Download Patho Study guide for Exam 3 UCF and more Study Guides, Projects, Research Pathophysiology in PDF only on Docsity!
1 / 31
Patho Study guide for Exam 3 UCF
What is in lower portion of the pulmonary system: - Larynx
- Trachea
- Bronchi -Bronchopulmonary segments -The alveoli What is the lower portion of the pulmonary system known as: Respiratory portion What is the upper portion of the pulmonary system known as: Conducting portion What is in the upper portion of the pulmonary system: - Nasopharynx
- Oropharynx
- Laryngopharynx What is the blood supply of the trachea and bronchi: Bronchial artery system and pulmonary system Define type I alveolar cells: -Epithelial structural cells -This is where gas exchange occurs Define type 2 alveolar cells: -Produce surfactant, a phospholipid that: lowers surface tension, and facilitates gas exchange -causes a slippery effect Define autonomic nervous system: Control of bronchi and bronchiole muscu- lature What is parasympathetic stimulation: -Mediated by acetylcholine -via the vagus nerve -leads to constriction of muscle What sympathetic stimulation: -mediated by B2-adrenergic receptors -leads to relaxation of the smooth muscle
- epineephrine
2 / 31 What is involved in the breathing process: - Inhalation/inspiration
- Exhalation/expiration What is more active in the breathing process: Inhalation/ispiration What is more passive in the breathing process: Exhalation/expiration What muscles are involved in the process of Inhalation: -diaphragm and external intercostals Describe the process of inhalation: - The diaphragm contracts and increases lung volume The ribs elevate as the diaphragm moves downward (thus creating a negative intrapleural pressure The lungs have natural recoil tendency (the chest wall favors the expanded state) Describe the process of exhalation: - The diaphragm rises and ribs fall lower- ing the lung volume Can be active during forceful breathing using internal intercostals and abdominal muscles Push diaphragm up and pull ribs in More decrease in long volume At the end of normal expiration, alveoli still have some gas remaining, known as functional residual capacity Surfactant decreases surface tension, allowing the alveoli to open easily with each breath What factors affect breathing: - Airway resistance Lung Compliance Distribution of ventilation
4 / 31 True or False: Lung compliance is increased in neonates and young chil- dren: True, this is due to their chest wall flexibility What is involved in the neurological control of ventilation: - Neural control center for respiration located in the pons and medulla oblongata Efferent fibers travel from the brainstem to the diaphragm via phrenic nerve to stimulate inspiratory muscles Medullary dorsal neurons stimulate inspiratory muscles (intercostals, diaphragm) What is the distribution of ventilation in the upright individual: - Alveoli at the apices of the lung are much larger than those at the base Ventilation is greatest at the bottom of the lung and decreases towards the apices Regional differences in ventilation are less in the supine position Define diffusion: movement of gas from high concentration to low concentration areas What are the 6 barriers to diffusion: - Surfactant Alveolar membrane Interstitial fluid Capillary membrane Plasma Red blood cells What is hypoventilation: air delivered to alveoli is insufficient to provide O and remove CO Hypoventilation results in increase of PaCO2 (respiratory acidosis) Causes of hypoventilation: - Morphine
5 / 31 Barbiturates Obesity Myasthenia gravis Obstructive sleep apnea Chest wall damage Paralysis of respiratory muscles Surgery of the thorax or abdomen What is hyperventilation: increase of air entering the alveoli leads to hypocap- nia (respiratory alkalosis) What causes hyperventilation: - Pain Fever Anxiety Obstructive lung disease Sepsis -High altitude Brainstem injury What is hypoxemia/hypoxia: deficient blood oxygen What are the types of pulmonary disorders: - Obstructive pulmonary disor- ders Restrictive pulmonary disorders What does obstruction refer to in the pulmonary system: Cannot get air out Obstruction is small airway Resistance to expiration Wheezing Hyperexpansion of CXR What does restriction refer to in the pulmonary system: Cannot get air in
7 / 31 Who has asthma: - 5-12% of the U.S population Most common chronic disease in children High risk populations include: African Americans, Inner city residents, prema- ture/low birth weight children What are some predisposing factors to asthma: - Genetic for atopy and structural (smaller airways) Chromosomes 5,11, History of hay fever, eczema Family history Positive skin test reactions to allergens What is Intrinsic Asthma: - Non-allergic Adult onset Antigen-antibody reactions are not directly involved IgE levels may be elevated What is Extrinsic asthma: - Allergic Pediatric onset 1/3 to 1/2 of asthma cases An IgE mediated response is common What are some clinical manifestations for extrinsic asthma: - Elevated IgE levels Allergic rhinitis Eczema Positive family history of allergy Attacks associated with seasonal, environmental or occupational exposure
8 / 31 What is the mechanism of action for extrinsic asthma: Immediate phase: -Initiated by exposure to specific antigen that has previously sensitized mast cells in airway mucosa -Antigen reacts with antibody on surface of mast cell -Mast cell releases packets of chemical mediator substances Chemical mediators released
- Histamine -Slow-reacting substances of anaphylaxis (leukotrienes)
- Prostaglandins
- Bradykinins -Eosinophilic chemotactic factor
- Serotonin
10 / 31 Curschmann spirals (mucous casts of bronchioles)
11 / 31 What pulmonary function tests would you perform on a patient with bronchial asthma: - Peak expiratory flow rate Forced expiratory volume Bronchodilatation stimulation: -Parasympathetic stimulation (mediated by acetylcholine) via the vagus nerve (cranial nerve X) leads to constriction of muscle Sympathetic stimulation (mediated by B2 adrenergic receptors); leads to relaxation of the smooth muscle What is the treatment for asthma: - Avoid triggers Environmental control: removal of allergens, air purifiers, air conditioners Preventative therapy Desensitization (allergen specific immunotherapy) Medications O2 therapy Small-volume nebulizers What is chronic bronchitis: - Type B COPD "Chronic Obstructive Pulmonary Disease" Blue bloater Chronic or recurrent productive > 3 months> 2+ successive years Persistent, irreversible Who has chronic bronchitis: - Typical patient is overweight (1:2 male to female ratio)
30-40 years Commonly associated with emphysema
13 / 31 -Physical reconditioning --treadmill/stationary bike --alternating rest and exercise What is emphysema: Abnormal permanent enlargement of the gas exchange airways accompanies by destruction of alveolar walls without obvious fibrosis "hon- eycombing" -Loss of elastic recoil -Bronchioles are more likely to collapse -Referred to as Type A COPD or Pink Puffer Who gets emphysema: -Young to middle age adults <50 years (uncommon) --Hereditary low a1- antitrypsin activity in the lung
50 years (develops over time) -Like cirrhosis, thought of as end stage of multiple chronic small airway obstructive etiologies What causes emphysema (etiology): - Smoking >70 packs/year: causes alve- olar damage --Inflammation in lung tissue leading to release of proteolytic enzymes --inactivates a1 antitrypsin (protects lung parenchyma) -Air pollution -Certain occupations such as mining, welding, working with or near asbestos -a1 antitrypsin deficiency What is a1- antitrypsin: -a protein made in the liver -is a serine protease inhibitor, main targets are --neutrophil proteases (mainly elastase) What is pathogenesis for emphysema: -Release of proteolytic enzymes from inflammatory cells (neutrophils, macrophages) leading to alveolar damage -loss of elastic tissue in lung -results in decrease in size of smaller bronchioles -results in loss of radial traction (holds airway open) What are some clinical manifestations for emphysema: - Progressive, exter-
14 / 31 nal dyspnea Increased shortness of breath for past 3-4 years -Thin: due to increased caloric expenditure (increased respiratory efforts) and de- creased ability to consume adequate calories -Use of accessory muscles leads to difficulty breathing -pursed lip breathing -cough (minimal or absent) -barrel chest -leaning forward to breathe Bullae: "Peripheral blebs" are hallmarks of chronic obstructive lung disease, COPD What would happen if a "bleb" was so paper thin that it ruptured: - Pheumothorax Diagnosis of emphysema: Patient history and physical finding -thin, wasted individual hunched foward -barrel chest -digital clubbing -decreased breath sounds, lack of crackles with prolonged expiration -decreased heart sounds -decreased diaphragmatic excursion What will a pulmonary function test (pfts) show on a patient with emphyse- ma: Decreased FEV (forced expiratory volume), increased TLC (total lung capacity), decreased FVC (forced vital capacity) What will a chest xray show on a patient with emphysema: Hyperinflation Treatment for emphysema: -O2 therapy
- Medications --Inhaled anticholinergic bronchodilators --Cough suppressants --Antimicrobial agents (infections) --Inhaled/oral corticosteroids What is bronchiectasis: Not a specific disease but simply a condition which large bronchi are damaged and dilatated due to a variety of causes
16 / 31 -diffuse interstitial lung disease
17 / 31
- Sarcoidosis -Hypersensitivity pneumonitis -occupational lung disease atelectatic disorders -acute (adult) respiratory distress syndrome
- infant respiratory distress syndrome Fibrotic Interstitial Lung Disease: characterized by infiltration of alveolar walls by cells, fluid, and connective tissue -can be acute, subacute, chronic -if untreated can progress to irreversible fibrosis -incidence rate is 5 cases per 100, Diffuse Interstitial Lung Disease Pathogenesis: Immune reaction: -Begins with injury to alveolar epithelial of capillary endothelial cells -Interstitial and alveolar wall thickening -Increased collagen bundles in interstitium Inflammation: -occurs early, reversible -triggering event leads to inflammatory response and increased inflammatory cells --injury leads to increased membrane permeability and movement of fluid/debris into alveoli Fibrosis: -Fibroblastic proliferation and deposition of large amount of collagen -caused by increased mesenchymal cells and fibrobrlasts in interstitium -alveolar walls become thickened with increased amounts of fibrous tissue Destruction: -End stage disease -Loss of alveolar walls What are the clinical manifestations of Diffuse Interstitial Lung Disease: - -Progressive dyspnea with exercise with desaturation -rapid shallow breathing -irritating, nonproductive cough -clubbing of nail beds (40-80%) -Bibasilar end-expiratory crackle -cyanosis (late finding)
19 / 31 -Dyspnea of insidious onset -Dry, nonproductive cough -erythema nodosum -Macules, papules, hyperpigmentation, and subcutaneous nodule -hepatosplenomegaly, lymphadenopathy Diagnosis for Sarcoidosis: -Bronchoalveolar lavage --Monitors cell content --Fluid has increased lymphocytes and high CD4/CD8 cell ratio -Transbronchial lung biopsy --Noncaseating granulomas (definitive diagnosis) -Chest X-ray --Differentiates stages
- Treatment --Corticosteriods --Immunosuppressive agents Atelectatic Disorders: -Incomplete expansion -is strictly an anatomic/physiologic concept, NOT a disease, but seen in many disease states What is Acute (Adult) Respiratory Distress Syndrome (ARDS): -damage to the alveolar capillary membrane -occurs in association with other pathophysiologic process -125,000-150,000 cases/year in the United States -Mortality rate 30-60% What are the causes of ARDS: -Severe trauma -Sepsis (>40%) -Aspiration of gastric acid (>30%)
- Shock Pathogenesis of ARDS: -Widespread pulmonary inflammation leads to: --noncardiogenic pulmonary edema associated with "leaky" pulmonary capillaries --Atelectasis associated with lack of surfactant --Fibrosis: Associated with inflammatory deposition of proteins Injury to alveoli Changes in diameter of alveoli Injury to pulmonary circulation
20 / 31 Disruptions in O2 transport and utilization What are common findings of ARDS: -Severe hypoxemia caused by intrapul- monary shunting of blood --Perfusion of large numbers of alveoli that are poorly (areas of low ventilation-per- fusion) or not ventilated (areas of shunt) -Decrease in lung compliance --Due to loss or inactivation of surfactant with subsequent increased recoil pressure --Proteinaceous fluid fills alveoli and impairs ventilation -Diffuse, fluffy alveolar infiltrates -Noncardiogenic pulmonary edema Early clinical manifestations for ARDS: -sudden marked respiratory distress -slight increase in pulse rate
- dyspnea -low PaO -Shallow, rapid breathing Late clinical manifestations for ARDS: - Tachycardia
- Tachypnea
- Hypotension -Marked restlessness -Crackles, rhonchi on auscultation -Use of accessory muscles -intercostal and sternal retractions
- cyanosis Diagnosis for ARDS: -Hallmark is hypoxemia refractory to increased levels of supplemental O Arterial Blood Gases (ABGs) for someone who has ARDS: - Hypoxia
- Acidosis -Hypercapnia (increase in CO2) What would a chest X-ray for a patient with ARDS show: Normal with progression to diffuse "whiteout" What would an open-lung biopsy show with a person who has ARDS: -At- electasis -Hyaline membranes
