Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho Final Exam > Chapter 23: Restrictive Pulmonary Disorders > Flashcards

Chapter 23: Restrictive Pulmonary Disorders Flashcards

1
Q

Fibrotic Interstitial Lung Disease

A
  • Group of disorders (more than 180 disease entities)
  • Characterized by acute, subacute, or chronic infiltration of alveolar walls by cells, fluid, and connective tissue
  • If left untreated, may progress to irreversible fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Diffurse Interstitial Lung Disease

A
  • Also called diffuse interstitial pulmonary fibrosis and other names
  • Characterized by thickening of alveolar interstitium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pathogenesis of and pathological patterns of Diffuse Interstitial Lung Disease

A
  • Begins with injury to alveolar epithelial or capillary endothelial cells
  • Persistent alveolitis leads to obliteration of alveolar capillaries, reorganization of lung parenchyma, irreversible fibrosis
  • Leads to large air-filled sacs (cysts) with dilated terminal and respiratory bronchioles (honey-comb lung)
  • Pathologic patters include inflammation, fibrosis, and destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical Manifestations of Diffuse Interstitial Lung Disease

A
  • Progressive dyspnea with irritating, nonproductive cough
  • Rapid-shallow breathing
  • Clubbing of nail beds
  • Bibasilar end-expiratory crackles
  • Cyanosis (late finding)
  • Anorexia, weight loss
  • Inability to increase cardiac output with exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diagnosis of Diffuse Interstitial Lung Disease

A
  • Chest x-ray
  • PFTs (decreased VC,
  • TLC, diffusing capacity)
  • Open lung biopsy
  • Transbronchial biopsy
  • Gallium-67 scan
  • High resolution computed tomography (HRCT) and bronchoalveolar lavage: primary tests
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Treatment of Diffuse Interstitial Lung DIsease

A
  • Smoking cessation
  • Avoid environmental exposure to cause
  • Anti-inflammatory agents
  • Immunosuppressive agents
  • Oxygen for hypoxemia
  • Lung transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sarcoidosis (Etiology)

A
  • Acute or chronic systemic disease of unknown cause
  • Immunologic basis is most likely cause
  • Activation of alveolar macrophage to unknown trigger
  • First degree relative increases risk 5 fold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathogenesis of Sarcoidosis

A
  • Development of multiple, uniform, noncaseating epithelioid granulomas
  • Affects multiple organs
  • Abnormal T cell function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clinical Manifestations of Sarcoidosis

A
  • Malaise, fatigue
  • Weight loss
  • Fever
  • Dyspnea of insidious onset
  • Dry, nonproductive cough
  • Erythema nodosum
  • Macules, papules, hyperpigmentation, and subcutaneous nodules
  • Hepatosplenomegaly, lymphadenopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnosis of Sarcoidosis

A
  • Leukopenia, anemia
  • Increased eosinophil count, elevated sedimentation rate
    Increased Ca++ levels
  • Elevated liver enzymes
    Anergy
  • Elevated angiotensin-converting enzyme in active disease
  • Gallium-67 scan (Localize areas of granulomatous infiltrates)
  • PFTs
  • Transbronchial lung biopsy (Noncaseating granulomas (definitive diagnosis))
  • Bronchoalveolar lavage
  • Stages 0-4 (Progressing from normal to advanced fibrosis with evidence of honeycombing, hilar retraction, bullae, cysts, and emphysema)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of Sarcoidosis

A
  • Management of symptoms
  • Corticosteroids
  • Immunosuppressive agents
  • Hydroxychloroquine: for disfiguring skin lesions, hypercalcemia, and neurologic involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acute (Adult) Respiratory DIstress Syndrome (ARDS) Etiology

A
  • Damage to the alveolar-capillary membrane (Causes widespread protein-rich alveolar infiltrates and severe dyspnea)
  • Occurs in association with other pathophysiologic processes
  • More than 150,000 cases/year in United States
  • Mortality rate 30% to 63%
  • Associated with a decline in the Pao2 that is refractory (does not respond) to supplemental oxygen therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of ARDS

A
  • Severe trauma
  • Sepsis (>40%)
  • Aspiration of gastric acid (>30%)
  • Fat emboli syndrome
    Shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Characteristics of ARDS

A
  • Increased permeability of the pulmonary vasculature
  • Flooding of the alveoli with proteinaceous fluid
  • Leads to development of protein-rich pulmonary edema (noncardiogenic pulmonary edema)
  • Triggers the immune system to activate the complement system and to initiate neutrophil sequestration in the lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathogenesis of ARDS

A
  • Injury to alveoli from a wide variety of disorders
  • Changes in alveolar diameter
  • Injury to pulmonary circulation
  • Atelectasis and decrease in lung compliance from lack of surfactant
  • Fibrosis (hyaline membrane)
  • Diffuse, fluffy alveolar infiltrates
  • Disruptions in O2 transport and utilization (Severe hypoxemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical Manifestations of ARDS

A
  • History of a precipitating event that has led to a low blood volume state (“shock” state) 1 or 2 days prior to the onset of respiratory failure
  • Early: Sudden marked respiratory distress, Slight increase in pulse rate,Dyspnea
    Low PaO2, Shallow, rapid breathing
  • Late: Tachycardia, Tachypnea
    Hypotension, Marked restlessness, Frothy secretions,
    Crackles, rhonchi on auscultation, Use of accessory muscles, Intercostal and sternal retractions, Cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diagnosis of ARDS

A
  • Hallmark is hypoxemia refractory to increased levels of supplemental O2
  • ABG (Hypoxia, Acidosis, Hypercapnia)
  • Chest Xray (Normal with progression to diffuse “whiteout”)
  • PFTs (Decrease in FVR, Decreased lung volumes, Decreased lung compliance, VA/Q mismatch with large right-to-left shunt)
  • Open-Lung biopsy shows (Atelectasis, Hyaline membranes, Cellular debris,
    Interstitial and alveolar edema)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatments of ARDS

A
  • Mostly supportive (Enhance tissue oxygenation until inflammation resolves)
  • Identify and treat underlying cause
  • Maintain fluid and electrolyte balance (Increased fluid administration can produce or intensify pulmonary edema)
  • Volume ventilator using pressure support
  • Mechanical ventilation with positive end-expiratory pressure (PEEP) (Increases FRV and prevents alveolar collapse at end-expiration, Forces edema out of alveoli)
  • Supplemental O2 (>60% contributes to ARDS related to absorption atelectasis, FIO2 reduced as soon as possible)
  • High-frequency jet ventilation (HFJV)
  • Inverse ratio ventilation (IRV)
  • Inhaled nitric oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pneumothorax Etiology

A
  • Accumulation of air in the pleural space
  • Primary pneumothorax (Spontaneous, Occurs in tall, thin men 20 to 40 years, No underlying disease factors, Cigarette smoking increases risk)
  • Secondary Pneumothorax (Result of complications from preexisting pulmonary disease)
  • Catamenial pneumothorax (Associated with menstruation, Primarily in right hemothorax, Associated with endometriosis)
  • Tension Pneumothorax (Traumatic origin, Results from penetrating or nonpenetrating injury, May also be from iatrogenic causes, Medical emergency)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pathogenesis of Pneumothorax

A
  • Primary (Rupture of small subpleural blebs in apices; Air enters pleural space, lung collapses, and rib cage springs out)
  • Secondary (Result of complications from an underlying lung problem, May be due to rupture of cyst or bleb)
  • Tension (Results form buildup of air under pressure in pleural space; Air enters pleural space during inspiration but cannot escape during expiration; Lung on ipsilateral (same) side collapses and forces mediastinum toward contralateral (opposite) side; Decreases venous return and cardiac output)
  • Open “sucking” chest wall wound (Air enters during inspiration but cannot escape during expiration leads to shift of mediastinum)
21
Q

Clinical Manifestations of Pneumothorax

A
  • Small pneumothoraces (
22
Q

Diagnosis of Pneumothorax

A
  • ABG (Decreased PaO2, acute respiratory alkalosis)
  • ECG
  • Chest Xray (Expiratory films show better demarcation of pleural line than inspiratory;
    Depression of hemidiaphragm on side of pneumothorax)
23
Q

Treatment of Pneumothorax

A
  • Management depends on severity of problem and cause of air leak
  • Lung collapse 15% to 25% (Chest tube placement with H2O seal and suction; Oxygen)
  • Chemical pleurodesis (Promotes adhesion of visceral pleura to parietal pleura to prevent further ruptures; For recurrent spontaneous pneumothorax)
  • Thoracotomy (Permits stapling or laser pleurodesis of ruptured blebs)
24
Q

Pleural Effusion Etiology

A
  • Pathologic collection of fluid or pus in pleural cavity as result of another disease process
  • Normally, 5-15 ml of serous fluid is contained in pleural space
  • Constant movement of pleural fluid from parietal pleural capillaries to pleural space
  • Reabsorbed into parietal lymphatics
25
Q

Five major types of pleural effusion

A
  • Transudates (Low in protein (ratio 0.5 mg/dl); Causes: malignancies, infections, pulmonary embolism, sarcoidosis, postmyocardial infarction syndrome, pancreatic disease)
  • Empyema due to infection in the pleural space (High-protein exudative effusion)
  • Hemothorax (Presence of blood in pleural space;
    Result of chest trauma; Contains blood and pleural fluid: hemorrhagic)
  • Chylothorax or lymphatic
    (Exudative process that develops from trauma)
26
Q

Causes of Pleural Effusion

A
  • Changes in pleural capillary hydrostatic pressure, colloid oncotic pressure, or intrapleural pressure
  • Imbalance in pressure associated with fluid formation exceeding fluid removal
27
Q

Pathogenesis of Pleural Effusion

A
  • Transudates (Increased hydrostatic or decreased oncotic pressure)
  • Exudates increase production of fluid r/t (Increased permeability of pleural membrane; Impaired lymphatic drainage)
28
Q

Clinical Manifestations of Pleural Effusion

A
  • Vary depending on cause and size of effusion

- May be asymptomatic with

29
Q

Diagnosis of Pleural Effusion

A
  • Chest X-Ray (Pleural-based, densities, infiltrates,Signs of CHF, Hilar adenopathy, and Location of fluid
  • Thoracentesis (Analyze fluid and reduce amount of fluid)
  • CT or Ultrasonographic Tests (Assist in complicated effusions, and Distinguish mass from large effusion)
30
Q

Treatment of Pleural Effusion

A
  • Directed at underlying cause and relief of symptoms
  • Tension and spontaneous pneumothorax are medical emergencies requiring treatment to remove pleural air and re-expand lung
  • Closed chest tube drainage (adults) (Controversial in pediatrics)
  • Thoracentesis, if large amount of effusion (Ultrasound useful for thoracentesis guidance)
  • Thoracotomy (Control bleeding (>200 ml/hr))
31
Q

Guillian Barre Syndrome (Acute Polyneuritis) etiology

A
  • Immunologic basis
  • Demyelination of peripheral nerves
  • History of recent viral or bacterial illness (66% of cases) followed by ascending paralysis (Infection involving Campylobacter jejuni often precedes diagnosis)
32
Q

Clinical Manifestations of Guillian-Barre Syndrome

A
  • Weakness and paralysis begin symmetrically in lower extremities and ascend proximally to upper extremities and trunk
  • Severe cases show Respiratory muscle weakness accompanied by limb and trunk symptoms
  • Usually have full recovery
  • Minor residual motor deficits (15% to 20%)
33
Q

Myasthenia Gravis

A
  • Weakness and fatigue of voluntary muscles
  • Those innervated by cranial nerves
  • Peripheral and respiratory muscles can be affected
  • Hallmark finding: weakness worse with exercise and better with rest
  • 2-5 cases/year/million persons in U.S.
  • Females more than males (3:2)
  • Primary abnormality at neuromuscular junction
  • Transmission from nerve to muscle impaired from decreased number of receptors on muscle
  • Symptoms often managed by appropriate therapy
  • Respiratory failure can be due to increasing severity of illness or overmedication
  • Individual episodes of respiratory failure are potentially reversible
34
Q

Pneumonia

A
  • Inflammatory reaction in the alveoli and interstitium caused by an infectious agent
  • Causes include Aspiration of oropharyngeal secretions composed of normal bacterial flora or gastric contents (25% to 35%), Inhalation of contaminants, and Contamination from the systemic circulation
35
Q

Classifications of Pneumonia

A
  • Community acquired
  • Hospital acquired
  • Bacterial
  • Atypical
  • Viral
36
Q

Those who are at high risk for Pneumonia

A
  • Elderly
  • Those with a diminished gag reflex
  • Seriously ill
  • Hospitalized patients
  • Hypoxic patients
  • Immune-compromised patients
37
Q

Types of Pneumonia

A
  • Anaerobic bacteria: present as a lung abscess, necrotizing pneumonia, or empyema; usually caused by aspiration of normal oral bacteria into the lung
  • Mycoplasmal pneumonia: commonly seen in the summer and fall in young adults; common between the ages of 5 and 20
  • Legionnaires Disease (Organism lives in H2O;
    Transmitted by portable H2O, condensers, cooling towers;
    Fever, diarrhea, abdominal pain, liver and kidney failure, pulmonary infiltrates; Treatment: macrolide antibiotic)
  • Opportunistic Pneumonias (Pneumocystis jiroveci & Aspergillus)
  • Pneumocystis jiroveci
    (Opportunistic fungal infection,
    Common in patients with cancer or HIV)
  • Aspergillus (Opportunistic fungal infection, Released from walls of old buildings under reconstruction)
38
Q

Pathogenesis of Pneumonia

A
  • Acquired when normal pulmonary defense mechanisms are compromised
  • Organisms enter lung, multiply, and trigger pulmonary inflammation
  • Inflammatory cells invade alveolar septa
  • Alveolar air spaces fill with exudative fluid (Consolidates and difficult to expectorate)
  • Viral pneumonia doesn’t produce exudative fluids
39
Q

Clinical Manifestations of Pnemonia

A
  • Severity of disease and patient age cause variation in symptoms
  • Crackles (rales) and bronchial breath sounds over affected lung tissue
  • Chills
  • Fever
  • Cough, purulent sputum
  • Viral (Upper respiratory prodrome: Fever, nonproductive cough, hoarseness, coryza accompanied by wheezing/rales)
  • Chlamydia Pneumonia (Cough, tachypnea, rales, wheezes, and no fever)
  • Mycoplasma (Fever, Cough, Headache, Malaise)
40
Q

Diagnosis of Pneumonia

A
  • Chest x-ray (Parenchymal infiltrates (white shadows) in involved area)
  • Sputum C&S (Sputum from deep in lungs)
  • CURB-65
  • Laboratory (WBC >15,000 (acute bacterial)
41
Q

Treatment of Pneumonia

A
  • antibiotic therapy based on sensitivity of culture
42
Q

Pulmonary Tuberculosis Etiology

A
  • Estimated 10 million infected in United States
  • High-risk individuals include those with Prior infection (90%), Malnourishment, immunosuppression, Living in overcrowded condition, Incarcerated persons, Immigrants, and Elderly
  • Multidrug-resistant TB
  • Cases are reported to local and state health departments
43
Q

Causes of Pulmonary Tuberculosis

A
  • Mycobacterium tuberculosis (Acid-fast aerobic bacillus Infects lungs and lymph nodes)
  • Infection (Inhalation of small droplets containing bacteria;
    Droplets expelled with cough, sneeze, or talking)
  • Involvement of distant organ systems (Hematogenous spread during primary or reactivation phase)
  • Disseminated disease
    (Miliary tuberculosis causes hematogenous dissemination of organisms)
44
Q

Classifications of Pulmonary Tuberculosis

A
  • Primary (usually clinically/radiographically silent)
    (May lie dormant for years or decades)
  • Reactivating (May occur many years after primary infection;
    Impaired immune system causes reactivation; HIV, corticosteroid use, silicosis, and diabetes mellitus have been found to be associated with reactivation)
45
Q

Pathogenesis of Pulmonary Tuberculosis

A
  • Entry of mycobacteria into lung tissue
  • Alveolar macrophages ingest and process microorganisms (Microorganisms destroyed OR persist and multiply)
  • Lymphatic and hematogenous dissemination (T-cells and macrophages surround organisms in granulomas)
  • Reactivation occurs if immunosuppressed
  • Pathologic manifestation is Ghon tubercle or complex
46
Q

Clnical Manifestations of Pulmonary Tuberculosis

A
  • History of contact with infected person
  • Low-grade fever
  • Chronic cough (most common); as disease progresses becomes productive with purulent sputum
  • Night sweats
  • Fatigue
  • Weight loss
  • Malaise
  • Anorexia
  • Apical crackles (rales)
  • Bronchial breath sounds over region of consolidation
  • Malnourished
47
Q

Diagnosis of Pulmonary Tuberculosis

A
  • Sputum culture (definitive diagnosis) (Three consecutive, morning specimens; Identify slow-growing acid-fast bacillus:
    Takes 1-3 weeks for determination)
  • DNA or RNA amplification techniques (diagnosis)
  • PFTs
  • Chest x-ray (Nodules with infiltrates in apex and posterior segments)
  • TB skin test (Mantoux or PPD test) (Doesn’t distinguish between current disease or past infection; False-positive PPD results may occur in persons with other mycobacterial infections or if they have received bacille Calmette-Guérin vaccine)
48
Q

Treatment of Pulmonary Tuberculosis

A
  • Administer multiple drugs (antibiotics) to which organism is susceptible (Therapy is for 9-12 months for active disease;
    Therapy shorter in persons exposed with no active disease)
  • Add at least 2 new agents to drug regimen when treatment failure is suspected
  • Providing safest, most effective therapy for shortest period of time
  • Ensuring adherence to therapy by using directly observed therapy (Nonadherence to therapy is major cause of treatment failure; Negative pressure isolation room to prevent spread)

Patho Final Exam (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions