Respiratory System Disorders - 2 Flashcards

1
Q

Lobar Pneumonia

A

Usually caused my streptococcus pneumoniae (pneumococcus) and the infection is localized in one or more lobes.
First stage is congestion - microbe sometimes colonizes the nasopharynx without producing symptoms. Inflammation and vascular congestion develop in the alveolar wall, exudate forms in the alveoli, interferes with oxygen diffusion. Neutrophils, RBCs and fibrin accumulate in the alveolar exudate, forming a solid mass in the lobe, called consolidation. Presence of RBCs products typical rusty sputum. Produces pleuritic pain (pleurisy or pleuritis).
Infection can spread into the pleural cavity causing empyema - can cause adhesions between the pleural membranes.
Filling of alveoli with exudate reduces diffusion of gases, decreases blood flow, hypoxia results.
Oxygen deficit leads to metabolic acidosis.

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2
Q

Typical manifestations of pneumococcal pneumonia

A

Sudden onset
High fever with chills, fatigue and leukocytosis
Dyspnea, tachypnea, tachycardia
Pleuritic pain with splinting
Rales - initially over affected lobe, then disappearing
Productive cough with rusty sputum
Confusion and disorientation if infection is severe.
Treated with antibacterial medications and supportive measures, fluids, drugs to reduce fever and oxygen.

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3
Q

Bronchopneumonia

A

Diffuse pattern of infection in both lungs, more often lower lobes
Caused by multiple bacteria, begin in the bronchial mucosa and spread into the local alveoli. Pooled secretions in the lungs become infected by organisms draining from upper passages, inflammation forms in the alveoli and interferes with oxygen diffusion.
Onset insidious with moderate fever, cough and rales
Dyspnea
Productive cough with yellow / green sputum.

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4
Q

Legionnaires’ Disease

A

Pneumonia caused by gram-negative bacteria - Legionella pneumophilia.
Thrives in moist environments like spas.
Nosocomial
Organism is found inside pulmonary macrophages
Causes severe congestion and consolidation with necrosis in lung, possibly fatal.

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5
Q

Primary Atypical Pneumonia

A

Often viral or mycoplasma (small bacterium, lacks cell wall)
Involves interstitial inflammation
Transmitted by aerosol, not highly contagious
Frequent cough
Viral caused by influenza A or B, as well as adenoviruses and RSV.
Starts with inflammation in the mucosa of the upper respiratory tract, then descends to involve lungs
Inflammation is diffuse and interstitial, little exudate, unproductive cough, rales not pronounced
Severe cases can be complicated by secondary bacterial infection.
Self-limiting

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6
Q

Pneumocystis carinii Pneumonia

A

PCP
Atypical
Occurs as opportunistic, often fatal infection in patients with AIDS.
Fungal, inhaled, attaches to alveolar cells causing necrosis and diffuse interstitial inflammation. Alveoli fill with exudate and fungi.
Difficulty breathing, nonproductive cough

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7
Q

Severe Actue Respiratory Syndrome (SARS)

A

Atypical pneumonia
Coronavirus - RNA virus, transmitted by respiratory droplets during close contact
Incubation period 2-7 days
Flulike syndrome - fever, headache, myalgia, chills, anorexia, diarrhea
Dry cough, dyspnea
Patchy areas of interstitial congestion and hypoxia increases rapidly, mechanical ventilation often required.
Lymphopenia and thrombocytopenia often present
Elevated liver enzymes - liver damage
Third stage - severe, sometimes fatal respiratory distress.
Identification difficult because antibodies are not present until 3 weeks after onset and nonspecific early manifestations.

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8
Q

Tuberculosis

A

Increasing particularly among AIDS patients in Africa.
1-2% drugs resistant
Disease of poverty and crowding
Large number of latent cases, 10% will progress to active pulmonary TB
Mycobacterium tuberculosis - primarily affects lungs, may invade other organs.
Aerobic, slow-growing, can survive in dried sputum for weeks, normal response by neutrophils does not occur.
Two stages: TB infection and TB disease.
Primary infection: microorganisms first enter lungs, are engulfed by macrophages and cause local inflammatory reaction, usually on periphery of upper lobe.
Lymphocytes and macrophages cluster to form a granuloma at site of inflammation. Forms a tubercle, in the center caseation necrosis develops - dead macrophages and necrotic material
Healthy person - lesions remain small, become walled off by fibrous tissue, calcifying - called Ghon complexes. Bacilli may remain viable in the dormant state
Hypersensitivity reaction - basis for tuberculin test - several weeks aftern exposure the person has become hypersensitive and will produce a positive skin reaction in response to tuberculoprotein.
Low resistance - primary infection may progress.
Miliary or extrapulmonary tuberculosis - rapidly progressive form, multiple granulomas affect large areas of lungs and rapidly disseminate into the circulation and to other tissues like bone or kidney, often arises years after primary infection, bacilli are reactivated.
Secondary or reinfection - stage of active infection
Cavitation occurs - formation of a large open area in the lung and erosion into bronchi and blood vessels.Bacilli are present in sputum, where they can be passed.

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9
Q

How do you become infected with tuberculosis?

A
Mycobacterium tuberculosis - transmitted by oral droplets released from a person with active infection that are inhaled into the lungs
Crowded conditions
Lowered immunity
Malnutrition
Alcoholism
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10
Q

Signs and symptoms of TB

A

Primary is asymptomatic, onset of secondary and active is insidious, systemic signs often appear first like anorexia, malaise, fatigue and weight loss. Low-grade fever and night sweats, prolonged cough becomes increasingly severe. As cavitation develops sputum becomes purulent and often contains blood.

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11
Q

Histoplasmosis

A

Fungal infection
Histoplasma capsulatum and its spores can be inhaled on dust particles
Opportunistic
Common in AIDS
Found as a parasite inside macrophages.
Effects are similar to TB
First stage asymptomatic, followed by 2nd stage of active infection
Second stage involves granuloma formation and necrosis and consolidation in lungs as well as possible spread to other organs
Cough, fatigue, fever, night sweats

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12
Q

Anthrax

A

Bacterial infection of skin, respiratory tract and GI tract of humans and cattle
Causative organism is gram-positive bacillus that forms grayish-white spores that remain visible for long periods of time
Flulike symptoms, incubation period of 1 to 7 days
Acute respiratory distress occurs with mediastinal widening and fever
Shock due to release of toxins

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13
Q

Cystic fibrosis

A

Inherited disorder, common in children
1 in 3600 live births in Canada, mean survival is 37 years.
Relate to a protein involved in chloride ion transport in the cell membrane. This defect in the exocrine lands causes abnormally thick secretions such as tenacious mucus
First seen in the lungs and pancreas where sticky mucus obstructs passages
In lungs - mucus obstructs airflow causing air trapping or atelectasis with permanent damage to the bronchial walls
Stagnant mucus promotes bacterial growth and causes infections and add to destruction of lung tissue.
Pancreas - ducts of exocrine glands become blocked - leads to deficit of pancreatic digestive enzymes and malabsorption and malnutrition, can result in diabetes mellitus.
Liver - bile ducts may be blocked by viscid mucus preventing bile from reaching the duodenum and interfering with digestions and absorption of fats and fat soluble vitamins. Can cause biliary cirrhosis.
Thick mucus obstructs vas deferens and cervix.
Autosomal recessive disorder

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14
Q

Signs of cystic fibrosis

A

Meconium ileus at birth
Salty skin
Malabsorption - steatorrhea, abdominal distention, failure to gain weight
Chronic cough, frequent respiratory infections
Hypoxia, fatigue, exercise intolerance.

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15
Q

Treatment for cystic fibrosis

A

Replacement therapy for pancreatic enzymes bile salt replacement
Dietary changes
Avoiding dehydration
Intensive chest physiotherapy
Bronchodilators and humidifiers
Cause of death is usually respiratory failure

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16
Q

Lung cancer

A

Benign tumors are rare
90% of lung cancers are related to smoking
Secondary metastatic cancer develops because venous return and lymphatics bring tumor cells from distant sites in the body - provides first hospitable environment where tumor cells can lodge
First change - metaplasia - associated with smoking and chronic irritation, leaves lung tissue more vulnerable to irritants and inflammation from smoking.
Stage 1 are localized, Stage 3 are disseminated
Common sites of metastases are brain, bone and liver.

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17
Q

Effects of lung tumors

A

Obstruction of airflow
Inflammation surrounding tumor stimulates cough, predisposes to secondary infection.
Pleural effusion, hemothorax, pneumothorax
Paraneoplastic syndrome - tumor cell secretes hormones like ADH or ACTH - can complicate diagnosis and treatment.
Persistent productive cough, dyspnea, wheezing
Pneumonia
Hemoptysis - tumors errode tissue
Chest pain
Hoarseness (laryngeal nerve compression), facial or arm edema and headache (compression of superior vena cava), dysphagia (compression of esophagus), atelectasis (large tumors or involved lymph nodes
Systemic signs - weight loss, anemia, fatigue

18
Q

What happens when liquids are aspirated?

A

Irritating liquids like acids (vomit) alcohol, oils (milk) tend to disperse into several bronchi. Cause severe inflammation, narrow airways, increased secretions, makes lungs more difficult to expand. Gas diffusion is impaired.Can be called aspiration pneumonia.
Respiratory distress syndrome
Pulmonary abscess may develop if microbes are in aspirate
Solvents can be absorbed into blood

19
Q

Risk factors of aspiration

A

Small children choking
When swallowing or gag reflex is depressed = anesthesia or stroke, coma, neurologic damage, anesthetics, drugs
Eating or drinking lying down

20
Q

Signs of aspiration

A

Coughing, choking, marked dyspnea
Stridor, hoarseness - upper airway
Wheezing - aspiration of liquids into lungs
Tachycardia and tachypnea - respiratory distress
Nasal flaring, chest retractions, marked hypoxia - severe respiratory distress

21
Q

Sleep apnea

A

Pharyngeal tissues collapse during sleep leading to repeated and momentary cessation of breathing.
Increases with age and obesity
Loud snoring, intermittent gasps for ear
Complications: Hypoxia, fatigue, type 2 diabetes, pulmonary hypertension, right-sided congestive heart failure, cerebrovascular accident, ED, depression, daytime sleepiness.
Treatment: CPAP, oral appliances

22
Q

Asthma

A

Periodic episodes of severe but reversible bronchial obstruction in people with hypersensitive or hyperresponsive airways.
Can lead to irreversible damage in lungs and development of chronic asthma (chronic obstructive lung disease)

23
Q

Extrinsic asthma -

A

Involves acute episodes triggered by a type I hypersensitivity reaction to an inhaled antigen - related to familial history of other allergic conditions - eczema and allergic rhinitis.

24
Q

Intrinsic

A

Onset during adulthood
Other types of stimuli target hyper-responsive tissues in the airway, initiating the acute attack e.g. respiratory infections, exposure to cold, exercise, drugs such as aspirin, stress, and inhalation of irritants
Antigen reacts with immunoglobulin E on the previously sensitized mast cells in the respiratory mucosa, releasing histamine, kinins, prostaglandins, and other chemical mediators causing inflammation. The reaction stimulates branches of the vagus nerve causing reflex bronchoconstriction.
Second stage - increased leukocytes (eosinophils) release additional chemical mediators such as leukotrienes, results in prolonged inflammation, bronchoconstriction, and epithelial damage. White blood cells are drawn to the area.
Air can get trapped, and only be partially expired, becomes difficult to inspire fresh air or cough effectively
Oxygen levels further depleted by muscle activity and the stress response as the individual fights for air.
Respiratory and metabolic acidosis
Hypoxemia causes vasoconstriction in the pulmonary blood vessels

25
Q

Pathophysiologic changes related to asthma

A

Inflammation or the mucosa with edema, contraction of smooth muscle (bronchconstriction), increased secretion of thick mucus in the passages - creates obstructed airways.

26
Q

Status asthmaticus

A

Persistent severe attack of asthma that does not respond to therapy - may be fatal

27
Q

Chronic asthma and chronic obstructive lung disease

A

may develop from irreversible damage in the lungs when frequent and severed acute asthmatic attacks form a pattern. Bronchial walls become thickened, fibrous tissue resulting from frequent infections develops in atelectatic areas, impossible to remove all tiny mucus plugs in small passages.

28
Q

Causes of asthma

A

Family history of hay fever, asthma and eczema
Viral upper respiratory infections
Increase in sedentary lifestyles, increased air pollution and exposure to allergens

29
Q

Signs of an asthma attack

A

Cough, dyspnea, tightness in chest, agitation, unable to talk, wheezing, rapid and labored breathing, accessory muscles
Thick and tenacious mucus
Tachycardia, hypoxia, respiratory alkalosis initially from hyperventilation, respiratory acidosis develops in time due to air trapping and marked fatigue - decreased respiratory effort with weaker cough.
Metabolic acidosis
Severe respiratory distress, failure - decreased responsiveness, cyanosis

30
Q

Treatment of asthma

A

Minimizing number and severity of acute attacks to prevent lung damage, reduce risk of infection, prevent emphysematous changes and chronic obstructive lung disease.
Skin test for allergic reactions, avoidance of triggering factors, good ventilation, regular swimming sessions to strengthen chest muscles and increase cardiovascular fitness, prophylactic medication at first sign of a cold

31
Q

Measures for acute attacks:

A

Controlled breathing - panic frequently aggravates
Bronchodilator
Glucocorticoids - effective in reducing second stage inflammation in airways.

32
Q

Prophylaxis treatment of chronic asthma

A

Leukotriene receptor antagonists block inflammatory responses in presence of stimuli - prevents attacks due to allergens, exercise and aspirin
Cromolyn sodium - inhalation, daily basis, inhibits release of chemical mediators from sensitized mast cells in the respiratory passages and decreases number of eosinophils, thus reduces hyperresponsiveness of the tissues.

33
Q

COPD

A

Sometimes called chronic obstructive lung disease
Group of disorders
Characterized by progressive tissue degeneration and obstruction in the airways of the lungs.
Debilitating
E.g. Emphysema, chronic bronchitis, chronic asthma.
Irreversible and progressive damage - respiratory failure may result from hypoxia or hypercapnia.
Leads to development of cor pulmonale (right-sided congestive heart failure
4th most common cause of mortaility

34
Q

Emphysema

A

Causes: Smoking, genetic (elastase, breaks down elastic fibers)
Location: Alveoli
Pathophysiology: Destruction of alveolar walls, loss of elasticity, permanently inflated, impaired expiration, barrel chest, hyperinflation
Some coughing and dyspnea
Little sputum
No cyanosis
Some infections
Breakdown of alveolar wall: loss of surface area for gas exchange
Loss of pulmonary capillaries affecting perfusion and diffusion
Loss of elastic fibers, affecting lung recoil
Altered ventilation-perfusion ratio
Decreased support for other structures such as small bronchi which leads to collapse of walls
Fibrosis and thickening of bronchial walls - resulted from chronic irritation and frequent infections associated with smoking and increased mucus production - causes narrowed airways, weakened walls, interference with passive expiratory airflow
Difficulty with expiration leads to: Air trapping and increased residual volume, overinflation, fixation of ribs in inspiratory position (barrel chest), diaphragm appears flattened
Advanced: Damaged alveoli coalesce forming large air spaces - blebs, bullae. Pleural membrane can rupture causing pneumothroax, hypercapnia becomes marked, hypoxic drive for inspiration develops as adaption to increased co2 happens.
Frequent infections
Pulmonary hypertension and cor pulmonale - increased pressure in pulmonary circulation increases resistance to right ventricle, eventually ventricle fails

35
Q

Signs and symptoms of emphysema

A

Dyspnea with exertion then at rest
Hyperventilation with a prolonged expiratory phase, use of accessory muscles and hyperinflation lead to “barrel chest”
Anorexia and fatigue
Club fingers and polycythemia

36
Q

Treatment for emphysema

A

Avoidance of respiratory irritants, smoking
Immunization against flu and pneumonia
Pulmonary rehab programs
Maintenance of adequate nutrition and hydration
Bronchodilators, antibiotics and oxygen therapy
Lung reduction surgery.

37
Q

Chronic Bronchitis

A

Significant changes in the bronchi resulting from constant irritation from smoking or pollution - irreversible and progressive
Inflammation, obstruction, infections, chronic coughing
Mucosa is inflamed
Hypertrophy and hyperplasia of mucous glands, increased secretions, number of goblet cells is increased, decreased ciliated epithelium
Fibrosis and thickening of bronchia wall, secretions pool distal to obstructions and are difficult to remove
Cyanosis during episodes of coughing
“blue bloater”
Dyspnea and fatigue
Pulmonary hypertension and cor pulmonale

38
Q

Signs and symptoms

A

Constant productive cough, tachypnea and shortness of breath, secretions are thick and purulent, cough and rhonchi more severe in morning
Hypoxia, cyanosis, hypercapnia, secondary polycythemia, weight loss, cor pulmonale

39
Q

Bronchiectasis

A

Usually secondary problem
Develops in patients with COPD and cystic fibrosis, childhood infection, aspiration or congenital weakness. Most often is in both lungs.
Abnormal dilation of medium-sized bronchi, arise from recurrent inflammation and infection, leads to obstruction or weakening of muscle and elastic fibers in bronchial wall. Fibrous adhesion may pull the wall outward.
In dilated areas fluid collects and becomes infected. Causes loss of cilia and metaplasia, additional fibrosis, progressive obstruction.

40
Q

Signs and symptoms of bronchiectasis

A

Chronic cough
Production of copious amounts of purulent sputum
Rales and rhonchi in the lungs, foul breath, dyspnea, and hemoptysis, weight loss, anemia, fatigue.

41
Q

Restrictive lung disorder

A

Group of diseases - lung expansion is impaired, total lung capacity reduced e.g. kyphosis or scoliosis, poliomyelitis or amyotrophic lateral sclerosis or botulism
Can be from abnormality in chest wall that limits lung expansion or from a lung disease that impairs expansion