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First aid Chs Part 1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What disorder should you think about in a child with nasal polyps?

A

Cystic Fibrosis

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2
Q

Why should you avoid aspirin in patients with nasal polyps?

A

Adults with nasal polyps and asthma are at a high likelihood of aspirin allergy (aspirin intolerant asthma).

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3
Q

What subgroup is angiofibroma of the nasal mucosa most commonly seen in?

A

Adolescent males (almost exclusively)

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4
Q

What virus can cause nasopharyngeal CA?

A

EBV

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5
Q

What two demographics are at high risk for nasopharyngeal cancer from EBV?

A

African children, Chinese adults

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6
Q

Describe the histology of nasopharyngeal carcinoma.

A

Pleomorphic keratin-positive epithelial cells in a background of lymphocytes

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7
Q

What is the #1 cause of acute epiglottitis?

A

H. influenza b

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8
Q

What viruses cause laryngeal papillomas?

A

HPV 6 and 11

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9
Q

How many papillomas are seen in adults with laryngeal papillomas?

A

One

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10
Q

How many papillomas are seen in children with laryngeal papillomas?

A

Multiple

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11
Q

What are the two most common causes of lobar pneumonia?

A

S. pneumo and K. pneumoniae

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12
Q

What are the 4 phases of lobar pneumonia?

A

Congestion, red hepatization (lots of RBCs), grey hepatization (RBCs broken down), resolution

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13
Q

Which cells are stem cells of lungs that help regenerate the alveolar air sacs after lung damage?

A

Type II pneumocytes

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14
Q

Grossly, how does bronchopneumonia appear?

A

Patchy (“shotgun”) appearance

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15
Q

What is the #1 cause of bacterial pneumonia following a viral infection of the lung (influenza)?

A

S. aureus

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16
Q

What are two major complications of staph aureus pneumonia?

A

Abscess, empyema

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17
Q

What two bacteria are most commonly seen in patients with COPD?

A

H. influenzae, M. catarrhalis

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18
Q

What stain is best to identify Legionella Pneumophila?

A

Silver stain

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19
Q

What is the #1 cause of atypical pneumonia in infants?

A

RSV

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20
Q

What is the classic location of aspiration pneumonia?

A

Right lower lobe

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21
Q

Meningitis caused by TB classically presents in what location?

A

The base of the brain

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22
Q

What happens to the FEV1/FVC ratio in COPD?

A

Decreases (Both FVC and FEV1 decrease, but FEV1 decreases more)

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23
Q

What is the symptomatic time period necessary for a diagnosis of chronic bronchitis?

A

Productive cough lasting at least 3 months over a minimum of 2 years.

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24
Q

What is the Reid index and what is its normal value?

A

Reid index- thickness of mucus glands in bronchi relative to the thickness of the entire wall. Normally <40%.

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25
Q

What is the Reid index in chronic bronchitis?

A

> 50% (increased thickness of mucinous glands relative to the entire thickness of the bronchial wall).

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26
Q

A “blue bloater” has what disease?

A

Chronic bronchitis

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27
Q

What causes centriacinar emphysema?

A

Smoking (usually in upper lobes)

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28
Q

What causes panacinar emphysema?

A

Alpha 1 antitrypsin deficiency (destroy the entire acinus)

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29
Q

In which lobes is centriacinar emphysema usually found?

A

Upper (smoke travels up in the lungs)

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30
Q

In which lobes is panacinar emphysema usually found?

A

Lower lobes

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31
Q

Pink PAS positive globules on liver biopsy is indicative of…

A

Alpha 1 antitrypsin deficiency

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32
Q

What is the most common mutation seen in A1AT deficiency?

A

PiZ allele

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33
Q

Where does alpha-1 antitrypsin accumulate in individuals with A1ATD?

A

Endoplasmic reticulum

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34
Q

Explain the mechanism of wall collapse in emphysema.

A

Normally, recoil of alveoli serves to hold lower airways open during expiration. When their septa are destroyed in emphysema, they lose this ability, and the airways collapse.

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35
Q

Why do patients with emphysema breathe with pursed lips?

A

It creates back pressure to keep the small airways open (they would otherwise collapse in emphysema because of loss of recoil from alveoli to keep them open)

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36
Q

What disease does a “pink puffer” have?

A

Emphysema

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37
Q

What 3 cytokines do TH2 cells secrete?

A

IL-4, IL-5, IL-10

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38
Q

What does IL-4 do?

A

Promotes class switching to IgE/IgG

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39
Q

What cytokine is a key eosinophil activator?

A

IL-5

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40
Q

What are the two mechanisms that cause early inflammation in asthma?

A

Mast cell destabilization and release of preformed histamine. Production of LTC4, LTD4, LTE4

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41
Q

What are Curschmann spirals?

A

Twisted mucous plugs admixed with sloughed epithelium in asthma

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42
Q

What are Charcot-Leyden crystals?

A

Crystals in sputum formed from breakdown of eosinophils in sputum

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43
Q

What is bronchiectasis?

A

Permanent dilation of bronchioles and bronchi (large airways)

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44
Q

What are some causes of bronchiectasis?

A

Bronchial obstruction, Kartagener’s syndrome (dysfunction of dynein arms of cilia), CF, allergic bronchopulmonary aspergillosis.

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45
Q

What is paraseptal (distal acinar) emphysema?

A

Emphysema of distal airway structures - associated with apical bullae that can rupture in tall, thin, male patients, creating a spontaneous pneumothorax.

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46
Q

What happens to the FEV1/FVC in restrictive diseases?

A

The ratio increases (Both FEV1 and FVC decrease, but FVC decreases more)

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47
Q

What induces fibrosis in idiopathic pulmonary fibrosis?

A

TGF-beta released from injured pneumocytes

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48
Q

What causes fibrosis in pneumoconiosis?

A

Alveolar macrophages responding to small particles

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49
Q

What is Caplan syndrome?

A

Black lung (coal worker pneumoconiosis) + rheumatoid arthritis

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50
Q

What is anthracosis?

A

A clinically insignificant anthracosis of the lung caused by mild exposure to carbon in pollutants.

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51
Q

What does silica do to alveolar macrophages?

A

Impairs phagolysosome formation, thus increasing risk for TB (only pneumoconiosis that increases TB risk)

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52
Q

In what lobe of the lung does silicosis typically occur?

A

Upper lobe (also increases the risk for TB, which preferentially infects upper lobe)

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53
Q

What category of patients are at risk for exposure to beryllium, and what does it cause?

A

Workers in the aerospace industry. Beryllium exposure causes noncaseating granulomas in the lung (similar to sarcoidosis) and increases risk of lung cancer.

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54
Q

What four general things can be caused by asbestos?

A

Fibrosis of the lung, fibrosis of the pleura, cancer of the lung, cancer of the pleura (mesothelioma).

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55
Q

What is the most common cancer that individuals exposed to asbestos get?

A

Lung cancer (bronchogenic) NOT mesothelioma!.

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56
Q

Patients in what occupation are at high risk for exposure to silica?

A

Sandblasters, miners.

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57
Q

What can cause “eggshell” calcifications of hilar lymph nodes?

A

Silicosis

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58
Q

What is the pathophysiology of idiopathic pulmonary fibrosis?

A

Repeated cycles of lung injury and healing with increased collagen deposition.

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59
Q

Where are non-caseating granulomas commonly seen in sarcoidosis?

A

Lung and hilar lymph nodes

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60
Q

What enzyme is commonly elevated in the blood of patients with sarcoidosis?

A

ACE

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61
Q

Why do patients with sarcoidosis have hypercalcemia?

A

Macrophages in non-caseating granulomas have 1-alpha hydroxylase activity and can activate vitamin D.

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62
Q

Explain the signs and symptoms of hypersensitivity pneumonitis.

A

Granulomatous reaction to inhaled organic antigens (pigeon feces, hay, etc.) with dyspnea, cough, chest tightness, etc. that GOES AWAY with removal of the stimulus. Can lead to interstitial fibrosis. Will see eosinophils in the tissue.

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63
Q

What is a plexiform lesion?

A

A tuft of capillaries resembling a primitive glomerulus seen in irreversible pulmonary hypertension.

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64
Q

What is normal pulmonary artery pressure?

A

10-14 mm Hg

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65
Q

What are some signs and symptoms of pulmonary hypertension?

A

Exertional dyspnea, right sided heart failure, RVH

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66
Q

What gene is inactivated in familial forms of primary pulmonary hypertension?

A

BMPR2

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67
Q

BMPR2 inactivation leads to…

A

Proliferation of vascular smooth muscle and pulmonary hypertension

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68
Q

What are some causes of secondary pulmonary hypertension?

A

Hypoxemia (COPD), increased volume in pulmonary circuit (left heart failure, mitral stenosis), recurrent pulmonary embolism.

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69
Q

What is a sequelae of recurrent pulmonary embolism?

A

Pulmonary hypertension secondary to thickening of the vascular wall due to repeated embolus deposition.

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70
Q

What is the microscopic hallmark of ARDS?

A

Formation of thickened hyaline membranes in alveoli.

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71
Q

What causes a diffuse “white out” of the lung on CXR?

A

ARDS

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72
Q

What cells are damaged in ARDS?

A

Type I and type II pneumocytes (injury to type II pneumocytes causes fibrosis upon recovery)

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73
Q

What is seen on CXR in newborns with neonatal ARDS?

A

Diffuse granularity

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74
Q

What test is used to screen for neonatal ARDS?

A

Lecithin:sphingomyelin ratio (lecithin increases as lungs mature). Ratio >2 = good.

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75
Q

What is the main component of surfactant?

A

Phosphatidylcholine (lecithin)

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76
Q

What are polycyclic aromatic hydrocarbons?

A

Extremely carcinogenic compounds found in cigarette smoke.

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77
Q

What two benign lesions can present as “coin lesions” on CXR or CT?

A

Granuloma and Bronchial hamartoma (Lung tissue and cartilage)

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78
Q

What types of tissue does a bronchial hamartoma contain?

A

Lung tissue and cartilage

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79
Q

Which type of lung cancer is not amenable to resection?

A

Small cell

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80
Q

What are some of the paraneoplastic syndromes that can be seen with small cell lung cancer?

A

Lambert-Eaton syndrome (antibodies against presynaptic calcium channels), ADH-producing tumor, ACTH-producing tumor

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81
Q

What are Kulchitsky cells?

A

Neuroendocrine cells (small, dark, blue cells) seen in small cell lung cancer.

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82
Q

What is the most common lung tumor in male smokers?

A

Squamous cell carcinoma

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83
Q

What are two major histologic characteristics of squamous cell carcinoma?

A

Intercellular bridging or keratin pearls

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84
Q

What is a common paraneoplastic syndrome seen with squamous cell carcinoma?

A

Hypercalcemia (tumor produces parathyroid-related peptide)

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85
Q

What lung tumor is cavitating?

A

Squamous cell carcinoma

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86
Q

What protein is released by squamous cell carcinoma to cause hypercalcemia?

A

Parathyroid hormone-related protein

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87
Q

What is the most common lung tumor in nonsmokers?

A

Adenocarcinoma

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88
Q

What is the most common lung tumor in female smokers?

A

Adenocarcinoma

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89
Q

What is the histologic characteristic of adenocarcinoma of the lung?

A

Glandular appearance with mucin production

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90
Q

Where (anatomically) is adenocarcinoma of the lung typically located?

A

In the periphery of the lung

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91
Q

Biopsy of a lung mass shows no evidence of intercellular bridging, keratin pearls, gland formation, or mucin. What is it?

A

Large cell carcinoma.

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92
Q

Bronchioloalveolar carcinoma is a cancer of which cells?

A

Clara cells

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93
Q

What is the hisologic appearance of bronchioloalveolar carcinoma?

A

Walls of alveolar air sacs replaced by columnar cells - apparent “thickening” of alveolar walls

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94
Q

What is the classic presentation of bronchioalveolar carcinoma on CXR?

A

Hazy infiltrates, similar to pneumonia

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95
Q

What is the prognosis of bronchioloalveolar carcinoma?

A

Excellent

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96
Q

Lung carcinoid tumor can be stained with..

A

Chromogranin

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97
Q

How can lung carcinoid tumor be differentiated from small cell carcinoma?

A

Both are neuroendocrine tumors. Small cell carcinoma is poorly differentiated, carcinoid tumor is well differentiated.

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98
Q

What lung tumor presents as a polyp-like mass in the bronchus?

A

Carcinoid tumor

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99
Q

What is the classic appearance of metastasis to the lungs?

A

Cannonball appearance - multiple nodules

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100
Q

What is a unique place that lung cancer likes to metastasize?

A

Adrenal gland

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101
Q

Which primary lung tumor will most commonly affect the pleura?

A

Adenocarcinoma (grows on the periphery of the lung and can cause pleural puckering)

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102
Q

What are the signs and symptoms of SVC syndrome?

A

Distended head and neck veins with edema and blue discoloration of the arms and face.

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103
Q

What thoracic tumor shows psammoma bodies on histology?

A

Mesothelioma

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104
Q

What lung cancer results from a k-ras mutation?

A

Adenocarcinoma

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105
Q

What is lepidic spread?

A

Cancer spreading along alveolar septa like a picket fence. Seen in bronchioloalveolar carcinoma.

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106
Q

What lung tumor will have nodular growth with central necrosis and cavitations?

A

Squamous cell

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107
Q

Biopsy of a lung tumor shows cells with salt and pepper chromatin with nuclear molding. Dx?

A

Small cell carcinoma

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108
Q

What lung tumor is associated with peripheral leukocytosis/eosinophilis?

A

Large cell

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109
Q

What lung tumor is associated with amplification of myc oncogenes?

A

Small cell carcinoma

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110
Q

To what side does the trachea shift in a spontaneous pneumothorax?

A

The side of the collapsed lung

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111
Q

What is the most common cause of spontaneous pneumothorax?

A

Rupture of apical blebs (seen in tall, thin males)

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112
Q

To what side does the trachea shift in a tension pneumothorax?

A

Away from the lesion

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113
Q

What are the three types of atelectasis?

A

Resorption (obstructive), compression, contraction

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114
Q

What causes resorption atelectasis?

A

Complete obstruction of airway (asthma, chronic bronchitis, bronchiectasis, foreign bodies)

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115
Q

To which side does the mediastinum shift with resorption atelectasis?

A

Toward the atelectatic lung

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116
Q

Explain the pathophysiology of resorption atelectasis.

A

Complete obstruction of the airway causes diminished lung volume. As a result, the mediastinum shifts TOWARDS the atelectatic lung.

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117
Q

How do you treat resorption atelectasis?

A

Remove the obstruction (it is also known as obstructive atelectasis)

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118
Q

To what side does the mediastinum shift in a compression atelectasis?

A

AWAY from the atelectatic lung (an example is a tension pneumothorax)

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119
Q

Explain the pathophysiology of compression atelectasis.

A

Something in the pleural cavity (air, fluid, tumor, etc.) causes compression of the lung, pushing the mediastinum AWAY from the atelectatic lung.

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120
Q

Which form of atelectasis is irreversible?

A

Contraction

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121
Q

What causes contraction atelectasis?

A

Fibrotic changes of the lung and/or pleura, preventing full expansion.

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122
Q

What are the 3 most common causes of otitis media?

A

Strep pneumo, H. influenza, Moraxella catarrhalis (gram - diplococci)

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123
Q

What serotypes of C. trachomatis cause neonatal conjunctivits?

A

D-K (from mom having an STD)

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124
Q

What are the two causes of neonatal conjunctivitis?

A

C. trachomatis (D-K), N. gonorrheae

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125
Q

What causes trachoma?

A

C. trachomatis A-C subtypes

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126
Q

What are the 3 F’s of trachoma?

A

Fomites, flies, fingers (all 3 spread the disease)

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127
Q

How does trachoma cause blindness?

A

Repeated infection with C. trachomatis types A-C results in scarring and inversion of the eyelid. The eyelashes abrade the cornea, causing blindness. The disease is spread by the 3 F’s: fingers, flies, fomites.

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128
Q

What is the most common cause of otitis externa?

A

Pseudomonas

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129
Q

What is the most common cause of viral conjunctivits?

A

Adenovirus (non-enveloped DNA virus) - swimming pool conjunctivitis.

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130
Q

What is the #1 cause of retinitis in AIDS patients?

A

CMV (herpesvirus - enveloped DS DNA)

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131
Q

What agar grows Fusarium?

A

Sabourad dextrose

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132
Q

What is Fusarium, what does it cause, and how do you get it?

A

Fusarium is a fungus (grows on sabourad dextrose) acquired through homemade contact lens solutions or trauma. It can cause keratitis of the eye and blindness.

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133
Q

What is Acanthamoeba, what does it do to your eyes, and how do you get it?

A

Acanthamoeba is a parasite acquired from deep water in lakes (association with contact lenses and swimming) that causes keratitis and blindness.

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134
Q

Explain the correlation between toxoplasmosis and blindness.

A

Mother is exposed (changing cat litter or eating contaminated food) during pregnancy, toxo crosses the placenta, and causes irreversible blindness to the child in the child’s teens or 20s.

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135
Q

What receptor does rhinovirus use to enter cells?

A

ICAM-1 (zinc blocks ICAM-1, hence ZICAM)

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136
Q

What are some signs and symptoms of epiglottitis and in what patient population are you concerned about it?

A

Fever, sore throat, drooling, “catchers-stance”, hoarsness, dysphagia. Concerned in unvaccinated individuals because it is caused by Hib.

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137
Q

What causes the green color of sputum?

A

Myeloperoxidase

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138
Q

After a lung transplant, what is most commonly attacked in a chronic rejection?

A

Small airways (bronchioles - bronchiolitis obliterans)

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139
Q

What is asbestosis?

A

Formation of fibrocalcific plaques on the parietal pleura with subsequent thickening and fibrosis of the lower lung.

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140
Q

What are ferruginous bodies?

A

Asbestos covered with a protein-iron matrix.

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141
Q

Which parts of the respiratory tree are within the conducting zone?

A

Large airways: nose, pharynx, trachea and bronchi

small airways: bronchioles and terminal bronchioles

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142
Q

Where in the respiratory tree does cartilage and goblet cells extend to?

A

The end of bronchi

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143
Q

What is the purpose of the anatomic dead space of the respiratory tree?

A

The conducting zone warms, humidifies and filters the air

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144
Q

What is the epithelial lining to the end of the terminal bronchioles before you get into the respiratory zone?

A

pseudostratified ciliated columnar cells to beat mucus up and out of the lungs

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145
Q

what is included in the respiratory zone?

A

respiratory bronchioles, alveolar ducts, and alveoli

146
Q

what is the epithelial lining in the respiratory bronchioles?

A

In respiratory bronchioles it’s cuboidal cells then squamous cells up to the alveoli

147
Q

which cell types in the lung participate in gas exchange?

A

Type 1 pneumocytes - squamous cells that line the alveoli

148
Q

Which cell types secrete surfactant?

A

Type 2 pneumocytes - cuboidal cells that are clustered

149
Q

What are Clara cells?

A

Nonciliated, columnar cells with secretory granules. Secrete components of surfactant, degrade toxins and act as reserve cells

150
Q

Which lung cancer arises from Clara cells?

A

Bronchoalveolar caricinoma

151
Q

how many lobes does the right lung have? the left lung?

A

Right - 3

left - 2 (and lingula)

152
Q

If a patient aspirates a peanut - no matter the position they are in where will it most likely go?

A

Via the right main stem bronchus into the inferior Right lobe

153
Q

If a patient aspirate a peanut while upright - where will it go?

A

Via the right main stem bronchus into the lower portion of the inferior Right lobe

154
Q

If a patient aspirate a peanut while supine- where will it go?

A

Via the right main stem bronchus into the superior portion of the inferior Right lobe

155
Q

Describe the relation of the pulmonary artery to the bronchus at each lung hilus…

A

RALS
Right - Anterior
Left - Superior

156
Q

What type of epithelium lines the trachea? How does this change in a smoker?

A

Ciliated columnar epithelium

Smoker - squamous metaplasia

157
Q

What is the mnemonic for the structures perforating the diaphragm and what are they?

A

I ate ten eggs at twelve

I ate - IVC 8
ten eggs - 10 esophagus (also the vagus)
at twelve - aorta 12 (also the thoracic duct and azygous vein)

158
Q

Name 3 muscles you use for inspiration during exercise

A

External intercostals, scalenes, SCM

159
Q

Name 5 muscles you use for expiration during exercise

A

rectus abdominus, internal and external obliques, transversus abdominus, internal intercostals

160
Q

Where is the location of the largest amount of functional dead space?

A

In a health person - the apex of the lung

161
Q

What is the equation for determining physiological dead space?

A

Vd = Vt x ((PaCO2 - PECO2)/PaCO2)

162
Q

what is the lungs compliance?

A

The lungs ability to stretch during inspiration (change in lung volume for a given change in pressure)

163
Q

What is FRC?

A

Functional residual capacity - the point at which the inward pull of the lung is balanced by the outward pull of the chest wall.

At this point - the airway and alveolar pressures are 0 and the intrapleural pressure is negative (preventing a pneumothorax)

164
Q

Is FRC decreased or increased in emphysema?

A

FRC is increased in emphysema - The lungs are more compliant - barrel chested patients

165
Q

Is FRC decreased or increased in patients with pulmonary fibrosis or edema?

A

FRC is decreased in pulmonary fibrosis or edema - these patients have decreased lung compliance, the total lung volume is decreased

166
Q

Name 3 situations where you would see decreased lung compliance?

A

decreased in pulmonary fibrosis, pneumonia, and pulmonary edema

167
Q

Name 2 situations where you would see increased lung compliance?

A

normal aging, emphysema

168
Q

What is mean by the taut and relaxed forms of hemoglobin?

A

T = Taut = Tissue, taut form has low affinity for O2 to give it away to the tissue

R = Relaxed = Respiratory, Relaxed form has higher affinity for O2

169
Q

Does hemoglobin exhibit positive or negative allostery?

A

Negative

but positive cooperativity

170
Q

What side of the dissociation curve favors the taut form?

A

a right shift - Increased Chloride, increased H+, CO2, 2,3 BPG and increased temperature

171
Q

Is the dissociation curve shifted to the right or left for fetal hemoglobin?

A

Fetal hemoglobin has lower affinity for 2,3 BPG and therefore higher affinity for O2 so it is shifted to the left

172
Q

What’s wrong with methemoglobin?

A

This is the oxidized form of hemoglobin (Fe 3+ ferric) that does not bind O2 as readily but has increased affinity for cyanide

173
Q

What causes methemoglobin?

A 
Nitrates/nitrites
anti-malarial drugs
dapsone
sulfonamides
metoclopramide
local anesthetics
174
Q

What drug is known to gradually lower methemoglobin?

A

Cimetidine

175
Q

How do I know the difference between Fe3+ and Fe2+

A 
Ferric = 3+ = abC
Ferrous = 2+ = Ferrou2 - binds to O2 better
176
Q

How do you treat methemoglobinemia?

A

Methylene blue + Vitamin C

177
Q

How do you traet cyanide poisoning?

A

use nitrates to oxidze hemoglobin to methemoglobin which will bind up the cyanide - then use thiosulfate to bind this cyanide forming thiocyanide which is renally excreted

178
Q

How is cyanide toxic?

A

It uncouples the electron transport chain by binding to cytochrome C

179
Q

What’s wrong with carboxyhemoglobin?

A

This form of hemoglobin is bound to CO instead of O2

180
Q

What does hemoglobin bound to CO instead of O2 do to the dissociation curve?

A

It causes a left shift with a decreased in oxygen binding capacity - you get decreased oxygen unloading in tissues

181
Q

How do you measure PO2?

A

Measured as a dissolved gas (arterial blood gas)

182
Q

why doesn’t myoglobin show the positive cooperativity that hemoglobin does?

A

Myoglobin is monomeric unlike hemoglobin which is a tetramer

183
Q

if the dissociation curve shifts to the right - does that mean you have increased or decreased affinity for O2?

A

Decreased affinity for O2 - unload at the tissue

184
Q

An increased in all factors, except pH, causes a shift of the curve to which way?

A

To the right - decreased affinity

185
Q

What’s the mnemonic for a right shift of the dissociation curve?

A

C-BEAT

CO2, BPG, Exercise, Acid/Altitude, Temperature

186
Q

what is the progression that’s seen in a patient with constant hypoxemia?

A

Low alveolar O2 –> chronic vasoconstriction –> pulmonary HTN –> cor pulmonale and subsequent RV failure

187
Q

Name 3 conditions that exhibit a perfusion limited gas exchange limitation?

A

O2 (normal health), CO2, N2O

188
Q

What is perfusion limitation?

A

Gas equilibrates early along the length of the capillary. Diffusion can be increased only if the blood flow is increased

189
Q

Name 3 conditions that exhibit a diffusion limited gas exchange limitation?

A

O2 - emphysema, fibrosis, CO

190
Q

What is a diffusion limitation?

A

Gas doesn’t equilibrate by the time the blood reaches the end of the capillary

You get a decreased in area in emphysema and you get an increase in thickness in pulmonary fibrosis

191
Q

At what pressure does a patient have pulmonary hypertension?

A

≥ 25mm Hg normal or ≥35 mm Hg during exercise

192
Q

what’s seen histiologically with pulmonary hypertension?

A

Arteriosclerosis, medial hypertrophy and intimal fibrosis of the pulmonary arteries

193
Q

what is primary pulmonary hypertension?

A

BMPR2 gene inactivating mutation (bone morphogenic protein receptor 2)

194
Q

What is the function of BMPR2 when it’s working correctly?

A

inhibits vascular smooth muscle proliferation

195
Q

Name some things that can cause secondary pulmonary hypertension?

A 
COPD
Mitral stenosis
recurrent thromboemboli
autoimmune disease
left to right shunt
sleep apnea 
living at high altitude (hypoxic vasoconstriction)
196
Q

What is the equation for pulmonary vascular resistance?

A

PVR = (P in pulmonary artery - P in L atrium) / Cardiac output

197
Q

A patient presents with normal Pa O2, decreased SaO2 and decreased O2 content - what might they have?

A

CO poisoning

198
Q

What is SaO2?

A

% saturation

199
Q

A patient presents with normal PaO2, normal SaO2 and decreased O2 content - what might this be?

A

Anemia - low Hb

200
Q

A patient presents with normal PaO2, normal SaO2 and increased O2 content - what might this be?

A

Polycythemia - increased Hb

201
Q

What is the O2 content of the blood?

A

O2 content = (O2 binding capacity x O2 saturation) + dissolved O2

202
Q

what causes O2 content of the blood to decrease without changing the O2 saturation or arterial PO2?

A

decreased hemoglobin

203
Q

What is the equation for oxygen delivery to tissues?

A

Oxygen deliver to tissues = cardiac output x oxygen content of the blood

204
Q

What is the alveolar gas equation?

A

PAO2 = 150 - PaCO2/0.8

205
Q

what occurs as you increased alveolar PCO2?

A

alveolar PO2 decreases

206
Q

what is the value for a normal A-a gradient?

A

A-a gradient = PAO2 - PaO2 = 10-15 mmHg

207
Q

What can cause an increased A-a gradient?

A

Hypoxemia

causes include R to L shunting, V/Q mismatch, or fibrosis (diffusion limitation)

208
Q

What causes hypoxemia but still has a normal A-a gradient?

A

High altitude or hypoventilation

209
Q

What is normal value of PaO2/FiO2?

A

normally 300 - 500

< 200 = severe hypoxia (like in ARDS)

210
Q

A patient inhaled a piece of food - what are going to see on V/Q?

A

This is an airway obstruction = SHUNT
V/Q = 0; in a shunt, 100% O2 will not improve PO2

you have low ventilation and high perfusion

211
Q

A patient gets a PE - what are you doing to see on V/Q?

A

This is a blood flow obstruction = PHYSIOLOGICAL DEAD SPACE

V/Q = infinity; assuming s not being perfused

212
Q

Does V/Q increased or decreased during exercise?

A

V/Q decreases during exercise because you get vasodilation in the lungs
This leads to increased perfusion in the apices so you’re not wasting as much ventilation

213
Q

Describe what’s happening at the apex of the lung in terms of ventilation and perfusion

A

Apex has decreased perfusion over all (increased V and decreased Q)
so V/Q = >1, it’s wasted ventilation – physiologic dead space

214
Q

What is V/Q at the apex of the lung?

A 
Apex = top of the lung
V/Q = >1
215
Q

why does TB prefer the apices of the lung upon reactivation?

A

more oxygen

216
Q

Describe what’s happening at the base of the lung in terms of ventilation and perfusion

A

The base has increased perfusion over all
V/Q = <1
This is a form of shunting - the blood leaves the lungs without being adequately oxygenated
Gravity pulls more blood down tot he bases so perfusion is better in the base of the lung than the apex

217
Q

What are the pressures in Zone 1 of the lung?

A

Zone 1 = apex

PA>Pa>PV

218
Q

What are the pressures in Zone 2 of the lung?

A

Zone 2 = middle

Pa>PA>PV

219
Q

What are the pressures in Zone 3 of the lung?

A

Zone 3 = base

Pa>Pv>PA

220
Q

How is CO2 transported in the lungs?

A

Bicarbonate (90%)
Carbaminohemoglobin of HbCO2 (5%)
Dissolved CO2 (5%)

221
Q

What is the Haldane effect?

A

In the lungs, the oxygenated of Hb promotes dissociation of H+ from Hb. this shifts equilibrium toward CO2 formation - therefore, CO2 is released from the RBCs

222
Q

What is the Bohr effect?

A

In peripheral tissues, Increased H+ from tissue metabolism shifts the dissociation curve tot he right resulting in unloading of O2

223
Q

A person climbs a bajillion feet to the top of a mountain and they decide they want to live there. They are ventilating - what is your kidney going to start to excrete more of?

A

Bicarb - this compensates for the respiratory alkalosis due to hyperventilating.

224
Q

What drug can you use to help with high altitudes?

A

Acetazolamide - gets rid of XS bicarb

225
Q

what is Virchow’s triad?

A
  1. stasis
  2. hypercoagulability (defect in coag cascade proteins - most commonly factor V leiden) or xs estrogen, sickle cell, polycythemia
  3. endothelial damage (exposed collagen triggers clotting cascade)
226
Q

A patient presents after hip surgery with calf pain and a positive homans sign - and a palpable cord in their leg - how should you treat them?

A

This is a DVT
You want to acutely manage with heparin (should have been given to prevent it) and use warfarin for long term prevention of DVT recurrence

227
Q

What’s the concern with a DVT?

A

can lead to a pulmonary embolus

228
Q

What is Homan’s sign?

A

Positive in a DVT - dorsiflexion of the foot leads to calf pain

229
Q

Name the emboli: Long bone fracture and liposuction

A

Fat embolus

230
Q

Name the emboli: Caisson disease - decompression illness from rising too quickly while diving

A

Air embolus

231
Q

If you have a defect in the perfusion phase when you check a V/Q scan - what should you think?

A

Possible PE

232
Q

A patient presents with a sudden-onset of dyspnea, chest pain, tachypnea. They have hypoxemia, neurologic abnormalities and a petechial rash - what is happening?

A

PE

233
Q

A patient gets a PE and develops DIC - what most likely happened?

A

They probably just delivered a baby and got an amniotic fluid emboli

234
Q

What is the imaging test of choice for a PE?

A

CT pulmonary angiography

235
Q

What will you see on an EKG with a PE?

A

most PE’s are minor so you will see non-specific ST segment and T wave changes

236
Q

What will you see on an EKG with a MASSSIVEEE like patient is freaking out vitals all over the place PE?

A

S1 Q3 T3 - wide S in lead 1, large Q and inverted T in lead 3
due to increased pressure and volume to RV

237
Q

What will you see the A-a gradient do when a patient has PE?

A

A-a gradient will be increased

238
Q

Where will a particle between 10-15 um get trapped?

A

URT

239
Q

Where will a particle between 2.5 - 10 um get trapped?

A

particles enter trachea and bronchi but are cleared by mucocilliary transport

240
Q

Where will a particle less than 2 um get trapped?

A

will reach terminal bronchiole and alveoli and get phagocytosed by alveolar macrophage

241
Q

what are the lines of Zahn?

A

Interdigitating areas of pink and red found in thrombi formed BEFORE death = pre-mortem PE

242
Q

Name the 4 types of Obstructive lung diseases

A

Chronic bronchitis, emphysema, asthma and bronchiectasis

243
Q

Name some times of restrictive lung diseases?

A

poor breathing mechanics due to poor effort or poor structural
interstitial lung diseases - ARDS, pneumoconiosis, Sarcoidosis, idiopathic pulmonary fibrosis, goodpastures, Wegener’s, langerhans histiocytosis, hypersensitivity pneumonitis, drug toxicity

244
Q

why do you have to be careful when you supplement O2 to COPD patients?

A

hypoxia drives their respiratory function - whereas in normal patients the PCO2 mediates respiratory drive - in patients with longstanding COPD - O2 supplementation can lead to respiratory suppression and coma

245
Q

What is the main problem with COPD?

A

Obstruction - obstructed from getting are OUT of the lung

246
Q

What is the main problem in restrictive diseases?

A

Can’t fill the lung

247
Q

COPD is a disease of the….

A

small airways

248
Q

A patient presents with wheezing, crackles, cyanosis (early onset hypoxemia due to shunting) and late onset dyspnea

A

Chronic bronchitis

249
Q

How do you determine a patient has chronic bronchitis?

A

Productive cough for > 3 months per year (not necessarily consecutive) for >2 years

250
Q

Name the disease: Hypertrophy of mucus-secreting glands in the bronchi leading to in Reid index of >50%

A

Chronic bronchitis

251
Q

What leisurely activity do patients with chronic bronchitis most likely partake?

A

smoking

252
Q

Why does air get trapped in patients with obstructive lung diseases?

A

Airways close prematurely at high lung volumes

253
Q

A patient has an increased RV, decreased FVC and they have a decreased FEV1/FVC ratio

A

Obstructive lung disease

254
Q

A patient has enlarged air spaces and decreased recoil due to a loss of elastic fibers

A

Emphysema

255
Q

Emphysema associated with smoking

A

Centriacinar

256
Q

Emphysema associated with alpha 1 anti-trypisin deficiency

A

panacinar

257
Q

What other organ is typically involved with panacinar emphysema?

A

The liver

258
Q

A patient presents with a barrel chest, hyperinflated lungs with flattening of the diaphragm and blunting of the costophrenic angles, they are very thin and breath through pursed lips - what is this and why do they do this?

A

Emphysema - they need to increased airway pressure to prevent airway collapse during respiration

259
Q

What is a Hoover sign?

A

Seen in emphysema
Hyperexpansion of the lungs due to air trapping causes the diaphragm to flatten, which causes it to contract inward instead of down - thereby paradoxically pulling the inferior ribs inwards during inspiration

260
Q

Name the disease: bronchial hyperresponsiveness causes reversible bronchoconstriction leading to smooth muscle hypertrophy

A

Asthma

261
Q

What will you see on histology of a patient with asthma?

A

Curschmann’s spirals, Charcot Leyden crystals,

262
Q

What are Curschmann’s spirals?

A

Seen in asthma, shed epithelium forms mucus plugs

263
Q

What are Charcot Leyden crystals?

A

Seen in asthma, formed from breakdown of eosinophils in sputum

264
Q

How can you test Asthma?

A

Methacholine challenge

265
Q

A patient presents with coughing, wheezing, tachypnea, dyspnea, hypoxemia, decreased inspiratory/expiratory ratio, pulsus paradoxus and mucus plugging

A

Asthma attack

266
Q

What is Bronchiectasis?

A

Obstructive lung disease
Chronic necrotizing infection of bronchi leading to permanently dilated airways, purulent sputum, recurrent infections, hemoptysis

267
Q

What are some conditions that can be associated with Bronchiectasis?

A

Bronchial obstruction, poor ciliary motility (smoking), Kartagener’s, cystic fibrosis, allergic bronchopulonary aspergillosis

268
Q

What can you see in the brain due to COPD?

A

Decreased cerebral vascular resistance…
A patient with long standing COPD is likely to have hypoxia and hypercapnea - the hypercapnia produces cerebral vasodilation via a decreased in cerebral vascular resistance - so you get increased cerebral blood flow

269
Q

a patient has decreased TLC but they have an increased FEV1/FVC ratio - what is this?

A

Restrictive lung disease

270
Q

In what type of restrictive lung disease will you still have a normal A-a gradient?

A

Poor muscular effort or poor structural apparatus leading to poor breathing mechanics

271
Q

In what type of restrictive lung disease will you see an increased A-a gradient?

A

Interstitial lung diseases

272
Q

Name 4 types of Pneumoconioses

A

Anthracosis
Silicosis
Asbestosis
Berylliosis

273
Q

Name the Pneumoconioses: Associated with coal mines - affects the upper lobes, is not associated with smoking and there’s no increased risk of lung cancer

A

Anthracosis

274
Q

What is Caplan syndrome?

A

Coal worker’s pneumoconioses + rheumatoid arthritis

275
Q

Name the Pneumoconioses: associated with foundries, sandblasting, and mines

A

Silicosis

276
Q

Name the Pneumoconioses: Macrophages eat the particles but phagolysome formation is impaired

A

Silicosis

277
Q

Name the Pneumoconioses: INCREASED risk of infection with TB

A

Silicosis

278
Q

Name the Pneumoconioses: Increased risk of bronchogenic carcinoma

A

Silicosis

279
Q

Name the Pneumoconioses: Affects upper lobes and causes an “egg shell” calcification of the hilar lymph nodes

A

Silicosis

280
Q

Name the Pneumoconioses: Associated with shipbuilding, roofing and plumbing

A

Asbestosis

281
Q

Name the Pneumoconioses: Ivory white clacified pleural plaques are pathonomonic of this - are NOT precancerous

A

Asbestosis

282
Q

Name the Pneumoconioses: Associated with in increased incidence of bronchogenic carcinoma and mesothelioma

A

Asbestosis

283
Q

Name the Pneumoconioses: Affects the lower lobes and has dumbbell shaped golden brown rods

A

Asbestosis

284
Q

Name the Pneumoconioses: Seen in mining and people that work in aerospace indusrty

A

Berylliosis

285
Q

Name the Pneumoconioses: Noncaseating granulomas in the lung, hilar lymph nodes and systemic organs and have an increased risk of cancer. Seen in mining and people that work in aerospace indusrty

A

Berylliosis

286
Q

What causes neonatal respiratory distress syndrome?

A

Premature birth with a lecithin:sphingomyelin ratio <1.5

287
Q

Why can maternal diabetes lead to neonatal respiratory distress syndrome?

A

The mom’s excess glucose leads to increased insulin in the baby which leads to decreased surfactant production

288
Q

What’s the concern with giving O2 for neonatal respiratory distress syndrome?

A

may result in blindness due to hyperoxemia because oxygen free radicals can damage the retinal arteries

289
Q

what is normal FEV1/FVC ratio?

A

80%

290
Q

what is a potential late finding seen in acute respiratory distress syndrome?

A

a progressive interstitial fibrosis = restrictive lung disease
due to repair of the lungs

291
Q

In what situations do you see hyaline membrane deposition in the alveoli?

A

ARDS and Neonatal RDS

292
Q

what progression can be seen in sleep apnea?

A

Hypoxia –> increased EPO released –> increased erythropoiesis

293
Q

What’s the lung abnormality: Decreased breath sounds, dull percussion, decreased fremitus

A

Pleural effusion

294
Q

What’s the lung abnormality: Decreased breath sounds, dull percussion, decreased fremitus and tracheal deviation toward the side of problem

A

Atelectasis (bronchial obstruction)

295
Q

What’s the lung abnormality: Decreased breath sounds, hyperresonant percussion, decreased fremitus and tracheal deviation toward the side of problem

A

Spontaneous pneumothorax

296
Q

What’s the lung abnormality: Decreased breath sounds, hyperresonant percussion, decreased fremitus and tracheal deviation AWAY from the side of problem

A

Tension pneumothorax

297
Q

What’s the lung abnormality: bronchial breath sounds with late inspiratory crackles, dull percussion and increased fremitus

A

Consolidation (like in lobar pneumonia or pulmonary edema)

298
Q

What type of breathing is commonly seen in congestive heart failure or in increased intracranial pressure?

A

Cheyne-Stokes Respirations

299
Q

What is the most common cause of cancer?

A

Metastatic! from breast, colon, prostate and bladder

300
Q

Where does lung cancer like to go?

A

Adrenals, brain, bone, liver

301
Q

Name the lung cancer: Located peripherally, is CEA + and is associated with k-ras activating mutation

A

Adenocarcinoma

302
Q

Name the lung cancer: most common lung cancer in nonsmokers and in smoking females

A

Adenocarcinoma

303
Q

Name the lung cancer: contains glands or mucin and is located peripherally

A

Adenocarcinoma

304
Q

Name the lung cancer: CXR shows hazy infiltrates like a pneumonia because the tumor cells are columnar cells that grow along bronchioles and alveoli

A

Bronchioalveolar carcinoma

305
Q

Name the lung cancer: is a subtype of Adenocarcinoma

A

Bronchioalveolar carcinoma

306
Q

Name the lung cancer: grows along alveolar septa leading to apparent “thickening” of alveolar walls, has a very good prognosis

A

Bronchioalveolar carcinoma

307
Q

Name the lung cancer: Centrally located, Hilar mass arising from the proximal bronchus, associated with smoking and cavitary lesion, also produces PTHrP leading to hypercalcemia and low PTH levels

A

Squamous cell carcinoma

308
Q

Name the lung cancer: Keratin pearly and intercellular bridging

A

Squamous cell carcinoma

309
Q

Name the lung cancer: Undifferentiated and very aggressive, located centrally and commonly has amplification of myc oncogenes

A

Small cell carcinoma

310
Q

Name the lung cancer: Neoplasm of neuroendocrine Kulchitsky cells leading to small dark blue cells

A

Small cell carcinoma

311
Q

Name the lung cancer: May produce ACTH, ADH or antibodies against presynaptic calcium channels

A

Small cell carcinoma

312
Q

Name the lung cancer: Inoperable tumor that is treated with chemotherapy

A

Small cell carcinoma

“too small for the surgeons to see”

313
Q

Name the lung cancer: Peripheral highly anaplastic undifferentiated tumor with a poor prognosis that gets removed surgically because it doesn’t really respond to chemo

A

Large cell carcinoma

314
Q

Name the lung cancer: Excellent prognosis, has nests of neuroendocrine cells that are chromogranin positive

A

Bronchial carcinoid tumor

315
Q

Name the lung cancer: Symptoms are usually due to a mass effect, you may see a carcinoid syndrome with serotonin secretion leading to flushing, diarrhea and wheezing

A

Bronchial carcinoid tumor

316
Q

Name the lung cancer: Psammoma bodies within the pleura results in hemorrhagic pleural effusions and pleural thckening

A

Mesothelioma

317
Q

Where else can you see a mesothelioma besides the pleura?

A

in peritoneum, pericardium and tunica vaginalis

318
Q

What are the most common causes of lobar pneumonia?

A

S. pneumonia most frequently, klebsiella

319
Q

What are the most frequent causes of Bronchopneumonia?

A

S pneumo, S aureus, H flu, Klebsiella

320
Q

Which pneumonia has acute inflammatory infiltrates with patchy distribution in 1 or more lobes?

A

Bronchopneumonia

321
Q

Which pneumonia involves patchy inflammation localized to interstitial areas at alveolar walls only?

A

interstitial atypical pneumonia

322
Q

What causes interstitial pneumonia

A

viruses (RSV, adenovirus, influenza), mycoplasma, legionella, chlamydia

323
Q

what are the gross phases of lobar pneumonia?

A

congestion
red hepatization
gray hepatization
resolution

324
Q

what are the most common bacteria seen in aspiration pneumonia leading to a lung abscess?

A

anaerobes: fusobacterium, bacteroides, peptostreptococcus

also S aureus

325
Q

What type of hypersensitivity is seen in hypersensitivity pneumonitis?

A

Mixed type III/IV HS reaction to environmental antigen

326
Q

Name the pleural effusion: decreased protein content, due to CHF, nephrotic syndrome or hepatic cirrhosis

A

Transudate

Transudate = transparent

327
Q

Name the pleural effusion: increased protein content, cloudy. Due to malignancy, pneumonira, collagen vascular disease, trauma

A

Exudate

must be drained in light of risk of infection

328
Q

Name the pleural effusion: due to thoracic duct injury from trauma, malignancy, milky-appearance, has increased triglycerides

A

Lymphatic aka chylothorax

329
Q

What’s the leading cause of a chylothorax?

A

lymphoma

330
Q

A patient presents with a unilateral chest pain and dyspnea. they have unilateral chest expansion, decreased tactile fremitus, hyperresonance and diminished breath sounds - what’s happening?

A

pneumothorax

331
Q

What type of pneumothorax has an accumulation of air in the pleural space, occurs most frequently in tall, thin, young males due to rupture of apical blebs and causes the trachea to deviate toward the affected lung?

A

Spontaneous pneumothorax

332
Q

What type of pneumothorax usually occurs in a setting of trauma or lung infection and leads to air entering the pleural space but not able to exit and leads to the trachea deviating away from the affected lung?

A

Tension pneumothorax

333
Q

what is the gold standard treatment for tension pneumothorax?

A

chest tube at midaxillay 4th intercostal space

334
Q

What is the rough and dirt job for treating tension pneumothorax?

A

needle thoracostomy is immediate and life saving in someone with dropping vital signs - this is midclavicular needle insertion at the 2nd intercostal space

335
Q

Name 3 first generation H1 blockers

A

Diphenhydramine, dimenhydrinate, chlorpheniramine

336
Q

Name 4 2nd generation H1 blockers

A

Loratadine, fexofenadine, desloratadine, cetirizine

337
Q

What drug relaxes bronchial smooth muscle via Beta 2 and is used during acute exacerbation of asthma

A

Albuterol

338
Q

What drug is long acting agent beta 2 agonist used for prophylaxis

A

Salmeterol, formoterol

339
Q

What are the adverse side effects of Salmeterol and formoterol?

A

tremor and arrhythmia

340
Q

What drug is a methyxanthing?

A

Thophylline

341
Q

How does theophylline work?

A

likely causes bronchodilation by inhibiting phosphodiesterase leading to increased cAMP levels due to decreased cAMP hydrolysis

342
Q

What drug does theophylline block?

A

denosine

343
Q

Why do you use theophylline?

A

TX COPD or asthma

344
Q

Name two muscarinic antagonists for treating bronchoconstriction and COPD

A

Ipratropium and tiotropium

345
Q

What are the side effects of Ipratropium and tiotropium?

A

metallic taste and a cough

346
Q

What corticosteroids are first line therapy for chronic asthma?

A

Beclomethasone, fluticasone

347
Q

How do Beclomethasone and fluticasone work?

A

Inhibit synthesis of cytokines - inactivates NF-kB which is the transcription factor that induces the production of TNF-alpha

348
Q

Which antileukotrienes block the leukotriene receptor?

A

Montelukast and zafirlukast

349
Q

What antileukotrienes are good for aspirin induced asthma?

A

Montelukast and zafirlukast

350
Q

How does Zileuton work?

A

5-lipoxygenase pathway inhibitor - blocks conversion of arachidonic acid to leukotrienes

351
Q

How does Omalizumab work?

A

Monoclonal anti-IgE antibody that binds mostly unbound serum IgE

352
Q

When would you use Omalizumab?

A

Used in allergic asthma resistant to inhaled steroids and long acting beta 2 agonists

353
Q

What is Guaifenesin?

A

Expectorant - thins respiratory secretions but does NOT suppress the cough reflex - would want to give a cough suppressant with it

354
Q

How is N-acetylcysteine a mucolytic?

A

Loosens mucous plugs in CF patients by cleaving disulfide bonds within mucous glycoprotein

355
Q

What is Bosentan use to traet?

A

pulmonary arterial hypertension

356
Q

how does Bosentan work?

A

competitively antagonizes endothelin-1 receptors, decreasing pulmonary vascular resistance

357
Q

What is dextromethorphan?

A

Antitussive that antagonizes NMDA glutamate receptors.

358
Q

What is dextromethorphan an analog of?

A

Synthetic analog of codeine - has mild opioid effect when used in XS and has mild abuse potential
Naloxone can be given for overdose

359
Q

How do pseudoephedrine and phenylephrine work?

A

sympathomimetic alpha agonistic nonprescription nasal decongestants

360
Q

What would you use pseudoephedrine and phenylephrine for?

A

reduces hyperemia, edema and nasal congestion; open obstructed Eustachian tubes
pseudoephedrine is also used as a stimulant

361
Q

What is the toxicity seen with pseudoephedrine and phenylephrine?

A

Hypertension

pseudoephedrine can also cause CNS stimulation/anxiety

362
Q

What is Methacholine?

A

Muscarinic receptor agonist - used in asthma challenge testing

First aid Chs Part 1 (8 decks)

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