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Step 1 > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

What is primary HTN most often associated with?

A

An inactivation mutation of BMPR2, which leads to proliferation of vascular smooth muscle.

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2
Q

On the histology, what is a sign of long-standing pulmonary HTN?

A

Plexiform lesion - a tuft of capillaries that occurs together

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3
Q

What type of pneumoconiosis predisposes a person to Tb and why?

A

Silicosis because silica impairs phagolysosome formation by macrophages, leading to increased risk of Tb.

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4
Q

What is the primary driver of pneumocytes to induce fibrosis?

A

TGF-Beta - remember macrophages induce fibrosis as the healing process by releasing TGF-beta and IL-10.

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5
Q

Why do people with sarcoidosis have hypercalcemia?

A

Granulomas have 1-alpha-hydroxylase activity activating vitamin D. Any disease with non-caseating granulomas will lead to hypercalcemia. You might see this with berylliosis as well.

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6
Q

What are two common causes of emphysema?

A

1) smoking 2) alpha-1-antitrypsin deficiency - both of these lead to destruction of alveolar air sacs and consequently loss of elastic recoil and airway collapse in the lung

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7
Q

What is cor pulmonale?

A

Blood vessels in lung vasoconstric when no ventilation, which shunts blood away. In a disease like chronic bronchitis, all vessels clamp down increasing the pressure that right ventricle must pump against, which can lead to RVH and eventually RH failure.

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8
Q

What other organ system beside the lung does A1AT deficiency affect?

A

The liver - it can lead to cirrhosis because the ER of hepatocytes get clogged up with misfolded A1AT proteins.

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9
Q

Why do patients with emphysema use purse lipped breathing?

A

This leads to an increase positive back pressure keeps the airways open in the lung, which is necessary since elastic recoil is damaged.

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10
Q

What class III anti-arrhythmic can lead to interstitial fibrosis?

A

Amiodarone

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11
Q

What are considered the stem cells of the lung?

A

Type II pneumocytes

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12
Q

What would be signs of endothelial cell damage in association with damage of the alveolar air sacs?

A

vWF and endothelin. Might also see LDH or D-dimer.

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13
Q

What is the cause of neonatal respiratory distress syndrome? How do you treat it?

A

Inadequate surfactant production by type II pneumocytes - treat with exogenous lecithin (AKA phosphatidylcholine)

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14
Q

When does surfactant production begin?

A

At 28 weeks of gestation but adequate levels not reached till 34 weeks. Premature babies before this are at risk of NRDS.

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15
Q

Why would you not want to give a baby suffering from NRDS supplemental O2?

A

This could lead to free radical formation which can damage the retina leading to blindness and bronchopulmonary dysplasia.

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16
Q

In terms of tracheal deviation, how do you differentiate between a spontaneous and tension pneumothorax?

A

Spontaneous pneumothorax has tracheal deviation towards the side with the damage. Tension pneumothorax has tracheal deviation away from the hole in the pleura (air get in the pleural space like a basketball and cannot escape so it “pumps” the tracheal away from the pneumothorax).

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17
Q

How would you treat an isoniazid overdose?

A

Pyridoxine - because INZ is a competitive antagonist of pyridoxal kinase, an essential component in the biosynthesis of GABA from vit B6 (pyridoxine)

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18
Q

What other signs or symptoms do patients with aspirin induced asthma often present with?

A

Also known as Samter’s triad: a combination of nasal polyps, asthma, and aspirin sensitivity.

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19
Q

In a patient with CF, the mutation results in a defect in which aspect of the CFTR protein assembl?

A

ER processing from the ER to the Golgi apparatus.

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20
Q

What is a Curschmann’s spiral?

A

Mucoid exudate forming a cast of the airways (associated with asthma)

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21
Q

What is a Charcot-Leyden crystal?

A

Collections of crystalloid made up of eosinophil membrane protein

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22
Q

If a patient has a sulfa allergy, what is the next best choice for prophylaxis of pneumocystis jirovecci?

A

Pentamidine (then dapsone)

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23
Q

What are the four major mechanisms of hypoxemia (PaO2 < 80 mmHg on room air)?

A

1) anatomic shunt
2) physiologic shunt (atelectasis)
3) low V/Q
4) hypoventilation

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24
Q

What are two mechanisms for hypercarbia (PaCO2 > 45)?

A

1) hypoventilation

2) increased dead space

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25
Q

Menthol acts on what channel to alleviate a cough?

A

TRPM8

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26
Q

What is the alveolar gas equation?

A

PAO2 = FiO2 (Pb - PH20) - (PACO2/0.8)

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27
Q

What is the O2 content equation?

A

Ca02 = (Hgb x 1.34) x SaO2 x Dissolved O2

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28
Q

What airways are flow dependent?

A

The large airways - greater effort = greater peak flow. Small airways are not flow dependent.

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29
Q

What are the 6 parameters of good effort on PFT?

A

1) Rapid rise on flow/volume curve
2) Early peak
3) Gradual decrease in flow to baseline
4) Plateau on spirogram
5) Expiratory time is > 6 sec.

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30
Q

What does the extent of restriction and obstruction depend on?

A

For restriction, extent depends on FVC. For obstructive, severity depends on FEV1.

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31
Q

What kind of breathing for those suffering from restrictive lung disease do?

A

Rapid, shallow breathing. This increase in frequency minimizes the work of breathing for individuals with a loss of lung compliance.

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32
Q

True or False: Idiopathic pulmonary fibrosis responds to corticosteroid therapy.

A

False - the only treatment is a lung transplant.

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33
Q

What lung disease is associated with honeycombing on a chest?

A

Idiopathic pulmonary fibrosis (this pattern is seen due to dense fibrosis)

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34
Q

What are the two most common causes of hypersensitivity pneumonitis?

A

1) Avian proteins found in bird excrement and feathers

2) Saccharopolyspora rectivirgula, a thermophilic actinomyces found in moldy hay.

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35
Q

Compared to normal, patients with a restrictive lung disease have a _______ RV/TLC.

A

Increased ratio; both are decreased though. TLC is decreased out of proportion to RV (remember this is a problem with filling)

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36
Q

What pulmonary disease is often associated with scleroderma?

A

Nonspecific interstitial pneumonitis

37
Q

Hypersensitivity pneumonitis is what type of hypersensitivity reaction?

A

Type IV resulting in lymphocytic alveolitis.

38
Q

Pleural effusions develop secondarily to?

A

An increase in permeability (inflammatory or neoplastic diseases - exudate) or a change in driving forces (CHF - fluid is a transudate).

39
Q

How is Duchenne’s MD inherited and what is the gene that is abnormal?

A

It is X-linked recessive and involves the dystrophin gene, a protein that links the normal contractile apparatus to the sarcolemma in skeletal muscle.

40
Q

What are the four common pathological features seen in someone with asthma?

A

1) Airway smooth muscle hypertrophy
2) Mucus plugs
3) Mucosal edema
4) Thickening of basement membrane (increased airway remodeling)

41
Q

What happens to airway resistance and ventilation during an asthma attack?

A

R(aw) increases, which lowers ventilation. V/Q < 1, which brings down PaO2 (hypoxemia), which is responsive to O2. In a severe attack, V/Q is close to 0 so it is like a physiologic shunt.

42
Q

What is the effect of increased airway resistance on RV and TLC during an asthma attack?

A

Increased R(aw) causes air trapping, which increases RV and increases RV/TLC ratio. There will be decreased expiratory flow so decreased FEV1 and decreased FVC, resulting in a decreased FEV1/FVC.

43
Q

Explain the Type I HSR that is occurring with asthma.

A

1) Allergen exposure induces TH2 phenotype in CD4+ T cells (in genetically predisposed people).
2) TH2 cells secrete IL-4 (class-switching to IgE), IL-5 (attract eosinophils) and IL-10 (stimulation TH2 and inhibits TH1)
3) Re-exposure to allergen leads to IgE mediated activation of mast cells

44
Q

What occurs in early phase reaction of asthma?

A

IgE mediated activation of mast cells leads to release preformed histamine granules and generate leukotrienes which leads to bronchoconstriction, inflammation, and edema.

45
Q

What occurs in the late phase reaction of asthma?

A

Inflammation, especially major basic protein derived from eosinophils, damages cells, and perpetuates bronchoconstriction.

46
Q

What is the equation for PVR?

A

PVR = [(MPA - PCWP)/CO] x 80

47
Q

What is the hemodynamic definition of pulmonary hypertension? How do you officially diagnosis it?

A

A mean pulmonary artery pressure of greater than or equal to 25 mmHg. Diagnosis uses a right-heart catheterization.

48
Q

How do systemic-to-pulmonary shunts, AV fistulas, chronic anemia, thyrotoxicosis, and other high cardiac output states contribute to pulmonary hypertension?

A

These are all high-flow states. Pulmonary system is usually low flow, low resistance system.

49
Q

How do you differentiate between pre-capillary pulmonary HTN and post-capillary HTN?

A

1) Pre-capillary: PCWP less than or equal to 15 mmHg; PVR greater than 240 dynes/sec/cm-5; with mean PAP of greater than or equal to 25 mmHg.
2) Post-capillary: PCWP > 15 mmHg; PVR is normal

50
Q

What are three medications that can be used to treat pulmonary hypertension?

A

Bosentan (endothelin receptor antagonist), Epoprostenol (prostacyclin - vasodilator), Sildenafil (PDE-5 inhibitor)

51
Q

What is the only curable form of pulmonary hypertension?

A

Chronic thromboemobolitic pulmonary hypertension. A pulmonary thromboendarectomy is performed and results in a cure of 90% of people.

52
Q

Which pneumoconiosis produces “egg shell” calcifications in the hilar nodes?

A

Silicosis -these are dystrophic calcifications

53
Q

What lung disease is associated with stellate inclusion/”asteroid” bodies?

A

Sarcoidosis - these are found in the granulomas

54
Q

What type of hypersensitivity reaction is hypersensitivity pneumonitis like Farmer’s lung?

A

Type III HSR; first exposure patient develops precipitating IgG antbodies (present in serum), second exposure antibodies combine with inhaled allergens to form immune complexes. There is no IgE or eosinophils. Chronic exposure can lead to Type IV with granulomas.

55
Q

What happens to TLC and RV in emphysema?

A

There is air trapping behind the collapsed distal bronchiole which distends the respiratory bronchiole. This increase RV and TLC. The total ratio of RV/TLC increases because RV increases more than TLC.

56
Q

What happens when IgE antibodies cross-link on mast cells?

A

Release of histamine and other preformed mediators which lead to bronchoconstriction, mucus production, and influx of leukocytes.

57
Q

Why are anticholinergics prescribed in lung diseases?

A

Acetylcholine acting on M3 receptor causes airway muscle contraction

58
Q

What is the suggested mechanism by which aspirin can induce asthma in some people?

A

It blocks cycloxygenase activity therefore inhibits formation of prostaglandins and thromboxanes. This leaves the cyclooxygenase pathway open for production of leukotrienes, which are bronchoconstrictors.

59
Q

What is bronchiectasis?

A

It is the permanent dilation of the bronchi and bronchioles causing repeated episodes of airway infection and inflammation. This due to destruction of cartilage and elastic tissue by chronic necrotizing infections.

60
Q

What is the major problem with primary cilia dyskinesia?

A

The dynein arm in cilia is absent. This arm contains ATPase for movement of the cilia. Without it, you cannot beat infections/mucus out of the aiway.

61
Q

What are the major causes of bronchiectasis?

A

1) CF
2) Infections like Tb
3) Bronchial obstruction from something like bronchogenic carcinoma occluding the lumen
4) Primary ciliary dyskinesia
5) ABPA

62
Q

What is the inheritance pattern of CF?

A

Autosomal recessive

63
Q

What is the pathogenesis of CF?

A

The mutation is a three-nucleotide deletion of chromosome 7 that normally codes for phenyalanine. The defective protein causes misfolding in the CFTR.

64
Q

What is the main problem with CF?

A

Secretion of the body become dehydrated because there is increased Na and H20 reabsorption from lumen and decreased Cl- into lumens. This leads to thickened mucus in bronchioles, pancreatic ducts, bile ducts, meconium, cervix, and seminal fluid.

65
Q

What can be used to treat CF?

A

1) N-acetylcysteine to loosen mucus plugs.

2) Dornase alfa (DNAse) to clear leukocytic debris

66
Q

Why are CF patients often deficient in vitamins A, D, E, and K?

A

There are fat-absorbable vitamines and since the patients have pancreatic insuffieciency there is impaired digestion of fats.

67
Q

What microorganism leads to most infection of CF patients?

A

Pseudomonas

68
Q

Isoniazid is used as prophylaxis for those exposed to Tb. What is its mechanism?

A

It decreases synthesis of mycolic acids. Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolite.

69
Q

ARDS is characterized by diffuse alveolar damage, which leads to protein-leakage into alveoli and eventually formation of an intra-alveolar hyaline membrane. What cell most likely enables exudation from the interstitium of the lungs into alveoli?

A

Type I pneumocytes because they line 97% of the surface of alveoli.

70
Q

What is the mechanism of action of zileuton?

A

It is a 5-lipoxogenase pathway inhibitor that blocks conversion of arachidonic acid into potent bronchoconstrictors called leukotrienes.

71
Q

What is the chloride shift?

A

It is the process by which bicarbonate ions created by carbonic anhydrase in response to rising carbon dioxide leaves an RBC in exchange for chloride.

72
Q

Other than blocking elastase and other protease activity, what other role might AIAT play?

A

It may inhibit alveolar cell apoptosis and protect against emphysema in the absence of neutrophilic inflammation.

73
Q

What lung conditions would giver hyperresonance upon percussion?

A

Emphysema, pneumothorax, asthma

74
Q

What are best drugs for COPD?

A

Long lasting B2 agonists. Really any long lasting bronchodilators.

Roflumilast is a PDE-4 inhibitor and is anti-inflammtory and reduces COPD exacerbations.

75
Q

What is the innate immunity of the upper airway?

A

It does mucociliary transport/clearance - this is an important role in defense of airway against inhaled microbes.

76
Q

How much does the nose contribute to total airway resistance?

A

50%!

77
Q

What is Waldeyer’s ring?

A

It is a ring of lymphoid (tonsil) tissue. If it gets inflammed, it can lead to hypertrophy of the adenoids leading to chronic mouth breathing, Eustachian tube dysfunction, and nasal obstruction.

78
Q

What is meant by “unified airways”?

A

The epithelial lining of the respiratory tract from the lining of the middle ears through nose and sinuses, through the larynx, down the trachea and bronchioles into the lungs is all similar.

79
Q

How do we defined respiratory failure?

A

PaO2 < 50 mmHg and PaCO2 > 50 mmHg

  • At PaO2 of 50 mmHg, pulmonary artery pressure rises; we want to be over 50 or else we can get cor pulmonale
80
Q

What is Type 1 Respiratory Failure?

A
  • Hypoxemic - “acute hypoxemic respiratory failure”
  • Occurs when alveolar flooding and intrapulmonary shunt develops
  • Pulmonary edema, pneumonia, and alveolar hemorrhage
81
Q

What is Type 2 Respiratory Failure?

A
  • Occurs as a result of alveolar hypoventilation
  • Inability to eliminate CO2 effecctively
  • Several etiologic mechanisms
  • Treat underlying cause
82
Q

What is Type 3 Respiratory Failure?

A
  • occurs as a result of atelectasis
  • “perioperative respiratory failure”
  • Decreased FRC (after general anesthesia)
83
Q

What is Type 4 Respiratory Failure?

A
  • Occurs in the setting of shock and multi-organ system failure
  • Hypo-perfusion of the respiratory muscles
84
Q

What is the pulmonary rule for arterial blood gases?

A

PaCO2:

  • pH change of 0.08 units/10 mmHg in PaCO2 if process is acute
  • pH change of 0.03 units/10 mmHG in PaCO2 if process is chronic (renal compensation)
85
Q

What is ARDS?

A

It is diffuse damage to the alveolar-capillary interface (diffuse alveolar damage). Leakage of protein-rich fluid leads to edema that combines with necrotic epithelial cells to form hyaline membranes.

86
Q

What is the pathophysiology of ARDS?

A

Insult –> Inflammation –> Cytokines –> Acute Lung Injury –> ARDS

87
Q

What would V/Q be for a patient with emphysema?

A

IT would be V/Q >1 because destruction of alveolar capillaries and alveolar septa leads to increased physiologic dead space (air trapping behind collapsed bronchioles).

88
Q

What are the J receptors in the lung?

A

These are juxtacapillary receptors (C-fiber receptors) that are located in alveolar walls and innervated by vagus nerve. They sense decrease in oxygenation and stimulate increase in ventilation. This can lead to a feeling of dyspnea.

89
Q

How does Bordetella pertussis classical present?

A

It is marked by bouts of multiple coughs in a single breath followed by a deep inspiration (“whooping cough”). This might also be followed by vomiting. This is the paroxysmal stage. The initial phase is flu-like for the first two weeks and can be treated with erythromycin.

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