Problem questions (ie ones I can't remember) Flashcards

Question

Pulmonary complications of IBD

Answer 1

``` Bronchiectasis (most common) Tracheal stenosis Ileobronchial colobronchial fistula COP (Cryptogenic organizing pneumonia) granulomatous and necrobiotic nodules ILD Pulmonary Vasculitis Drug induced disease (Sulfasalazine and Mesalamine can cause HP) Opportunistic infection Malignancy Pulmonary thromboembolism ```

Answer 2

Need 4 1. Symptoms compatible with HP 2. Evidence of exposure to antigen 3. Radiographic characteristics consistent with HP 4. BAL fluid lymphocytosis (CD8 > CD4) 5. Lung biopsy demonstrates histology consistent with HP 6. Positive natural challenge that produces symptoms and objective abnormalities after reexposure to the offending antigen

Answer 3

The classic triad of 1. Interstitial lymphocytic-histiocytic cell infiltrate. 2. Bronchiolitis obliterans. 3. Scattered poorly formed non-necrotizing granulomas

Answer 4

1. Giant cells, granulomas, or Schaumann bodies 2. Interstitial pneumonia (UIP)–like Pattern. 3. A nonspecific interstitial pneumonia (NSIP)–like pattern or a bronchiolitis obliterans organizing pneumonia like disease can also be seen in chronic HP

Answer 5

1. Interstitial mononuclear cell infiltrate. | 2. Granulomas and macrophages with foamy cytoplasm have also been reported.

Answer 6

- ABPA - Congenital tracheobronchomegaly - CF - Williams Campbell syndrome

Answer 7

- CF - TB (NTM can be middle too) - ABPA (mid and upper) - Chronic HP (mid, upper)

Answer 8

Most common location - post infectious - aspiration - immunodeficiency - PCD - with BO post transplant

Answer 9

Excessive proliferation of granulation tissue -> consists of loose collagen-embedded fibroblasts and myofibroblasts involving alveolar ducts + alveoli +/- bronchiolar intraluminal polyps

Answer 10

Steroids (IV or PO) | Macrolides

Answer 11

1) Lymphocytosis (increased CD4:CD8 ratio) 2) no eosinophils, stain S-100, CD1a, langerin 3) Acute = neutrophilia, >48hrs = lymphocytosis, increased CD8 4) Gross blood, increasing with each sample 5) Lipid laden macrophages

Answer 12

Foamy alveolar macrophages | Type 2 alveolar cell hyperplasia

Answer 13

Qf = Kf[(Pc − Pis) − σ(πpl − πis)] where Qf = net flow of fluid Kf = capillary filtration coefficient; this describes the permeability characteristics of the membrane to fluids and the surface area of the alveolar-capillary barrier Pc = capillary hydrostatic pressure Pis = hydrostatic pressure of the interstitial fluid σ = reflection coefficient; this describes the ability of the membrane to prevent extravasation of solute particles such as plasma proteins πpl = colloid osmotic (oncotic) pressure of the plasma πis = colloid osmotic pressure of the interstitial fluid Note that the surface area of the alveolar-capillary barrier is included in the Kf. The Starling equation is very useful in understanding the potential causes of pulmonary edema, even though only the plasma colloid osmotic pressure (πpl) can be measured clinically.

Answer 14

1. Exclude patients with perinatal lung disease 2. Within 7 days of known clinical insult 3. Respiratory failure not fully explained by cardiac failure or fluid overload 4. Chest imaging findings of new infiltrate(s) consistent with acute pulmonary parenchymal disease 5. Oxygenation CPAP ≥ 5, P/F ≤ 300, SpO2/FiO2 ≤ 264 Mild = 4 ≤ OI ≤8 Moderate = 8 ≤ OI ≤ 16 Severe = OI ≥ 16

Answer 15

Consequence of inflammatory process at alveolar-capillary interface Increased alveolar capillary permeability à flooding of alveoli with protein rich fluid, leading to: - Impaired gas exchange - Impaired surfactant function

Answer 16

filtration constant = measure of membrane permeability to water

Answer 17

reflection coefficient; this describes the ability of the membrane to prevent extravasation of solute particles such as plasma proteins

Answer 18

1. Triggered by direct or indirect injury 2. Acute exudative phase with pulmonary edema, cytokine release, activated neutrophils 3. Fibroproliferative phase (may lead to fibrosing alveolitis) 4. Recovery Stage

Answer 19

1) fully aerated, normal "baby lung" 2) Poorly aerated (recruitable) 3) Non-aerated (collapsed, atelectatic)

Answer 20

Direct (pulmonary) causes

Answer 21

Characterized by a primary injury to the alveolar epithelium | Results in intra-alveolar edema, reduced lung compliance, with preservation of chest wall compliance

Answer 22

``` Pneumonia (viral, bacterial) Aspiration pneumonia Bronchiolitis Near drowning Lung contusion Toxic inhalation ```

Answer 23

Sepsis Nonthoracic trauma Transfusion of blood products Pancreatitis

Answer 24

Predominantly consolidation Differences in mechanism of injury and pathology may explain why pulmonary causes tend to have more refractory hypoxemia, with resistance to recruitment maneuvers and prone posturing, but respond better to surfactant

Answer 25

Primary insult is systemic, with the major injury occurring to the capillary endothelium Results in interstitial edema, with greater reduction of compliance in the chest wall Responds better to recruitment

Answer 26

Predominantly atelectasis

Answer 27

Also referred to as alveolar capillaritis, is characterized by neutrophilic infiltration of the alveolar septa (lung interstitium) -> necrosis of these structures, loss of capillary structural integrity and spilling of RBCs into the alveolar space and interstitium

Answer 28

``` The systemic vasculitides Anti-glomerular basement membrane (anti-GBM, Goodpasture’s) disease Rheumatic diseases Certain drugs Idiopathic pulmonary hemosiderosis, Idiopathic pulmonary capillaritis ``` Idiopathic pulmonary capillaritis, also known as pauci-immune pulmonary capillaritis, is characterized by the histopathologic findings of pulmonary capillaritis, but without clinical or serologic evidence of an associated systemic illness

Answer 29

Present with signs and symptoms of alveolar hemorrhage without renal or other systemic manifestation Diffuse alveolar opacities on imaging Low hemoglobin Hemosiderin-laden macrophages on BAL Normal kidney function Associated with lower hemoglobin and higher ESR (compared to IPH) Usually positive ANCA - if not, need biopsy

Answer 30

Subtype of group 1 (PAH) PVOD may represent a common aberrant response to an inciting event of endothelial injury that leads to widespread fibrosis of pulmonary venules Many patients with PVOD additionally have findings of capillary congestion and lymphadenopathy, but with a normal-sized left atrium and normal-sized major pulmonary veins The presence of venous congestion and lymphadenopathy with a normal-sized left atrium and normal-sized major pulmonary veins are features that may help distinguish PH due to PVOD from other causes of post-capillary PH, namely that due to left-sided heart disease These features are likely due to chronic pulmonary capillary hypertension, transudation of fluid into the interstitium, and enlargement of pulmonary lymphatic channels.

Answer 31

PVOD is a fibroproliferative disease primarily affecting the small pulmonary veins with relative sparing of the larger veins. The pathologic hallmark of PVOD is extensive and diffuse occlusion of the pulmonary veins due to smooth muscle hypertrophy and collagen matrix deposition (ie, fibrous tissue).

Answer 32

1. Iron deficiency Anemia 2. Hemoptysis 3. Diffuse infiltrates on imaging

Answer 33

``` The triad of: 1) primary focus 2) local tuberculous lymphangitis (basically inflammation of surrounding lymphatic channels) 3) enlarged regional lymph nodes = the primary complex. ``` Ghon focus = happens when cellular infiltrates continue to the site of infection, the center for the granuloma because caseous (or necrotizing) and you can see a fibrocalcific residua on imaging Ghon complex = Ghon focus + calcified granulomatous focus in a draining lymph node

Answer 34

Inflammatory, such as granulomatous with polyangitis, rheumatoid arthritis, sarcoid Fat emboli Malignancy, such as squamous cell carincoma Langerhans cell histiocytosis

Answer 35

CAVITY is the acronym to remember C = cancer, such as squamous cell carcinoma A = autoimmune, such as GPA, rheumatoid arthritis (rheumatoid nodules) V = vascular, such as septic pulmonary emboli or I = infection, such as bacterial or fungal, such as pulmonary abscess, pulmonary TB, NTAM, aspergillus T = trauma, such as pneumatoceles

Answer 36

- Shares visceral pleura - More common with infections - Doesn't usually have associated anomalies - Blood supply = Aorta, Venous usually to left atrium but can also be to right side usu posterior basal LLL. More than 50% diagnosed as adult - often asymptomatic. - Usually drain into pulmonary system (=shunt)

Answer 37

- Own visceral pleura - Usually detected incidentally on imaging - More common to have associated anomalies - Blood supply = Aberrant vessel from Aorta, Venous drainage to right atrium usu beneath LLL, 15% abdominal. More often detected in neonates - assoc abn - Usu. drain into azygous

Answer 38

``` Location: periphery, centre or hilum Pulmonary cyst Regular shaped cyst Thin walled cyst, Water lily sign Meniscus, crescent sign Bronchial displacement Pericentric emphysema Air fluid level ```

Answer 39

``` Lymphoid interstitial pneumonitis Pulmonary tumours Bronchiolitis obliterans Bronchiectasis Immune reconstitution inflammatory syndrome (IRIS) Airway hyperreactivity/asthma Aspiration pneumonitis Pulmonary HTN (limited data in children) Upper airway disease ``` Respiratory disease is the most common complication occurring in human immunodeficiency virus (HIV)-infected children. Acute disease = most likely to be infectious

Answer 40

Pentamidine Dapsone Atovoquone

Answer 41

"Every Pulmonologist Can See Alveoli" 1) Embryonic 4-7 wks 2) Pseudoglandular 5-17 wks 3) Canalicular 16-26 wks 4) Saccular 24 wks- term 5) Alveolarization 36 wks to 21 years

Answer 42

Lung buds; trachea, main stem, lobar, and segmental bronchi; trachea and esophagus separate

Answer 43

Subsegmental bronchi, terminal bronchioles, and acinar tubules; mucous glands, cartilage, and smooth muscle

Answer 44

Respiratory bronchioles, acinus formation and vascularization; type I and II AEC differentiation

Answer 45

Dilation and subdivision of alveolar saccules, increase of gas-exchange surface area, and surfactant synthesis

Answer 46

Further growth and alveolarization of lung; increase of gas-exchange area and maturation of alveolar capillary network; increased surfactant synthesis

Answer 47

``` Drugs Idiopathic Infection (bacteria, fungi, mycobacteria, parasites, virus) Inflammation (acute/chronic eosinophilic pneumonia, Churg-strauss, Rheumatoid effusion) Malignancy (lymphoma) PE Toxicity Trauma ```

Answer 48

Diffuse infiltration of lymphocytes and scattered nodules of mononuclear cells Unclear etiology → ?lymphoproliferaton with response to the HIV alone or co-infection with another virus EBV = common co-infection Insidious course and slowly progressive Median age = 2.5-3yrs Dx = lung biopsy Tx = non-specific → bronchodilators, oxygen, steroids Some may progress to lymphoproliferative disease with polyclonal, polymorphic B-cell content with extranodal systemic and prominent pulmonary involvement or to malignant lymphoma

Answer 49

Ivacaftor is metabolized by cytochrome CYP3A. (don’t use a strong inducer with Ivacaftor. If it’s a strong inhibitor, you can still use the drug, but you need to do a dose adjustment). strong cyp3a inducers = Rifampin, Rifabutin, Phenytoin Phenobarb, herbal supplements (St Johns wort) is not recommended for use with Ivacaftor. strong cyp3a inhibitors -azoles,erythro clarithro telithromycin- needs dose adjustment seville orange, grapefruit-to avoid caution when co administering other cyp3a substrates -tacrolimus, cyclosporine ,digoxin

Answer 50

Highest PEF - Lowest PEF/Mean of both >13 = significant, take the highest of 3 values for each PEF PEF lowest in the early morning and highest in the afternoon

Answer 51

Inhaled nitric oxide selectively dilates pulmonary vasculature in ventilated areas of the lung. Mechanism of action: NO activates soluble guanylyl cyclase (sGC) to produce cyclic guanosine monophosphate (cGMP) leading to decrease vascular smooth muscle tone (ie, vasodilation) Additional effects of NO include suppression of both smooth muscle proliferation and platelet aggregation

Answer 52

Phosphodiesterase inhibitors (eg. Sildenafil): Prevent degradation of cyclic GMP → potentiates the effect of NO activity by inhibiting PDE 5

Answer 53

Endothelin Receptor Antagonists (eg. Bosentan-dual receptor): Block ET receptors (found in smooth muscle and endothelial cells) thus promoting vasodilation and prevents proliferation

Answer 54

Prostacyclin Analogs/receptor agonists (eg. Epoprostenol, Iloprost, Trepostinil): Acts as a pulmonary vasodilator, inhibits vascular smooth muscle proliferation, inhibits platelet aggregation, improves endothelial dysfunction and can also act as a possible cardiac inotrope

Answer 55

Mean Pulmonary arterial pressure at rest ≥ 20 mmHg Pulmonary artery wedge pressure (<15mmHg) Elevated Pulmonary Vascular Resistance > 3 woods units x m2

Answer 56

Ziehl-Neelsen

Answer 57

Prussian blue

Answer 58

Bombesin staining

Answer 59

Periodic Acid Shiff stain

Answer 60

Rapid increase Sharp peak Linear curve Inspiratory loop

Answer 61

Cinitial x Vsystem = Cfinal (Vsystem + FRC)

Answer 62

1) Inhibits pseudomonas growth, protein synthesis and biofilm formation 2) Decreased bacterial virulence factors for P 3) Most benefit in those + with P

Answer 63

"Aztreonam Lysine for Pseudomonas Infection Eradication": 28 days of AZLI treatment in pediatric patients 3 months to b18 years of age is both effective and well tolerated in the treatment of early Pa pulmonary infection associated with CF Results from ALPINE, ELITE, and EPIC support a short treatment course (28 days) as effective for initial eradication of Pa for most CF patients.

Answer 64

28 days of inhaled tobramycin was as beneficial as 56 days in treating first of early pseudomonas

Answer 65

EPIC: Inhaled tobramycin 300mg BID for 28 days and oral ciprofloxacin 14 days -->addition of cirpo didn’t make a difference to rate of eradication

Answer 66

Tracheomalacia and bronchomalacia Intralobar bronchopulmonary sequestration CPAM Acinar aplasia or dysplasia ACD-MPV Congenital pulmonary lymphangiectasia, and other pulmonary vascular malformations Hypoplasia with CDH

Answer 67

Congenital alveolar dysplasia Alveolar capillary dysplasia Pulmonary hypoplasia

Answer 68

Congenital alveolar dysplasia Alveolar capillary dysplasia Pulmonary hypoplasia

Answer 69

- Chronic wet cough >4 weeks – Absence of symptoms or signs (i.e. specific cough pointers) of other causes of wet or productive cough – Resolution of cough within 2 weeks of an appropriate oral antibiotic (usually amoxicillin-clavulanate) In a minority of children 4 weeks of antibiotics are required

Answer 70

1) Children with hemodynamically significant CHD or CLD (defined as a need for oxygen at 36 weeks’ GA) who require ongoing diuretics, bronchodilators, steroids or supplemental oxygen, should receive palivizumab if they are <12 months of age at the start of RSV season. 2) In preterm infants without CLD born before 30 + 0 weeks’ GA who are <6 months of age at the start of RSV season, it is reasonable (but not essential) to offer palivizumab. 3) Infants in remote communities who would require air transportation for hospitalization born before 36 + 0 weeks’ GA and <6 months of age at the start of RSV season should be offered palivizumab.

Problem questions (ie ones I can't remember) Flashcards

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