Respi 4 Flashcards

1
Q

What is the pathogenesis of Centriacinar Emphysema?

A

W/ cigarette smoke being an important risk factor, the components of cigarette smoke can activate alveolar macrophages to release cytokines that recruit neutrophils. Macrophages and neutrophils then release proteases that degrade the ECM, causing a protease-antiprotease imbalance and leading to dilated airspaces.

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2
Q

What does the morphology of the pulmonary artery look like in Idiopathic pulmonary HTN?

A

In PAH, there is inc. endothelial and smooth muscle proliferation. The PA may show inc. smooth muscle thickness (medial hypertrophy), intimal fibrosis, and luminal narrowing. Severe HTN can lead to formation of plexiform lesions due to extensive fibrosis w/in the lumen.

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3
Q

How if Pulmonary HTN managed?

A

Definitive management is lung transplant. Bosentan is a vasodilator and endothelin-receptor antagonist that may be given to improve ssx.

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4
Q

How to lung cavitary lesions occur in the setting of a TB infection or any dse that involves granulomatous inflammation?

A

W/ granulomatous inflammation, macrophages phagocytose the microbe and present the Ag to Th1 cells, w/c then stimulate other macrophages (TNF, IFN-gamma). These macrophages release lysosomal enzymes and proteases w/c may damage lung tissue.

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5
Q

What is the significance of a Chloride shift in RBCs?

A

CO2 produced by tissue respiration enters RBCs and is converted to HCO3 and H+ by Carbonic anhydrase. The HCO3 diffuse out, and to maintain electrical neutrality, Cl- ions diffuse into RBCs to take their place.

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6
Q

Why is Silicosis often associated w/ increased risk of TB infection?

A

Silicosis impairs the macrophage effector arm of cell-mediated immunity. Macrophage phagolysosomes are disrupted by internalized silica particles, causing release of viable mycobacteria as well as lysosomal enzymes, w/c can cause lung injury.

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7
Q

What specific cytokines are released by APCs to induce a naive T cell to differentiate into Th1 or Th2?

A

> Macrophages release IL-12 for Th1 differentiation.

>Other APCs release IL-4 for Th2 differentiation.

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8
Q

Why may patients w/ selective IgA deficiency present w/ anaphylaxis when given blood transfusions?

A

In IgA deficiency, patients can produce IgE antibodies against IgA. When transfused w/ blood products containing small amounts of IgA, patients can develop fatal anaphylaxis. Give these patients blood products washed of residual plasma.

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9
Q

What would be in the sputum findings of patients w/ allergic asthma?

A

> Eosinophils, w/c were recruited by IL-5 secreted by Th2 cells.
Charcot-Leyden crystals (crystalloid bodies).

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10
Q

What cardiovascular complications may arise in patients w/ chronic Obstructive Sleep Apnea?

A

W/ an occluded airway, there is dec. PO2 and inc. PCO2 until chemoreceptors trigger arousal and pharyngeal muscle tone returns. If chronic, OSA can lead to systemic and pulmo HTN (hypoxia-induced vasoconstriction of pulmo arteries) w/ RHF, and an inc. risk of arrhythmias.

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11
Q

What infections are patients w/ SCID susceptible to?

A

W/ T and B cell deficiency, patients may have severe viral and bacterial infections. They’re also more prone to mucocutaneous candidiasis, persistent diarrhea, and failure to thrive.
>LABS: thymic aplasia, hypogammaglobulinemia, dec. CD3+ T cells.

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12
Q

How would excessively high O2 concentrations induce hypercapnia in patients w/ COPD? (3 mechs)

A

> Hypoxia induces pulmo vasoconstriction and blood is shunted to better ventilated alveoli. Giving O2 reverses vasoconstriction and poorly ventilated alveoli become perfused (V/Q mismatch, inc. dead space).
O2 dec. peripheral chemoreceptor stimulation, thus dec. RR.
Inc. PaO2 dec. Hgb affinity for CO2, leading to inc. pCO2 levels in blood.

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13
Q

What pulmonary complication can arise from tricuspid valve endocarditis?

A

Septic pulmonary emboli can cause hemorrhagic infarction in the lungs, resulting in wedge-shaped lesions at the lung periphery.

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14
Q

What lung disease can arise from obstruction of a mainstem bronchus?

A

An obstructive lesion (ex. tumor) of a mainstem bronchus can prevent ventilation of an entire lung, leading to obstructive atelectasis and complete lung collapse.
>CXR: unilateral pulmo opacification, deviated mediastinum toward affected lung.

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