

What are the most common minerals that cause pneumoconioses?

A

Coal causes CWP.
Asbestos causes asbestosis.
Silica causes silicosis.
Beryllium.

67
Q

What particle size of a mineral dust determines where it will deposit in the lungs?

A

1-5 microm will reach the bifucation of the respiratory bronchioles and alveolar ducts.

Smaller than .5 microm will reach teh alveoli and are phagocytosed by alveolar macrophages.

68
Q

Of the mineral dust: asbestos, silica, coal, increase the risk of cancer? TB?

A

Abestos increases the risk of cancer.
Silica increases the risk of TB and cancer.
Coal dust doesn’t increase the risk of TB or cancer.

69
Q

What is anthracosis? What is a dust cell?

A

Accumulation of coal pigment without a cellular reaction.

Dust cells are alveolar macrophages with coal pigment. They are expelled via coughing or through the lymphatics.

70
Q

Fibroblast release _____ (a component of collagen type III) that traps macrophages and begin the fibrosing process of CWP.

A

Reticulin.

71
Q

What is Caplan’s syndrome?

A

Pneumoconiosis plus large cavitating rheumatoid nodules in the lungs.

72
Q

What is the “black lung disease’?

A

Complicated coal workers pneumoconiosis. Also known as progressive massive fibrosis.

73
Q

What is the most common occupational disease in the world?

A

Silicosis: acquired while casting metal, sandblasting, working in mines. Quartz deposits in the lung and increases the risk of both TB (tuberculosilicosis) and cancer.

74
Q 
Match the Xray findings with a disease:
A) Egg-shell calcification in the hilar nodes
B) Potato nodes (hilar or mediastinal)
C) Honeycomb lung
D) Ground glass appearance of the lung
A

A) Silicosis
B) Sarcoidosis
C) Idiopathic pulmonary fibrosis (but can also denote any late state fibrosis)
D) Neonatal RDS

75
Q

Where does quartz deposit in the lungs?

A

Upper lungs.

76
Q

What pathogenic cytokines contribute to the fibrotic changes in restrictive lung disease?

What other macrophage products contribute to fibrosis?

A

IL-1, TNF, LTB4, monocyte chemoattractent protein-1, MIF

Growth factors: TGF, GF, FGF, IGF, PDGF

Macrophages: oxygen free radicals

77
Q

What are the signs of cor pulmonale?

A 
Right ventricular heave
Large A waves
Loud pulmonary valve closure sound (P2)
Hepatomegaly
Edema
78
Q

What geometric forms of asbestos are clinically important?

A

Serpentine: curly and flexible - produce interstitial fibrosis and lung cancer.

Amphibole: straight and rigid - produce interstitial fibrosis, lung cancer, and mesothelioma.

79
Q

A man who worked his whole life on naval ships develops exertional dysnpea and a dry cough. Examination reveals finger clubbing and end-inspiratory crackles in lower lung fields. Diagnosis?

A

Asbestos pneumoconiosis.

80
Q

Name the asbestos related diseases:

A

Most common: benign pleural plaques.
Diffuse interstitial fibrosis with/without pleural effusion.
Primary bronchogenic carcinoma.
Malignant mesothelioma of pleura.

81
Q

What is the most common noninfectious granulomatous disease of the lung? What the pathogenesis of it?

A

Sarcoidosis: CD4 Th cells interact with an unknown antigen.

82
Q

Patient presents with dyspnea, a violaceous rash on his cheeks (lupus pernio), and erythema nodosum. The patient also complains of blurry vision. Labs show an increase in ACE. Diagnosis?

A

Sarcoidosis.

83
Q

What lab findings could you elicit from a sarcoidosis patient?

A

Increased ACE. Hypercalcemia due to increase in 1-alpha-hydroxlase in granulomas (hypervitaminosis D). Polyclonal gammopathy. Increased TNF.

84
Q

What is the definition of idiopathetic pulmonary fibrosis?

A

Repeated cycles of alveolitis triggered by an unknown agent.

85
Q

What are the types of hypersensitivity pneumonintis?

A

Farmer’s lung: due to thermophilic actinomycetes in moldy hay. Type III hypersensitivity.
Silo filler’s disease: inhalation of gases from plants.
Byssinosis: textile factories.

86
Q

What drugs can cause interstitial fibrosis of the lungs?

A

Amiodarone. Bleomycin. Cyclophophamide. Methotrexate. Nitrosurea.

87
Q

Define emphysema.

A

Emphysema is defined as abnormal permanent enlargement of air spaces distal to the terminal bronchioles (the respiratory unit), accompanied by the destruction of the walls and without obvious fibrosis.

88
Q

What are the two most commonest types of emphysema?

A

Centriacinar: most common type in smokers, involves the upper lung.

Panacinar: predominantly in the lower lungs and more associated with AAT deficiency.

89
Q

Define obstructive lung disease.

A

Characterized by an increase in airway resistance (particularly expiratory airflow) due to narrowing of airway lumen.

90
Q

Patient presents with decreased breath sounds, dyspnea, and hyperventilation. The patient is also very thin and has a pink complexion. Diagnosis?

A

This ‘pink puffer’ has the clinical signs of emphysema.

91
Q

Describe.

A

Hyperlucent lung field. Vertically oriented heart. Depressed diaphragm. = emphysema.

92
Q

Obstructive disorders are characterized by an increase in airway resistance. Explain how emphysema leads to airway resistance?

A

Distal terminal bronchioles lose elastic tissue which is responsible for the radial traction. This causes the airways to collapse, particularly on expiration.

93
Q

How does cigarette smoke cause emphysema?

A

Cigarette smoke is chemotactic to neutrophils and macrophages. They accumulate in the respiratory unit and release free radicals and elastases. Cigarette also inactivates AAT (acquired AAT deficiency) and antioxidants. The pathogenesis of emphysema is explained by this imbalance in ROS > antioxidants and elastases > AAT.

94
Q

Define chronic bronchitis.

A

The presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough were excluded).

95
Q

What is the pathogenesis of chronic bronchitis?

A

Hypersecretion of mucus in bronchi.
Obstruction to airflow in the terminal bronchioles: narrowing of the terminal bronchioles by mucus plugs, inflammation, and fibrosis.
Mucus plugs: located in a proximal terminal bronchiole prevents exodus of large amounts of CO2 causing respiratory acidosis.

96
Q

What changes occur in the bronchi in chronic bronchitis?

Changes in terminal bronchioles?

A

Bronchi: hypersecretion of submucosal mucus glands. Acute inflammation/chronic inflammation. Loss of ciliated epithelium and presence of squamous metaplasia.

TB: mucus plugs. Goblet cell metaplasia, hypertrophy of mucous glands, chronic inflammation and narrowing of lumen.

97
Q

How does chronic bronchitis differ from emphysema?

A

PaCO2 in chronic bronchitis is increased leading to respiratory acidosis. Cyanosis is also present, the patients are often stocky, and cor pulmonale is common. Additionally, chronic bronchitis has an early onset of hypoxemia and a late onset of dyspnea.

98
Q

What are the two types of asthma?

A

Extrinsic (atopic): type I hypersensitivity reaction.

Intrinsic: nonimmune. Virus-induced, air pollutants, NSAIDS, stress, exercise, cigarette smoke.

99
Q

What are the histologic changes that occur in the bronchi of asthmatics?

In the terminal bronchioles?

A

Bronchi: thickening of BM, edema, hypertrophy of submucosal gland, hypertrophy/hyperplasia of SMC.

Bronchioles: mucus plugs (with Curschmann spirals - shed epithelial cells), Charcot-Leyden crystals (eosinophil remnants), loss of epithelial cells, goblet cell metaplasia, thick BM, SMC hypertrophy/plasia.

100
Q

Patient presents with episodic expiratory wheezing, nocturnal cough and a barrel chest. Diagnosis?

A

Most likely asthma.

101
Q

Describe the late phase reaction in asthma.

A

Late phase (4-8 hrs later): eotaxin is produced (chemotactic for eosinophils), eosinophils release MBP and cationic protein (damage epithelial cells and produce airway constriction).

102
Q

Define bronchiectasis.

A

Permanent dilation of bronchi and bronchioles caused by destruction of cartilage and elastic tissue by necrotizing infections.

103
Q

A male patient commonly presents with bacterial pneumonia and sinusitis infections. He also learned recently he is infertile. What could explain this mans condition?

A

Kartagener syndrome: bronchiectasis, sinusitis, and situs inversus. Half of patients with primary ciliary dyskinesia have kartageners.

104
Q

Whats the pathogenesis of dyskinesia?

A

Autosomal recessive syndrome is characterized by an absence or shortening of the dynein arm in cilia (binds ATPase and moves).

105
Q

What are the gross findings in the lung of a patient with bronchiectasis?

A

Occurs in the lower lobes.
Dilated bronchi filled with pus.
Airways extend to the lung periphery.

106
Q

Patient presents with massive hemoptysis, digital clubbing, and cor pulmonale. Patient also has copious amounts of sputum. Diagnosis?

A

Bronchiectasis.

107
Q

You determine your patient has the most common cause of bronchiectasis in the US. Explain how a sweat test confirmed you suspicions.

A

CFTR is a chloride ion channel (ATP-channel). Loss of Cl- causes decreased Na+ and Cl- reabsorption in sweat glands, thus making the skin hypertonic. This channel also cause increased water reabsorption from luminal secretions (bronchioles, bile duct, vas deferens, pancreatic duct etc.)

108
Q

In COPD, what type of metaplasia occurs in the epithelium of the bronchi?

A

Pseudostratified columnar changes into stratified squamous.

109
Q

An AIDS patients presents fatigue and has diffuse, patchy infiltrates on CXR. A methenamine silver stain of bonchoalveolar lavage is positive. Because the patient is allergic to sulfa drugs we must treat him with _____.

A

Pentamidine is used to treat Pneumocystis jiroveci.

110
Q

Child presents with severe upper airway wheezing (stridor) and is unable to swallow. Observation of the mouth reveals a large cherry like formation at the base of the tongue. What does this child have?

A

The most common cause of epiglottitis in children is due to Haemophilus influenzae type b.

111
Q

On the wards you come across a child who has a fever, a soar throat and a dark exudate on his pharynx base. You realize that taking a scraping could lead to systemic infection. How do you confirm your suspicion on what bacteria it is?

A

Send a throat/nasopharynx swabs for culture on a potassium tellurite agar and Loeffler’s coagulated blood serum medium.

112
Q

What gram positive nonspore forming rod releases a powerful exotoxin into the bloodstream that damages heart and neural cells by inhibiting protein synthesis?

A

Corynebacterium diphtheriae.

113
Q

Woolsorter’s disease is not pneumonia. The bacteria that causes it is a gram positive spore forming rod. Explain how it causes respiratory issues.

A

Bacillus anthracis is normally contracted from goat hair (hides). Spores are taken up by macrophages and transported to mediastinal/hilar nodes. Here, they germinate and cause mediastinal hemorrhage. On CXR this shows up as an enlarged area on chest radiograph and CT scan.

114
Q

What are the two glycoproteins important for the virulence of the influenza viruses? Explain how an inactivated-virus vaccine provides protection against influenza.

A

HA - hemagglutinin: binds to sialic acid receptors allowing entry of virus into cell.

NA - neuraminidase: cleaves neuraminic acid (mucus) which exposes sialic acid.

Inactivated vaccines stimulate antibody production against HA. This prevents the virus from entering cells.

115
Q

How do you diagnose Legionnaires’ Disease?

A

This sever pneumonia (high fever and nonproductive cough) is caused by Legionella pneumophilia, a facultative intracellular parasite (in alveolar macrophages). It can be cultured on charcoal yeast extract agar (with L-cysteine).

116
Q

24 year old male presents with paroxysmal episodes of wheezing. Microscopic findings include crystallized masses. What IL is most likely responsible for this finding?

A

Crystalline granules in eosinophils coalesce to form Charcot layden crystals. IL-5 stimulates the production and activation of eosinophils.

117
Q

Explain the significance of a bronchial challenge test.

A

Methacholine is a non-selective muscarinic agonist which is used to assess bronchial hyperactivity in asthmatics.

118
Q

What is the proposed reason that silicosis is the only cause of pneumoconiosis that increases the risk of tuberculosis?

A

It is proposed that silicosis impairs macrophage phagolysosomes.

119
Q

What is the primary virulence factor of Mycoplasma pneumoniae that allows it to bind to epithelial cells? What is the primary defense of mycoplasma pneumoniae?

A

Protein p1, an adhesin virulence factor. This protein resembles proteins on RBCs, which explains how M. pneumoniae can cause anemia.

B-lymphocytes and Abs (IgA in the respiratory tract) provide protection against M. pneumoniae. Since this bacteria has no cell wall, other defenses are less effective.

120
Q

5 month old presents with a severe respiratory infection and signs of asthma (wheezing, infiltrate) requires intervention. What antiviral should be administered?

A

Ribavirin. Asthma in newborns is very rare. This child has RSV.

121
Q

Child presents with a laryngotracheobronchitis: fever, stridor, a brassy (barking) cough are observed on observation. Does this virus have an envelope and is it positive or negative stranded?

A

Paramyxovirus (croup): helical, enveloped, nonsegmented and negative stranded.

122
Q

What are the types of lung cancers and the frequency of each?

A 
Adenocarcinoma is the most common (25%-40%)
Squamous cell carcinoma (25-40%)
Small cell lung carcinoma (20-25%)
Large cell carcinoma (10-15%)
Bronchial carcinoid
123
Q

Which carcinomas of the lung are most often centrally located and which are peripherally located?

A

Central: small cell lung carcinoma, squamous cell carcinoma, bronchial carcinoid

Peripheral: adenocarcinoma and large cell carcinoma

124
Q

Patient presents with cough, dyspnea, weight lost and labs show hypercalcemia. What is the most likely lung tumor?

A

Squamous cell carcinoma.

125
Q

Patient presents with a puffy face, central obesity, thin extremities, and purple stria on her stomach. She also complains of a chronic cough and dyspnea. CXR shows a solitary coin lesion in her lungs. Diagnosis?

A

The lesion would most likely be centrally located, because these symptoms are being caused by a paraneoplastic syndrome from a small cell lung carcinoma which is secreting ACTH.

126
Q

Patient presents with cough, confused mental state, hemoptysis, weight loss, and chest pain. Labs also show hyponatremia. You decide to order a CXR because you have a suspicion that it might be lung cancer. How would you treat this paraneoplastic syndrome?

A

Small cell lung carcinoma with SIADH (syndrome of inappropriate secretion of ADH). Treat by reducing water intake or with demeclocycline (side effect is reduced ability to concentrate urine).

127
Q

What is the most likely lung cancer?

A

Squamous cell carcinoma showing a dense area of keratinization (squamous pearl).

128
Q

What is the most likely lung cancer?

A

Adenocarcinoma showing glandular formations.

129
Q

What is the most likely lung cancer?

A

Small cell lung carcinoma. Basophilic staining lymphocyte sized cells with scant cytoplasm.

130
Q

Lung cancer patient presents with muscle weakness. What sydrome does he have and what is the pathogenesis?

A

Eaton-Lambert syndrome: asthenia resulting from interference with the release of Ach due to immunologic attack against the presynaptic voltage-gated calcium channel.

131
Q

What is the lung tumor that causes Horner syndrome?

A

Horners: ptosis (lid drooping), miosis (pupil constriction), anhyrosis.

Tumor: superior sulcus tumor aka Pancoast tumor (normally of squamous cancer origin).

132
Q

Patient presents last week with cough, dyspnea, clubbing, and hypertrophic pulmonary osteoarthropathy. The male patient also complained about his gynecomastia. You sent a lung biopsy (from the periphery) to path. Histological inspection reveal undifferentiated cells that lacked any definitive features. What is the most likely tumor?

A

Large cell carcinoma.

133
Q

Name the most common sites for lung cancers to metastasize.

Name the most common origins of metastatic lung cancer.

A

To: hilar lymph nodes (most common), adrenal glands (50%), liver, right-subclavicular, brain, bone.

From: Breast (most common), colon cancer, renal cell carcinoma.

134
Q

Bronchoalveolar carcinoma is a type of adenocarcinoma of the lung. These tumors can arise from scar tissue. They also characteristically spread along alveoli without causing damage. What lung pathology do they mimic? What cells do adenocarcinomas arise from?

A

Mimic lobar pneumonia.

Arise from type II pneumocytes.

135
Q

Which lung cancers have the strongest association with smoking? Least association?

A

Strongest: small and squamous cell carcinoma.

Least: bronchoalveolar carcinoma (type of adenocarcinoma).

136
Q

Small cell carcinomas arise from what cell type?

A

Neuroendocrine cells (Kulchitsky).

Step 1 Complete (29 decks)

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