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Pathology 2 - Block 2 - Part 3

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davidwurbel7's version from 2016-06-23 16:24

Respiratory Diseases

Question Answer
Common coldRhinitis
Inflammation of paranasal air sinusesSinusitis
Most common cancer causing death in men and womenBronchogenic Carcinoma
Second most common cancer causing death in men and womenColon Carcinoma
Neuroendocrine cells of the lungKulchitsky Cells
This marker indicates a cancer is of neuroendocrine originS100
These cells are the reserve cells in the lungsType II Pneumocytes
This is how alveolar macrophages move from alveoli to anotherPores of Kohn
This is composed of Respiratory bronchiole, Alveolar ducts, Alveolar sacs and AlveolusRespiratory Unit
This is the basic gas exchange unit of lungsAcinus
Collapse of previously aerated lungAtelectasis
Incomplete lung expansionNeonatal Atelectasis
Results when complete airway obstruction prevents air from reaching the alveoli causing alveolar collapse due to lack of air and resorption of trapped airResorption Atelectasis
Mediastinum shifts in this way in a resorption atelectatic lung (due to decreased lung volume)Toward
The obstruction seen in Bronchial asthma, chronic bronchitis, bronchiectasis and post operative period is due to thisMucus Plug
Mucous or mucous plug, Aspiration of foreign bodies, Tumors and enlarged lymphnodes may cause this in the bronchiObstruction
The most common cause of fever 24 hours after surgery due to mucous plugs blocking the terminal bronchiolesResorption Atelectasis
Clinical findings include Fever and dyspnea, Absent breath sounds and vocal vibratory sensation (tactile fremitus) and Dullness to percussionResorption Atelectasis
This occurs when air or fluid in the pleural cavity collapses small airways under the pleuraCompression Atelectasis
Pleural effusion and pneumothorax will show this atelectasisCompression Atelectasis
Mediastinum shifts in this way in a compression atelectatic lungAway
This occurs when fibrotic changes in lungs or pleura prevent full expansionContraction Atelectasis
This occurs primarily due to lack or deficiency of surfactantRespiratory Distress Syndrome of the Newborn
The most common cause of Respiratory Distress Syndrome of the Newborn is due to thisLack of Surfactant
A newborn born before this gestational time is at increased risk of Respiratory Distress Syndrome of the Newborn36 Weeks
A newborn born is at increased risk of Respiratory Distress Syndrome of the Newborn born to a mother with this conditionDiabetes
A newborn born is at increased risk of Respiratory Distress Syndrome of the Newborn born by this methodCesarean Section
Surfactant synthesis is increased by theseCortisol, Thyroxine and Prolactin
Surfactant synthesis is decreased by thisInsulin
Clinical findings include Increasing Respiratory effort after birth, Tachypnea with use of accessory muscles, Nasal flaring, grunting, Hypoxemia and CyanosisRespiratory Distress Syndrome
The function of surfactant in the alveoli is to do thisReduce Surface Tension
This is composed of cellular debris and fibrin rich plasma leaking from damage pulmonary capillariesHyaline Membrane
Positive pressure ventilation therapy complication in which superoxide free radical damage the lens of the eye which may lead to blindnessRetrolental Fibroplasia
Positive pressure ventilation therapy complication in which there is permanent damage to small airwaysBronchopulmonary Dysplasia
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Acute Lung Injury and ARDS

Question Answer
Refers to acute injury to lung tissue (endothelial and epithelial cells- pneumocytesAcute Lung Injury
Clinically manifests as acute onset of dyspnea, decreased arterial oxygen pressure (hypoxemia) and development of bilateral pulmonary infiltrates (pulmonary edema)Acute Lung Injury
Pulmonary edema in acute lung injury is also known asNoncardiogenic Pulmonary Edema
Severe acute lung injury manifests as thisARDS
A clinical syndrome characterized by diffuse alveolar capillary and or epithelial damage with resultant in increased capillary permeability and formation of intra-alveolar hyaline membraneAcute Respiratory Distress Syndrome (ARDS)
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Respiratory-Vascular Diseases

(Insert 1-20)
Question Answer
RIsk factors for this include postoperative states, trauma, oral contraceptives, CHF, prolonged sitting, AT III deficiency, Protein C deficiency, Protein S deficiency, Factor V LeidenPulmonary Emboli
Most (95%) Pulmonary Emboli originate from deep veins of the lower extremity above this veinPopliteal Vein
May lodge in the bifurcation or large pulmonary artery branches and cause sudden deathLarge Emboli
May or may not cause infarction of lung. Usually No infarction – due to dual blood supplyMedium Emboli
A medium emboli usually does not cause lung infarction because of thisDual Blood Supply
Medium emboli usually do not cause infarction except in a case of thisCompromised Cardiac Function
Obstruction of >60% pulmonary circulation required to cause thisSudden Death
Recurrent pulmonary emboli may become incorporated into the pulmonary artery wall leading to thisPulmonary Hypertension
Clinical findings include sudden onset of shortness of breath (SOB). Tachycardia, fever, pleuritic chest pain, hemoptysis and nonproductive coughPulmonary Embolism
The gold standard confirmatory test for pulmonary embolismSpiral Computed Tomographic Angiography
Spiral computed tomographic angiography, Ventilation perfusion scan and Positive D-dimer assay. The chest X ray: may be normalPulmonary Embolism
Treatment of Pulmonary Embolism includes thrombolytics and thisSurgical Thrombolectomy
Once diagnosis of DVT is made- start Rx with thisAnticoagulants
Patients with DVT in whom anticoagulation is contraindicated, this is the treatmentInferior Vena Cava Filter
Majority of pulmonary infarcts occur in this area of the lungLower Lobes
Gross and microscopic findings of red-blue colored wedge shaped area that is hemorrhagicPulmonary Infarction
Clinical finding include sudden onset of dyspnea and tacyhpnea. Fever, pleuritic chest pain (pain on inspiration), pleural effusion, hemoptysisPulmonary Infarction
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Obstructive Lung Diseases

Question Answer
Obstruction to airflow out of the lungs due to partial or complete obstruction in airwayObstructive Lung Disease
An increase in lung compliance and a decrease in lung elasticityObstructive Lung Disease
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Question Answer
Normal FEV14 L
Obstructive FEV1<2 L
Normal FVC5 L
Obstructive FVC<4 L
Normal FEV1/FVC ratio80%
Obstructive FEV1/FVC ratio<70%
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Question Answer
Both chronic bronchitis and emphysema cause chronic or recurrent obstruction to the airflow out of the lungs. The damage to the lung tissue is this typeIrreversible
Dyspnea is first seen in this obstructive lung diseaseEmphysema
Permanent Enlargement of all or part of the respiratory unit - respiratory bronchiole, alveolar ducts and alveoliEmphysema
In emphysema, air trapping is due to thisLoss of Elastic Recoil
A genetic cause of emphysema is thisAlpha-1-Antitrypsin Deficiency
The most common cause of emphysema is thisCigarette Smoking
Cigarette smoke is chemotactic to these which then accumulate in the alveoliNeutrophils and Macrophages
The Neutrophils and Macrophages that accumulate in the alveoli release thisFree Radicals and Elastases
Due to the loss of radial traction, this happens to the small airways on expirationCollapse
The collapse of the small airways prevents egress of air out of the respiratory unit which traps air and distends the respiratory unit resulting inHyperinflated Lungs
Type of emphysema in which only the respiratory bronchioles is affectedCentriacinar
Type of emphysema in which all of the acinius is affectedPanacinar
Type of emphysema in which only the alveolar ducts and the alveoli are affectedDistal acinar
Most common type of emphysema in smokersCentriacinar Emphysema
primary site of elastic tissue damage in Centriacinar Emphysema is this part of the aciniusRespiratory Bronchioles
In Centriacinar Emphysema this part of the lung is most usually affectedApical Segments of Upper Lobes
This characterized by uniform destruction and enlargement of respiratory unitPanacinar Emphysema
In Panacinar emphysema this part of the lung is most usually affectedLower Lobes
Panacinar Emphysema is associated with this conditionAlpha-1-Antitrypsin Deficiency
The normal gene for Alpha-1-AntitrypsinPiMM
The abnormal gene for Alpha-1-AntitrypsinPiZZ
Liver cells with the PiZZ Alpha-1-Antitrypsin gene produce this type of Alpha-1-AntitrypsinMisfolded Alpha-1-Antitrypsin
The long term accumulation of misfolded Alpha-1-Antitrypsin in the hepatocytes can lead to thisCirrhosis of the Liver
A neonate with Alpha-1-Antitrypsin Deficiency may also present with this at birthJaundice
Emphysema particularly in the lower lubes of the lung seen in a young individual or a non-smoker suggests this conditionAlpha-1-Antitrypsin Deficiency
This type of emphysema does not usually cause obstructive lung diseaseDistal Acinar (Paraseptal) Emphysema
Emphysema that appears as large air filled spaces located beneath the pleuraDistal Acinar (Paraseptal) Emphysema
Distal Acinar (Paraseptal) Emphysema has an increased incidence of thisSpontaneous Pneumothorax
Clinical findings includes symptoms - Dyspnea (+/- exertion): Severe and occurs early, Decreased exercise tolerance, Tachypnea. Signs include pink skin, Pursed lip breathing, Hyperventilation: Well oxygenated blood (pink puffers). Cachectic appearance (weight loss) due to anorexia and increased work of breathing. Hyperinflation/ barrel chest, hyperresonant percussion. Decreased breath soundsEmphysema
Investigations show Decreased FEV1, Decreased FEV1/FVC ratio. Increased TLC, RV (gas trapping). Blood gas values is usually normalEmphysema
This is clinically defined by requiring - 1. Persistent cough and sputum production 2. Present for at least 3 months 3. Present for at least 2 consecutive yearsChronic Bronchitis
This part of the lung unit is affected by chronic bronchitisTerminal Bronchioles
Exposure to noxious or irritating inhaled substances such as tobacco smoke, from grain, cotton, and silica can lead to thisChronic Bronchitis
Inflammation, Mucus gland hyperplasia and Mucus hypersecretion seen in chronic bronchitis occurs in these airwaysLarge Airways
Inflammation, Goblet cell metaplasia, Mucus plugs and SMC hypertrophy seen in chronic bronchitis occurs in these airwaysSmall Airways
The presence of goblet cells in the terminal bronchioles due to chronic irritationGoblet Cell Metaplasia
The ratio of the thickness wall of the large airway to the thickness of the glandular layerReid Index
The normal Reid Index is this40%
The Reid Index in chronic bronchitis is this> 50%
Clinical features include Symptoms: Persistent cough productive of copious purulent sputum. Mild dyspnea initially. Signs: Severe hypoxemia, Cyanosis, peripheral edema from RVF (Cor pulmonale). Tend to be stocky and obeseChronic bronchitis
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