M9: Pulmonary Flashcards
Pneumonia causes general and specific bacteria (ch 35, pg 1176-1178)
-infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites.
-CAP most caused by Streptococcus pneumoniae also known as pneumococcus.
-Other common bacteria include Legionella (found in water systems), Moraxella catarrhalis, and Hemophilus influenzae (ch resp d/o).
-Staph Aureus: severe PNA, often p flu
-Atypical pathogens include Chlamydophila and mycoplasma (walking).
COPD-OBSTRUCTIVE Pg 1172
COPD – defined by the global initiative for COPD Gold 2022 report as – common preventable and treatable disease characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities.
Cluster of dx’s: emphysema, ch bronchitis, asthma
-Airflow limitation that is not fully reversible
-Usually progressive and associated with chronic bronchitis and emphysema.
-Risk factors
Tobacco smoke
Occupational dusts and chemicals
Indoor air pollution from biomass fuel used for cooking and heating.
Outdoor air pollution
Any factor that affects lung growth during gestation and childhood
Genetic susceptibilities
Emphysema pg 1173
Emphysema- is abnormal permanent enlargement of gas-exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis.
-larger but fewer air sacs=reduced surface area for gas exchange
-Hypoxemia
-Hyperinflated lungs
-Loss of elastic recoil
-Centrilobular
-septal destruction occurs in the respiratory bronchioles and alveolar ducts, usually in the upper lobes.
-alveolar sac (alveoli distal to the respiratory bronchiole) remains intact.
-tends to occur in smokers with chronic bronchitis
-involves the entire acinus
-damage is more randomly distributed.
Clubbing
-selective bulbous enlargement of the end of a digit (finger or toe). Recognized by measuring the nail-fold angle and phalangeal depth.
-severity can be graded from 1-5 based on the extent of nail bed hypertrophy and the number of changes in the nails themselves.
-usually painless, develops gradually over weeks or months.
-most common cause of clubbing in US is lung cancer.
Associated with disease that cause chronic hypoxemia (bronchiectasis, cystic fibrosis, pulmonary fibrosis, lung abscess, CHD)
-clubbing without underlying cancer or lung disease can occur in association with a variety of other conditions including GI, hepatobiliary diseases, and endocrine disorders. Can be congenital.
-exact cause unknown, in people with chronic hypoxemia suggested that decreaed oxygen causes the release of vascular endothelial growth factor which promotes proliferation of the connective tissue between the nail matrix and the distal phalanx. Rarely reversible.
Hemoptysis ch 35 pg. 1154 versus Hematochezia
Hemoptysis - coughing up of bloody sputum originating from the tracheobronchial branches of the pulmonary system.
-Can sometimes be confused with hematemesis.
-Bloody sputum is often froth and usually bright red with an alkaline PH.
-Can indicate lung cancer, bronchiectasis, or infection (PNA), TB, or lung abscess. Other causes include cancer or PE. The amount and duration of bleeding provide information about its source. -Chest imaging and bronchoscopy used to confirm site of bleeding.
Hematochezia: GI bleed from lower tract
Dyspnea versus Orthopnea pg 1153
Dyspnea- MC symptoms of pulmonary disease. Described as a subjective experience of breathing discomfort.
s/s: breathlessness, air hunger, shortness of breath, labored breathing.
C/B: pulmonary, acute pain, heart disease, trauma, and anxiety.
Stimulation of many receptors can contribute to the sensation of dyspnea, including afferent receptors in the brain and brainstem, mechanoreceptors in the chest wall and upper airway, and central and peripheral chemoreceptors that sense the effectiveness of gas exchange. These receptors communicate with the CNS respiratory control center, which then sends signals to the cerebral cortex and to the mechanical portions of the respiratory system to modulate breathing.
Dyspnea can occur transiently or chronically, and the magnitude of the dyspnea may not correlate with the severity of the underlying disease.
Orthopnea- is a dyspnea that occurs when an individual lies supine, which increases intrathoracic and intraabdominal pressure. This puts pressure on the diaphragm and the respiratory muscles, can be relieved by standing.
-common w/ HF, or other severe respiratory d/o.
Cannibis inhalation
pg 56 purple box
The inhalation of smoke from cannabis can irritate the bronchial passages and lead to respiratory problems such as chronic bronchitis. The long-term impacts on lung function are still uncertain, but potential for airway inflammation, increased airway resistance, and hyperinflation has been suggested.
Tuberculosis risk Pg 1178
-infection caused by mycobacterium tuberculosis, an acid-fast bacillus that usually affects the lungs but may invade other body systems.
-Affects an estimated 10 million worldwide resulting in 1.6 million deaths.
- leading cause of death in the world from a curable infectious disease.
-highly contagious and is transmitted person to person in airborne droplets.
Pathophysiology
Tubercle formation: Granulomatous lesion
Caseous necrosis: Cheeselike material
May remain dormant for life or cause active disease
Isolation of bacilli by enclosing them in tubercles and surrounding the tubercles with scar tissue
-Risk : hiv, immunosuppressive therapy, crowded institutional settings, homelessness, substance abuse, and lack of access to screening and medical care.
Pulmonary artery pressure pg 1181
-Normal 15-18 mm Hg.
pressure affecting artery from heart to lung
-Pulmonary hypertension is a mean artery pressure greater than 25 mm Hg at rest.
-Most important cause of pulmonary artery constriction: Low alveolar partial pressure of oxygen (Pao2)
-Vasoconstriction caused by alveolar and pulmonary venous hypoxia: Hypoxic pulmonary vasoconstriction
-Acidemia and inflammatory mediators: Pulmonary artery constriction
*C/b: LHF, chr lung ds, pulm han
PAH-Pulm Artery HTN (pg 1134 & 1181)
-PAH can be caused from idiopathic or secondary conditions.
Mean pulmonary artery pressure above 25 mmHg at rest
enhanced pulmonary arteriole contractility, endothelial dysfunction, remodeling and proliferation of both endothelial and smooth muscle cells, and local thrombi.
- partial occlusion of small pulmonary arteries, which leads to an increase in PVR, right ventricular failure, and death.
3 signaling pathway disruptions that lead to the progressive pulmonary vascular defects.
the nitric oxide (NO),
prostacyclin (PG12) and
thromboxane A2 (TXA2), and the endothelin-1 (ET-1).
Idiopathic, familial, or associated
Pathophysiology
Overproduction of vasoconstrictors and decreased production of vasodilators
Remodeling
Resistance to pulmonary artery blood flow, thus increasing the pressure in the pulmonary arteries
Workload of the right ventricle increases and subsequent right ventricular hypertrophy, may be followed by failure and eventually death
TX:
Prostacyclin analogs (epoprostenol, beraprost, iloprost)
Endothelin receptor antagonists (bosentan, ambrisentan)
Phosphodiesterase-5 inhibitors
Calcium channel blockers
Lung transplantation
Secondary pulmonary artery hypertension
Treat the primary disorder.
Once pulmonary hypertension has persisted long enough for hypertrophy to develop, it is no longer reversible.
Supplemental oxygen reverses hypoxic vasoconstriction.
Lung cancers (pg 1182-1185)
-Is also known as bronchogenic carcinomas.
-Is the most frequent cause of cancer death in the United States.
Most common cause: Cigarette smoking
(Smoking is related to cancers of the larynx, oral cavity, esophagus, and urinary bladder.)
-Genetic, environmental, or occupational risk factors are also associated with lung cancer.
- MC: Non–small-cell lung cancer
Squamous cell carcinoma
Nonproductive cough or hemoptysis
Adenocarcinoma
Tumor arising from glands
Asymptomatic or pleuritic chest pain and shortness of breath
Surgical resection
Large cell carcinoma (undifferentiated)
Surgical therapy limited to palliative procedures
Radiation and chemotherapy not helpful
Small cell carcinoma: Less common, more severe, asso w/ smoking
Limited vs. extensive disease
First manifestations: Paraneoplastic syndrome
Bronchial carcinoid tumors
Rare
Adenocystic tumors (cylindromas)
Mucoepidermoid carcinomas
Mesotheliomas
Associated with asbestos
May take 20–40 years before cancer appears
RF: radon gas, asbestos, genetics, other carcinogens
Mani:
Dyspnea and chest pain
TX:
Pleuropneumonectomy, chemotherapy, radiation, and hyperthermia
TNM classification system
T: Denotes the extent of the primary tumor.
N: Indicates nodal involvement.
M: Describes the extent of metastasis .
TX:
Preferred treatment: Surgical resection
Chemotherapy
Radiation
Dose-intensified radiation radiofrequency ablation, microwave ablation, cryotherapy, and brachytherapy
Ventilation and respiration control
(pg 1137 &1151)
Ventilation
-Is the mechanical movement of gas or air into and out of the lungs, facilitated by the diaphragm and accessory muscles.
-Is not the same as respirations.
-Minute volume
Ventilatory rate is multiplied by the volume of air per breath.
-Alveolar ventilation–ABG
Measures partial pressure of carbon dioxide (Paco2).
Respiratory center
-Is located in the brainstem. (Medulla oblongata)
-Dorsal respiratory group: Sets the basic automatic rhythm.
Receives impulses from peripheral chemoreceptors in the carotid and aortic bodies: Detects the Paco2 and the amount of oxygen in the arterial blood.
*responding to changes in CO2, O2, and pH levels. Chemoreceptors in the brain and in the arteries detect these changes and adjust the rate and depth of breathing.
-Pneumotaxic and apneustic centers: Are in the pons.
Modifiers of the inspiratory depth and rate are established by the medullary centers.
Neurochemical control of Ventilation
Central chemoreceptors:
-reflects the PaCO2
-stimulated by hydrogen (H+) in the cerebrospinal fluid (pH).
incr depth and rate
Peripheral Chemoreceptors:
-located in the aorta and carotid bodies
-stimulated by hypoxemia (PaO2)
-responsible for all the ventilation that occurs in response to arterial hypoxemia.
Lung receptors
Irritant receptors: Are sensitive to noxious substances.
When stimulated cause cough, bronchoconstriction, and increase respiratory rate.
Stretch receptors: Protect against excess lung inflation.
Decrease ventilatory rate and volume.
Juxtapulmonary capillary (J) receptors: Are sensitive to increased pulmonary capillary pressure.
Bronchiectasis (Pg 1162)
-persistent abnormal dilation of the bronchi.
-usually occurs in conjunction with other respiratory conditions that are associated with chronic bronchial inflammation, such as cystic fibrosis but can also be due to prolonged atelectasis, aspiration of a foreign body, recurrent pulmonary infection, TB, congenital weakness of the bronchial wall.
-Associated with systemic disorders such as RA, inflammatory bowel disease, and immunodeficiency syndromes.
-results from recurrent inflammatory and infectious insults to the bronchial epithelium leading to the infiltration of neutrophils and the release of neutrophil derived proteases that destroy the elastic and muscular components of the bronchial walls. This is followed by obstruction of the bronchial lumen, fibrois, and permanent dilation.
-Primary symptoms is a chronic productive cough. Dyspnea and fatigue are common, recurrent lower respiratory tract infections lead to expectoration of copious amounts of foul-smelling, purulent sputum.
-other signs include clubbing of the fingers and hemoptysis.
-Diagnosis confirmed with CT, treated with atb, anti-inflammatories, bronchodilators, mucolytic agents, chest physiotherapy, and supplemental O2.
OSA & it’s treatment (pg: 1167 & 1195)
-results from partial or complete upper airway obstruction that occurs during sleep d/t intermittent relaxation of throat muscles—-Obstruction.
-associated with snoring, labored, or obstructed breathing, and disrupted sleeping patterns.
-risk factors include: adenotonsillar hypertrophy, allergic rhinitis, craniofacial abnormalities, genetic disorders such as down syndrome
-environmental factors include smoking status and socioeconomic status
Patho: airway narrowing, increased upper airway collapsibility r/t obesity or neurological disorders (Central apneas) and airway inflammation (GERD, asthma, allergy)
-airway obstruction can be partial or complete.
-manifestations: snoring, labored breathing, sweating, restlessness during sleep which may be continuous or intermittent.
-may be episodes of increased respiratory effort but no audible airflow often terminated by snorting, gasping, repositioning, or arousal.
Evaluation: sleep study, if tonsillar than T&A, obesity = CPAP and weight loss, anti-inflammatories, dental treatment.
-comorbidities- hypertension, cv disease.
ABG interpret (pg 1149)
Normal pH 7.35-7.45
Acidosis <7.35
Alkalosis >7.45
Respiratory acidosis
Elevated pCO2
Ventilation depression
Respiratory alkalosis
Depressed pCO2
hyperventilation
Metabolic acidosis
Depression of HCO3
Increase in non carbonic acid
Focus on uremia
Metabolic alkalosis
Elevated HCO3
Excessive loss of metabolic acids
Incentive spirometry (pg 1148)
- Measures volume and flow of air inhaled an exhaled and plotted against time during different breathing maneuvers.
Forced Expiratory Volume in 1 second
Part of the Turn, Cough, Deep breath to prevent PNA’s and increase inflaton of lungs.
