DIT review - Pulmonary 2 Flashcards

1
Q

Will you see an increase or a decrease in the following values in obstructive lung disease:

  • Residual volume (RV)
  • Functional residual capacity (FRC)
  • Total lung capacity (TLC)
  • FEV1
  • FVC
  • FEV1:FVC
A
  • Residual volume (RV) - increased
  • Functional residual capacity (FRC) - increased
  • Total lung capacity (TLC) - increased
  • FEV1 - decreased
  • FVC - decreased
  • FEV1:FVC - decreased (< 80%)
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2
Q

What are the 4 obstructive lung diseases?

A

Asthma, chronic bronchitis, emphysema, bronchiectasis

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3
Q

What will be seen on histology in asthma patients

A
  • Curschmann’s spirals (shed epithelium forms whorled mucus plugs)
  • Charcot-Leyden crystals (eodsinophilic, hexagonal, double-pointed, needle-like crystals)
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4
Q

What is the diagnostic criteria for chronic bronchitis

A
  • Chronic productive cough for > 3 months per year for > 2 consecutive years
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5
Q

Describe characteristic histology of Chronic bronchitis

A
  • Characterized by hyperplasia of mucus-secreting glands in bronchi
    • Reid index (thickness of mucosal gland layer to thickness or wall) > 50%
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6
Q

Classic presentation of chronic bronchitis

A

“Blue bloaters”

  • Productive cough, wheezing, crackles, dyspnea
  • Cyanosis (“blue bloating”) due to shunting
    • Decreased paO2
  • CO2 retention due to mucus plugs trapping CO2
    • Increased paCO2
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7
Q

Describe the basic premise behind emphysema

A
  • Destruction of alveolar air sacs = loss of elastic recoil and collapse of airways during exhalation = obstruction and air trapping
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8
Q

What are the two types of emphysema, and which occurs in what part of the lung

A
  • Centriacinar
    • Associated with smoking
      • Pollutants in smoke = excessive inflammation = protease-mediated damage
    • Worse in upper lobes
  • Panacinar
    • Associated with alpha-1-antitrypsin (A1AT) deficiency
      • No A1AT to neutralize proteases (elastase)
    • Worse in lower lobes
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9
Q

Why is A1AT deficiency also associated with liver cirrhosis

A
  • A1ATD due to misfolding of mutated proteins
  • Misfolded proteins accumulate in the endoplasmic reticulum of hepatocytes
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10
Q

Classic presentation of emphysema

A
  • Dyspnea and cough with minimal sputum
  • Prolonged expiration with pursed lips (“pink puffer”)
  • Barrel-chest
    • Increased AP diameter on CXR
    • Flattened diaphragm
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11
Q

Describe the basic premise behind bronchiectasis

A
  • Chronic infection of the bronchi causes permanent dilation of airways
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12
Q

Common causes of bronchiectasis

A
  • Cystic fibrosis, Karagener sundrome, necrotizing infection, allergic bronchopulmonary aspergillosis
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13
Q

Presentation of bronchiectasis

A
  • Cough, dyspnea, foul-smelling sputum
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14
Q

What type of drug is Chlorpheniramine and Diphenhydramine

A
  • 1st generation H1-blockers
    • Are lipophilic and can cross the BBB
    • Diphenhydramine** and **Dimenhydrinate
      • = dragonfly fairy
    • Chorpheniramine
      • = color fairy
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15
Q

What type of drug are

  • Hydroxysine, Meclizine, Promethazine
A
  • 1st generation H1-blockers
    • Are lipophilic and can cross the BBB
  • Hydroxysine, Meclizine, Promethazine
    • = fairy cuisine
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16
Q

What are the 2nd generation H1-blockers

A
  • 2nd generation H1-blockers:
    • Are less lipophilic and so do NOT cross the BBB (less central effects)
  • Fexofenadine
    • à fox
  • Cetirizine
    • à Satyr
  • Loratidine
    • à rat
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17
Q

What effects do 1st generation H1-blockers have the 2nd generation do not?

A
  • Treats vestibular nausea or motion sickness
    • = seasick fairy sailors in front of the brain tree
    • Only 1st generation H1 blockers because they are lipophilic so can enter the CNS and act of the vestibular system and brainstem
  • Drowsiness (can be used to treat insomnia)
    • = guy sleeping
    • Only 1st generation
  • Antagonize peripheral and central muscarinic receptors (e.g. pupillary dilation, dry mouth, urinary retention, constipation, exacerbation of glaucoma, and delirium)
    • = anti-muscarinic tea party
  • Treat extrapyramidal side effects caused by antipsychotics (e.g. acute dystonia)
    • = falling “extra parking” cone
    • This is because the anti-muscarinic effects re-establish dopaminergic-cholinergic balance
  • Antagonize serotonin receptors in the CNS stimulating appetite and weight gain
    • = cut smiley face cake
    • = stuffed fairy next to cake
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18
Q

What are the main 2 drugs used in mild to moderate asthma

A

Beta-2 blockers

Inhaled cortocosteroids

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19
Q

MOA of Montelukast and Zafilukast

A

Direct inhibitors of leukotriene receptors (CysLT1)

Causes broncodilation

Used for persistent asthma, espcially aspirin-induced asthma

20
Q

MOA of Zileuton

A
  • Zileuton
    • = GodZILla
  • Mechanism:
    • Direct inhibition of LOX, which prevents the production of leukotrienes
      • = Godzilla falling on coach LOX
  • Uses:
    • Alternative therapy for mild persistent asthma
    • Especially goof for aspirin-induced asthma
  • Adverse effects:
    • Risk of hepatotoxicity
      • = liver spot on Godzilla
21
Q

What are the two long-acting Beta-2 agonists (LABA) used for asthma

A
  • Salmeterol** and **Formoterol
    • = Salute
    • = formation
    • = ROL call
  • Used for prophylaxis of asthma
22
Q

What is the muscarinic antagonist that can be used for asthma

A

Ipratropium

23
Q

MOA of Omalizumab

A
  • Omalizumab = limousine
    • Mechanism of action
      • Recall:
        • Mast cell degranulation is important to the pathogenesis of asthma
        • Antigen binding to IgE on mast cells causes degranulation and release of inflammatory mediators (e.g histamine)
      • Is an anti-IgE monoclonal antibody directed against the Fc portion of IgE (part that attaches IgE to mast cell), preventing mast cell sensitization
        • = limo guy grabbing end of IgE gun
24
Q

MOA of Theophyllin

A
  • Increases intracellular cAMP by inhibiting its breakdown by phosphodiesterases
    • = “Don’t PHOSTER disinterest”
    • = “go cAMPing”
  • Increased cAMP can aid in bronchial smooth muscle relaxation and inhibition of cytokine release
25
MOA of Cromolyn
* Mechanism of action: * Inhibits mast cell degranulation, preventing the release of histamine * = bee sedating smoke
26
Will the following value be high or low in restrictive lung disease: * TLC * FEV1 * FVC * FEV1:FVC
* Decreased TLC * Decreased FEV1 and FVC, but FVC is decreased more * FEV1:FVC ratio is increased (\> 80%)
27
What are the two main mechanisms that can cause restrictive lung disease
(1) Poor breathing mechanics (muscular or structural) (2) Interstitial lung disease
28
What will you see in idiopathic pulmonary fibrosis
* Repeated cycles of lung injury and wound healing with increased collagen deposition * “Honeycomb” lung appearance
29
What are the 2 interstitial lung diseases that also affect the kidney
Goodpasture syndrome Granulomatosis with polyangiitis (Wegener's) ?? microscopic polyangiitis ??
30
Besides pulmonary issues, what else does Langerhans cell histiocytosis present with?
* Neoplastic proliferation of specialized dendritic cells (especially in skin) * Birbeck (“tennis racket”) granules seen on EM * S-100 (+) and CD1a (+) * Presentation: * In children * Lytic bone lesions * Skin rash * Recurrent otitis media
31
What type of HSR is hypersensitivity pneumonitis
* Aka Pigeon breeder or Farmer’s lung * Mixed type III/IV HSR to environmental antigen * Presents with dyspnea, cough, chest tightness, and headache
32
What pneumoconiosis is caused by aerospace and manufacturing industries
Berylliosis
33
What pneumoconiosis is associated with sand blasting
Silicosis
34
What pneumoconiosis is associated with shipbuilding and roofing
Asbestos
35
What pneumoconiosis is associated with carbon dust exposure
Coal worker's pneumoconiosis
36
Of the 4 pnuemoconioses, which occur in the upper and which occur in the lower lobes: Asbestos, Coal worker's, Berylliosis, Silicosis
THINK: Asbestos is from the roof but affects the base; Silica and coal are from the bast but affect the roof Lower lobe = asbestos Upper lobe = berylliosis, coal worker, silicosis
37
What pneumoconiosis is assoicated with golden-brown fusiform rods resembling dumbbells?
Asbestos
38
Complications associated with Asbestos
* Causes fibrosis of lung or pleura; cancer of lung or pleura (mesothelioma) * Lung carcinoma more common than mesothelioma
39
What is anthracosis
Asymptomatic carbon in lungs Found in most urban dwellers
40
Describe presentation of Berylliosis
* Noncaseating granulomas in lung, hilar lymph nodes, and systemic organs * Looks similar to sarcoidosis
41
Complications associated with silicosis
* “Eggshell” calcifications of hilar lymph nodes * Silica impairs phagolysosome formation (increased risk for TB)
42
Characteristic findings of sarcoidosis
* Characterized by noncaseating granulomas in multiple organs * Granulomas most commonly involve the hilar lymph nodes and lung * Erythema nodosum (nodules on shins), uveitis, salivary and lacrimal glands (mimics Sjogren)
43
Elevated serum levels and histology of sarcoidosis
* Elevated serum levels: * ACE * Calcium * Histology = asteroid bodies * THINK: watching shooting stars (asteroids) on the beach with ice cream (hypercalcemia) while playing cards (ACE)
44
Describe the pathogenesis behind acute respiratory distress syndrome (ARDS)
* Due to diffuse damage to alveolar-capillary interface * Caused by neutrophil activation inducing protease- and free radical-mediated damage of type I and type II pneumocytes * Endothelial damage = increased capillary permeability = protein-rich leakage into alveoli = diffuse alveolar damage and noncardiogenic pulmonary edema * Results in intra-alveolar hyaline membrane
45
Causes of ARDS
* Sepsis, Pancreatitis, Pneumonia, Aspiration, Uremia, Trauma, Amniotic fluid embolism, Shock, Infection
46
Describe the defect that causes neonatal respiratory distress syndrome, and associated risk factors
* Respiratory distress due to inadequate surfactant levels * Associated with: * Prematurity, C-section delivery, maternal diabetes * Will show diffuse granularity (“ground glass”) appearance on lung