Pathophysiology II Final Exam Review CNM Fildes
Asthma etiology-ANSWER 1. Type of etiology
2. Reversible airway obstruction for some, bronchoconstriction.
3. Airway inflammation, bronchial mucosal edema and production of mucous.
4. Airway responsiveness increased to various stimuli, i.e., dog hair, pollen, etc.
Predisposing factors of asthma - ANS Genetic for aptopy and structural-smaller airways
[chromosomes 5, 11, 14], history of hay fever or eczema, family history, positive skin
test to allergens are all.
Extrinsic-allergic asthma - ANS 1. Accounts for 1/3 to 1/2 of these cases
2. An IgE mediated response is common
3. Clinical manifestations include: elevated IgE levels, allergic rhinitis, eczema, (+)
family history of allergens, attacks associated with
seasonal/environmental/occupational exposure
Common symptoms of asthma - ANSWER Wheezing, feeling tightness of the chest,
dyspnea, cough (dry or productive), increased sputum production (think, tenacious,
scant, and viscous) are all.
Radiographic finding - ANSWER 1. Test used to diagnose asthma
2. X-Ray shows hyperinflation w/ flattening of the diaphragm
Sputum examination- ANSWER 1. Test used to diagnose asthma
2. Charcot-Leyden crystals (formed from crystallized enzymes from eosinophilic
membranes)
,Pulmonary function tests- ANSWER 1. Test used to diagnose asthma
2. Forced expiratory volumes decrease
-FEV1 measured over 1 second
-FVC
-Ratio of FEV1/FVC before/after administration of short-acting bronchodilator
-OBSTRUCTION IS INDICATED BY FEV1/FVC <75%
Treatment of asthma- ANSWER 1. Medications
2. Oxygen therapy
3. B2 adrenergic agonists
4. Corticosteroids (status asthmaticus only)
5. Mast cell inhibitors
Are all examples of.
Chronic bronchitis - ANSWER 1. Type B COPD
2. "Blue bloater"
3. Chronic or recurrent productive cough >3 months, >2+ successive years
4. Persistent and irreversible
Causes of chronic bronchitis - ANSWER Cigarette smoking (90%), repeated airway
infections, genetic predisposition, inhalation of physical or chemical irritants are all.
Pathogenesis of chronic bronchitis - ANSWER Pathogenesis of this disease
1. Chronic inflammation and edema of the bronchial mucosa with subsequent scarring
2. Hyperplasia of the bronchial mucous gland/goblet cells (increased mucous
production, mucus combines with purulent exudate [bronchial plugs] to form a mucus
plug, increased thickness of the bronchial wall
3. Pulmonary hypertension (inflammation in the walls of the bronchial with associated
vasoconstriction of pulmonary blood vessels and pulmonary arteries, may lead to
,right-sided heart failure, INCREASES PULMONARY ARTERY RESISTANCE, WHICH
LEADS TO COR PULMONALE
Clinical manifestations of chronic bronchitis-ANSWER SOB on exertion, excessive
sputum, chronic cough-more symptomatic in am, evidence of excess body fluids such as
edema, hypervolemia, and cyanosis are all.
Diagnosis of chronic bronchitis-ANSWER Pulmonary function tests help with
diagnosis-normal TLC, increased RV, and decreased FEV1.
Treatment of chronic bronchitis - ANSWER Drugs, inhaled short-acting B2 agonists,
inhaled anticholinergic bronchodilators, cough suppressants (antitussive drugs),
antimicrobial agents, inhaled/oral corticosteroids, and theophylline products are
all.[hint: Tx of this disease]
Emphysema - ANSWER 1. Type A COPD
2. "Pink puffer"
3. Uncommon in young to middle-age adults <50 years old (Hereditary low
α1-antitrypsin(proteolytic enzyme) activity in lung)
4. Affects adults >50 years (takes time to develop)
Causes of emphysema - ANS Smoking >70 pack/year, air pollution, certain occupations
(mining, welding, working w/ or around asbestos), and α1-Antitrypsin deficiency are all.
Pathogenesis of emphysema - ANS Pathogenesis of this disease
1. Release of proteolytic enzymes from inflammatory cells (neutrophils, macrophages)
leading to alveolar damage → loss of radial traction → air trapping (and a barrel chest).
Reduction in pulmonary capillary bed
2. Impaired exchange of O2 and CO2 between alveolar and capillary blood secondary to
decrease in surface area available for gas exchange.
Medication: Supplemental oxygen should be given to patients with emphysema.
, Clinical manifestations of emphysema - ANSWER 1. Breathes using the accessory
muscles
2. Pursed-lip breathing
3. Cough-minimal or absent
4. Leans forward to breathe
5. Barrel chest
6. Digital clubbing
7. Dyspnea on exertion-late sign
Diagnosis of emphysema - ANSWER -Pulmonary function tests help in this
-Increased functional residual capacity
-Increased RV
-Increased TLC
-Increased FEV
-Increased FVC
Treatment of emphysema - ANSWER Oxygen therapy and medications (inhaled
short-acting B2 agonists, antimicrobial agents [infections], inhaled/oral corticosteroids,
theophylline products are all.
Etiology of bronchiectasis - ANSWER Etiology of the disease
1. Bronchial wall dilatation
2. Obstructive and suppurative (pus forming) disorder
Pathogenesis of bronchiectasis - ANS 1. Recurrent infection and infection of bronchial
walls results in persistent dilatation
2. Inflammation causes destruction of wall
3. Destructive process results in loss of ciliated epithelium it changes to squamous cells
and pus formation, leads to obstruction)
Asthma etiology-ANSWER 1. Type of etiology
2. Reversible airway obstruction for some, bronchoconstriction.
3. Airway inflammation, bronchial mucosal edema and production of mucous.
4. Airway responsiveness increased to various stimuli, i.e., dog hair, pollen, etc.
Predisposing factors of asthma - ANS Genetic for aptopy and structural-smaller airways
[chromosomes 5, 11, 14], history of hay fever or eczema, family history, positive skin
test to allergens are all.
Extrinsic-allergic asthma - ANS 1. Accounts for 1/3 to 1/2 of these cases
2. An IgE mediated response is common
3. Clinical manifestations include: elevated IgE levels, allergic rhinitis, eczema, (+)
family history of allergens, attacks associated with
seasonal/environmental/occupational exposure
Common symptoms of asthma - ANSWER Wheezing, feeling tightness of the chest,
dyspnea, cough (dry or productive), increased sputum production (think, tenacious,
scant, and viscous) are all.
Radiographic finding - ANSWER 1. Test used to diagnose asthma
2. X-Ray shows hyperinflation w/ flattening of the diaphragm
Sputum examination- ANSWER 1. Test used to diagnose asthma
2. Charcot-Leyden crystals (formed from crystallized enzymes from eosinophilic
membranes)
,Pulmonary function tests- ANSWER 1. Test used to diagnose asthma
2. Forced expiratory volumes decrease
-FEV1 measured over 1 second
-FVC
-Ratio of FEV1/FVC before/after administration of short-acting bronchodilator
-OBSTRUCTION IS INDICATED BY FEV1/FVC <75%
Treatment of asthma- ANSWER 1. Medications
2. Oxygen therapy
3. B2 adrenergic agonists
4. Corticosteroids (status asthmaticus only)
5. Mast cell inhibitors
Are all examples of.
Chronic bronchitis - ANSWER 1. Type B COPD
2. "Blue bloater"
3. Chronic or recurrent productive cough >3 months, >2+ successive years
4. Persistent and irreversible
Causes of chronic bronchitis - ANSWER Cigarette smoking (90%), repeated airway
infections, genetic predisposition, inhalation of physical or chemical irritants are all.
Pathogenesis of chronic bronchitis - ANSWER Pathogenesis of this disease
1. Chronic inflammation and edema of the bronchial mucosa with subsequent scarring
2. Hyperplasia of the bronchial mucous gland/goblet cells (increased mucous
production, mucus combines with purulent exudate [bronchial plugs] to form a mucus
plug, increased thickness of the bronchial wall
3. Pulmonary hypertension (inflammation in the walls of the bronchial with associated
vasoconstriction of pulmonary blood vessels and pulmonary arteries, may lead to
,right-sided heart failure, INCREASES PULMONARY ARTERY RESISTANCE, WHICH
LEADS TO COR PULMONALE
Clinical manifestations of chronic bronchitis-ANSWER SOB on exertion, excessive
sputum, chronic cough-more symptomatic in am, evidence of excess body fluids such as
edema, hypervolemia, and cyanosis are all.
Diagnosis of chronic bronchitis-ANSWER Pulmonary function tests help with
diagnosis-normal TLC, increased RV, and decreased FEV1.
Treatment of chronic bronchitis - ANSWER Drugs, inhaled short-acting B2 agonists,
inhaled anticholinergic bronchodilators, cough suppressants (antitussive drugs),
antimicrobial agents, inhaled/oral corticosteroids, and theophylline products are
all.[hint: Tx of this disease]
Emphysema - ANSWER 1. Type A COPD
2. "Pink puffer"
3. Uncommon in young to middle-age adults <50 years old (Hereditary low
α1-antitrypsin(proteolytic enzyme) activity in lung)
4. Affects adults >50 years (takes time to develop)
Causes of emphysema - ANS Smoking >70 pack/year, air pollution, certain occupations
(mining, welding, working w/ or around asbestos), and α1-Antitrypsin deficiency are all.
Pathogenesis of emphysema - ANS Pathogenesis of this disease
1. Release of proteolytic enzymes from inflammatory cells (neutrophils, macrophages)
leading to alveolar damage → loss of radial traction → air trapping (and a barrel chest).
Reduction in pulmonary capillary bed
2. Impaired exchange of O2 and CO2 between alveolar and capillary blood secondary to
decrease in surface area available for gas exchange.
Medication: Supplemental oxygen should be given to patients with emphysema.
, Clinical manifestations of emphysema - ANSWER 1. Breathes using the accessory
muscles
2. Pursed-lip breathing
3. Cough-minimal or absent
4. Leans forward to breathe
5. Barrel chest
6. Digital clubbing
7. Dyspnea on exertion-late sign
Diagnosis of emphysema - ANSWER -Pulmonary function tests help in this
-Increased functional residual capacity
-Increased RV
-Increased TLC
-Increased FEV
-Increased FVC
Treatment of emphysema - ANSWER Oxygen therapy and medications (inhaled
short-acting B2 agonists, antimicrobial agents [infections], inhaled/oral corticosteroids,
theophylline products are all.
Etiology of bronchiectasis - ANSWER Etiology of the disease
1. Bronchial wall dilatation
2. Obstructive and suppurative (pus forming) disorder
Pathogenesis of bronchiectasis - ANS 1. Recurrent infection and infection of bronchial
walls results in persistent dilatation
2. Inflammation causes destruction of wall
3. Destructive process results in loss of ciliated epithelium it changes to squamous cells
and pus formation, leads to obstruction)
