Medical Surgery Notes PDF

# Pneumonia ## If pt is an outpatient - Antinausea drink: azithromycin (coral), krefloxacin - HAP → vancomycin + piptaz ## Health Teachings - Get pneumococcal and flu vaccines - Advise to religiously take the antibiotic - Advise to follow-up chest x-ray after 2 weeks upon discharge - Report any si...

# Pneumonia ## If pt is an outpatient - Antinausea drink: azithromycin (coral), krefloxacin - HAP → vancomycin + piptaz ## Health Teachings - Get pneumococcal and flu vaccines - Advise to religiously take the antibiotic - Advise to follow-up chest x-ray after 2 weeks upon discharge - Report any signs of fever ## Nice to know - **High pressure alarm** - Obstruction: mucus secretion, kinks, biting - **Low pressure alarm** - Disconnection ## Management: Pneumonia - Goal: Patient to stay only for 3-5 days 1. Advise to ambulate 2. Increase of unkor contraindicated: If didn’t work, check patient further 3. Biet: Increase calories, increase proteins 4. Incentive spirometry to prevent lung collapse: If rubricks, contraindicated to patient with LOPD 5. Huff laughing ## Fever 1. Culture and sensitivity: Should be performed before giving antibiotic 2. Check for CBC 3. Imaging: X-ray and CT Scan to know presence of pleural effusions and malignancy ## Antibiotic Management - **CAP** - Azithromycin - **If in patient:** - IV: Ceftriaxone, moxifloxacin, levofloxacin - **If patient is already septic:** Piperacillin - Tazobactam combined with ## Things to avoid: 1. **Milking** - Can increase pressure in lungs 2. **Clamping** - Don’t clamp the chest tube especially during transport of the patient. Can cause increased pressure in the lungs: Pneumothorax. ## Repris: - Various condition that happens when the body's immune system has an extreme response to an infection: - C- confusion: Sign of impending sepsis - A-emia: Accumulation of urea in the blood - R- increased respirations (alkalosis) - B- decreased BP ≥90 mmHg - T- temperature: Hyperthermia (sign of impending sepsis), Hypo (late sign of sepsis) ## ARDS: - Called pulmonary edema - Non-cardiogenic type - Build up of fluid due to repario (inflammation) - Hallmark: Hypoxemia - Inadequate arterial oxygenation despite high oxygen given ## Management: - Support: 8-10L High Flow - Give diuretics (Furosemide): Don't give in patients with BP <90 mmHg - Antiobiotics ## Thoracentesis: - Insertion of a needle in the intercostal space - Monitor BP (hypotension) - Important because analysis of fluid for cell cytology, culture and sensitivity. - 71L removed from the patient can relieve symptoms - Chest tube thoracentesis: Attached to chest tube draining fluid. ## 3 Chambers: 1. **Collection chamber** - Measures amount of fluid from the patient collected here - Allows passage of air to water seal chamber - Expected to be bright red verous/anguinous - After several hours, color changes to pink → anguinous → clear 2. **Water seal chamber** - Measures any air exiting: Fluctuation is normal - Fluctuation: Sign that the lungs is fully inflated. - Water is bubbling: Sign that there's an air leakage 3. **Suction regulation chamber** - Negative pressure, amount of negative pressure exerted to suction - Normal: Gentle and continuous bubbling - Intermittent: You need to check the gauge - No bubbling: Check the connection ## Need to remember - Notify the provider if the fluid drain is ≥100 mL/hr: Hypotension ## Other Signs - Dyspnea on exertion - Fatigue - Increased respiration - Body aches ## Auscultate: - Crackles - Chest pain (pleuritic chest pain during inspiration) - LOC: Altered mental status - Signs of sepsis ## 3 most common complications: 1. **Pleural effusion**: Abnormal collection of fluid in the pleural space, ≥15-20 mL or more - **Types:** - **Hemothorax** - Accumulation of blood in the pleural space - **Pyothorax/emphyrema** - Pus in the pleural space - **Hydrothorax** - Water in the pleural space - **Chylothorax** - Lymphatic fluid in the pleural space - **Chylous fluid**: Milky white with high lipid content - **Signs/Symptoms:** - Chest pain due to pleurisy/pleuritis: Inflammation of the membrane surrounding the lungs - Sharp pain when breathing - Pleural friction rub: When you auscultate, you will hear grating/creaking - Asymmetrical lung expansion: Delayed expansion on the area of the lung with effusions. - Decreased tactile fremitus: Vibration produced by the voice that is transmitted to the chest wall 2. **Pneumonia**: - **Types:** - **Community acquired pneumonia**: LIRT infection, occurs 48 hours - **Hospital acquired pneumonia**: Occurs 48-72 hours after intubation - **Ventilator acquired pneumonia**: Candida albicans - **Fungal pneumonia**: History of LOC, stroke, seizure, anesthesia; Gag and cough reflex are deprived. - **Aspiration pneumonia**: Sequela (condition of a consequence of previous injury, disease) - **Opportunistic pneumonia**: Patient with altered immune system. Common causative agent: Pneumo Cystic Jiroveci (common in AIDS). - Cytomegalovirus: Common cause of viral pneumonia in immunocompromised - Pneumococcal pneumonia: Most common cause of bacterial pneumonia. - **2 most common symptoms**: Fever and productive cough - **Chest X-ray**: Most convenient diagnostic finding of pneumonia. - Chest X-ray: Auscultate bronchitis, fever, cough. - **Bacterial pneumonia vs Congestive Heart Failure**: - BNP is used to rule out heart failure. - If BNP is high (>100 pg/mL) indicates heart failure. - **Staphylococcus Aureus**: MRSA, high potent kind of microorganism, strong enough to cause sepsis. - **Streptococcus pneumoniae**: Gram + microorganism. 3. **Bronchodilator**: Albuterol, levallbuterol, salbuterol - Common side effect: Tachycardia and palpitation (more common) 4. **Corticosteroid**: Medication ending in “-rone” 5. **Antibiotics**: -mycin - Anti-leukotriene: Montelukast (Singulair) - Prevents bronchoconstriction 6. **Pulmonary rehabilitation**: Huff laughing (combination of pursed lip breathing and evacuation of secretion) 7. **Comfort**: Low dose as morphine sulfate. - Look out for respiratory depression, RR, and O2 sat. 8. **Contraindicated:** For COPD - Aminophylline: More harm than therapeutic effect - Theophylline: Narrow therapeutic index, causes toxicity to the body ## Pneumonia: - Inflammation of the lung tissue. - Alveoli is filled with fluid or pus - Bronchiole is also inflamed. ## Risk Factors: - Elderly: Cat years old or older. - Children: Below 5 Years old - Patients that are immunocompromised (HIV, cancer) - Patients with chronic diseases (diabetes, COPD) - Smokers, alcoholics - Severe malnutrition. - Post operative patients - Patients with a tube and are ventilated ## Normal vs Chronic Bronchitis - **Normal Bronchus:** Open airway, smooth muscle, mucus gland - **Chronic Bronchitis:** Mouth muscle (constricted), narrow airway, mucus gland, excessive mucus production. ## Diagnosis: Chronic Bronchitis - May have mucus production - Emphysema wall: Chronic productive cough (≥ 3 months for ≥2 consecutive years) - **Clinical Appearance:** “Blue Bloaters" - Bluish and obese. Chronic hypoxemic, vasoconstriction ## Interprofessional and Collaborative Management 1. Smoking cessation 2. Prevent triggers: - Atopic dermatitis 3. Infection: Influenza and pneumococcal vaccines 4. Provide adequate nutrition 5. Increase fluid intake: Reduces on demand 6. Diet: High calorie (provide course of energy) - Protein: Maintain the integrity of alveolar walls - Low carb: Natural and product of carbs (LG) - Support : 1-3 L/min - 2 L/min (rapeutic) - VpO2 : 88% - 92% 7. Oxygen supplementation ## Pharmacological Therapy 1. **Mucolytics:** Acetylcysteine (Fluimucil) if there's secretions - Expectorant 2. **Antitussive**: Medications given to prevent night disturbances due to coughing. - Dextromethorphan ## Diagnosis: Emphysema - ↓ Alveolar surface area - ↓ Decreased in dead space (no gas exchange in that area) - ↓ Impaired 02 diffusion - ↓ Hypoxemia ## Emphysema: - Pathological (malikita talaga) - Permanent enlargement and damage to the air space. - Air trapped in the lungs causing to overinflate. ## Mechanism: - Whenever they inflate, alveoli expand - Exhale: Collapses during expiration, CO2 fuel retained ## Clinical Appearance: - Barrel chest due to air trapping - "Pink Puffer:" Compensating mechanism - Patient with emphysema: They are puffing (breathing heavily), pursed lip breathing (prolonged expiration), CO2 retained. ## Acute Bronchitis: - Short term - 90% due to viral infection - Pollution, bacterial infection ## Chronic Bronchitis: - Causes: Smoking, chemical exposure, air pollution - Pathological changes in airway - Further narrowing of bronchiole lumen - Irreversible lung changes - Emphysema - No genetic type: Inflammation of airway, goblet and mucus gland, mucus production, persistent coughs. - Can trigger: ## Clinical Manifestation: - Chronic cough - Sputum production - Dyspnea (severe: Worsening due to CO2) - COPD Dyspnea: Dyspnea even at rest. ## Position of Uncomfort: - Orthopneic position ## Diagnostic Tests: 1. **Chest X-Ray**: Hyperinflated lungs 2. **CT Scan**: Not routinely obtained 3. **Spirometry**: Used to evaluate airflow obstruction - PEV/FVC lower than 70% 4. **ABG**: Are baseline oxygenation and gas exchange 5. **Pulmonary Function Test**: FEV/FVC ## 2 Function of COPD 1. **Emphysema**: Impaired CO2 and O2 exchange due to destruction of the walls of over distended alveoli. - Overdistended non-functional alveoli, leading to the rupture of alveoli ## Causes: - Smoking - Chemical exposure - Air pollution - Genetic type: Alpha 1 anti-trypsin deficiency - Disequilibrium of elastase/anti elastase - Destruction of elastic recoil - Overdistention of alveoli (collapse) - Retention of CO2 (air trapping) - Destructed alveoli. ## Changes: 1. **Proximal airway (trachea and bronchi)** - Airway narrows due to excess mucus - Increased number of goblet cells (produce mucus) - Enlarged submucosal glands (secrete antimicrobial proteins) 2. **Respiratory airway (bronchioles)** - Thickening of the airway and overall narrowing of the airway - Bronchiolitis obliterans: Inflammation and fibrosis of the bronchiolar walls resulting to narrowing of the bronchiolar. 3. **Lung parenchyma (alveoli)** - Alveolar wall destruction: Leads to 100% alveolar attachment and decreased elastic recoil. 4. **Pulmonary vasculature:** - Thickening of the lining of the vessels and hypertrophy (excessive growth of smooth muscle): Pulmonary hypertension - High BP in the arteries of the lungs. - High pressure in pulmonary artery (vasoconstriction) ## Risk Factors: 1. **Cigarette smoking** (active, passive) - Alveoli: Greatly diminished lung capacity - Mucus: Irritates young goblet cells; more mucus. - End product: Carbon monoxide + hemoglobin - Carboxyhemoglobin: Does not carry 02 effectively. 2. **Prolonged exposure to occupational chemical exposure (coal/fuel)*** 3. **Age**: ≥70 4. **Family history (genetic abnormalities)**: Alpha 1 anti-trypsin deficiency ## Red zone - Less than 60% (medical emergency). ## Status asthmaticus: - Severe persistent asthma that no longer responds to treatment with conventional therapy. ## Manifestation: - Severe bronchospasm - If status asthmaticus worsens, causes hyperventilation leading to respiratory alkalosis - CO2 retains and pH levels decrease leading to respiratory acidosis. - Signs/Symptoms: - Labored breathing - Prolonged exhalation - Wheezing - Engorged neck veins - Inspiratory wheezing indicates that the condition is worsening ## Management: - Oxygenation: High-flow supplemental O2 through non-rebreather mask - Magnesium sulfate: Calcium antagonist; Induces smooth muscle relaxation leading to bronchodilation. ## COPD: - 3rd most leading cause death - Patients with COPD becoming symptomatic during middle adult year (≥70%) - The disease is categorized as slowly progressive; does not happen overnight but overtime. - Persistent airflow obstruction that is associated with chronic airway information. ## Salmeterol & Formoterol: - Long duration of bronchodilation (12 hours) - For long-term use. ## Anti-leukotrienes - Montelukast - Inhibits inflammatory pathway: The increase secretion and bronchoconstriction - Given to prevent acute exacerbation of asthma (maintenance.) ## Immunomodulators: - Promote binding of IgE to the high affinity receptors of mast cells/basophils. - Ex: Omalizumab - Monoclonal antibody and may be used for patients with allergies and recurrent asthma. ## Other ways to monitor the severity of asthma: - Peak flow monitoring: Measures the severity of asthma - Peak flow meter: Measures the highest airflow during a forced expiration. - Recommended to patients with asthma to monitor if they meet the 1-4 criteria: 1. Have moderate or severe persistent asthma 2. Poor perception of changes in airflow 3. Worsening symptoms - Unresponsive to the environment or occupational exposure - Discretion of the clinician and patient to use peak flow meter. ## How to know if asthma is controlled? - **Green zone**: Signifies 80-100%: Personal best (patient is doing well) - **Yellow zone**: 60-80% (asthma is getting worse) ## Pharmacological Therapy: - Quick-relief medications: Treatment of asthma (risks & exacerbations) - P (provide protection): Prevent triggers - 0- Oxygenation - C- Corticosteroids - S- Short-acting beta-agonist (SABA) - A: anti-cholinergics - R- Rest - SABA: Albuterol, levalbuterol - Enhances the function of beta 2 to cause bronchodilation - Prevents exercise-induced asthma. - Anti-cholinergics: Inhibit muscarinic cholinergic receptor - Form of nebulization meds (ipratropium, tiotropium) - Inhibits the leukotriene to release acetylcholine that causes bronchoconstriction to create bronchodilation. - Long-acting control medications: - Corticosteroids: Medications ending in “-one” (fluticasone) - Most potent and effective anti-inflammatory drug - Halts the inflammatory response - Cromolyn sodium: Mild to moderate anti-inflammatory agent - Stabilizes mast cells to prevent inflammatory response. - Long acting beta 2 agonist: LABA - Ex: Theophylline: Mild to moderate bronchodilator - If patient is taking this, it needs to be monitored closely, because it has a short therapeutic index, which can lead to toxicity. - Can also relieve night-time asthma symptoms. ## Mast cells - Will release inflammatory mediators and promote inflammatory pathways. ## Inflammatory Pathways: 1. **Cyclooxygenase pathways:** - G enzyme: Helps create prostaglandin 2 (important chemical in the body to check inflammation) - If active prostaglandin can lead to: - Vasodilation: Causing leakage of fluid. - Bronchoconstriction: Narrow airway. 2. **Leukotrienes**: Chemical mediator that initiates inflammatory response. - Stimulates the parasympathetic nervous system to release acetylcholine. - If stimulated, results in: - Bronchoconstriction - PNJ (increased mucous production) - Smooth muscle contraction. ## Alpha 1 & Beta 2 Adrenergic Receptors: - If stimulated, bronchoconstriction occurs. - Controlled by cAMP: Cyclic Adenosine Monophosphate ## Beta 2: - If stimulated results in increased level of cAMP which inhibits the release of chemical mediators causing bronchodilation ## Symptoms of exacerbation: - Diaphoresis - Widened pulse pressure (pulsus paradoxus: Difference of hypoxemia & cyanosis: sign of poor oxygenation ## "Pulsus Paradoxus" - Difference between systolic BP and diastolic BP. - Normal pulse pressure: 40-60 mmHg - Ex: More than (not normal) ## Intrinsic asthma: - Triggered by medication, dust ## Extrinsic Asthma: - Triggered by the environment and genetics (3-6x more likely) - Asthma: Antibodies which are produced when the immune system react with allergen. - IgE: Atopic dermatitis ## Rhinitis: - If you have these 3, you have an active antibody E: - rhinitis - Asthma - Atopic dermatitis ## For instance: - You have UKTI (triggered by microorganism) - Antigen is recognized by the Dendritic cells (antigen presenting cells) - Will bind to B-cells - Bind to antibodies (IgE): Interleukin 4&5 - Bind to mast cells (dominant asthma), cytokines (basophils) - By cleaning: Initiates inflammatory immune response. - Antigen will be presented to helper T-cells (thymus gland) - Orchestrates ## 3. Environment - Dust, chemicals ## 4. Infection: - URTI ## 5. Intrinsic factors: -"Stress", GERD - How it can cause asthma? - Weak esophageal sphincter: Causing the patient to vomit if there is a repeated flow of stomach acid in the lining (esophagus); It also can damage the lining of throat/airway leading to breathing difficulties and persistent cough. - If there’s a frequent exposure to acid, it also makes the lungs more sensitive to irritants (dust, pollen) which triggers asthma. - If a patient has stomach acid reflux it triggers a protective have reflex, which causes narrowing of the airway to prevent stomach acid to enter the lungs. ## 4. Irritants - Aerosols, perfume, smoke ## Classiic symptom of asthma: - Expiratory wheezing: Indicates that the patient’s condition is worsening. (Expected) ## 3 Common Symptoms: - **Other signs:** - Cough - Dyspnea - Wheezing - Use accessory muscle when breathing - Chest tightness: Due to air trapping/accumulation of CO2 - Diminished breath sounds: Due to hyperinflation - Tachycardia - Coughing - Increased secretion: Worse inflammation in your lungs. ## Endoscopic Procedures: - **Bronchoscopy**: Procedure that lets the doctor look at your lungs and air passages using a thin tube (bronchoscope). - **Thoracentesis**: Test that uses a thin flexible tube with a camera to examine the lungs and chest wall. - **Thoracentesis**: Removal of fluids/air in your lungs and chest wall. - **Biopsy**: Test to know the presence of malignancy. ## Asthma: -Heterogeneous disease: Means it has several etiologies. - Characterized by: - Chronic inflammation & hyperactivity of the airways. ## Triad pathology of asthma: 1. **Inflammation:** Lining of the airway is swollen; If swollen, it couldn't let in and out of the lungs. 2. **Obstruction:** There is a persistent limitation of airflow when you exhale 3. **Hyperactivity:** Hyperactivity of the airways in response to an allergic reaction; There’s twitching of the muscle in the airways (bronchospasm): Muscle around the airway constricts, which causes the airway to narrow. Also, causes irritation in the mucous gland, causing excessive mucus production. ## Asthma - A chronic condition: Waiting for a “trigger” to exacerbate the disease. ## Triggers of asthma: 1. **Allergens:** Pet dander (fur of cats and dogs). 2. **Drugs:** NSAIDs (ibuprofen): Disturbs the inflammatory pathways that trigger asthma. ## Diagnostic Evaluation. - **Pulmonary function test:** Assess respiratory function and determine the extent of dysfunction. - **Arterial blood gas:** Measures CO2 and O2 and pH levels from an artery. - **Pulse oximetry:** Measures saturation of hemoglobin. - **End tidal carbon dioxide**: Monitor partial pressure of CO2: COPD (88-92% is normal) - **Culture:** Identifies pathogens responsible for respiratory infections. - **Sputum studies:** Identify pathogens, organisms, determines malignant cells are present. ## Imaging Studies: - **Chest x-ray:** Produces images of your heart, lungs, blood, airways, and injuries. - **Computer tomography:** Helps health care providers detect disease and injuries: It uses a series of x-ray and computer to create detailed images. ## Contraindications for contrast dye: - Liancy function tests (creatinine and BUN) - Withhold metformin - Check for allergies in iodine. - **Pulmonary angiography:** Visualizes the pulmonary vessels. A radiopaque agent is injected. Used to investigate congenital anomalies and pulmonary emboli. - **Magnetic Resonance Imaging (MRI)**: Painless, non-invasive kit that uses magnetic and radio waves. - **Fluoroscopic studies:** Live x-ray images generated via camera to a video screen: Used to assist invasive procedures. ## Devices of Oxygenation: 1. **Nasal cannula:** - 1.4 L per min (flow rate) - FiO2: 20-40% 2. **Face mask:** - Flow rate: 4-6 L/ 6-10 L - FiO2: 40-60% 3. **Non-rebreather mask:** - Flow rate: 10-15 L - FiO2: 80-100% 4. **Venturi mask:** - FiO2: Up to 60%. ## Common sign and symptoms: - **Dyspnea:** Sudden dyspnea causes: pneumothorax, acute respiratory obstruction, allergic reaction, myocardial infarction. - **ARDS (Acute Respiratory Distress Syndrome):** Tachypnea, dyspnea, hypoxemia - **Cough:** Reflex of the lungs. - Coughing every night: Bronchial asthma and left sided heart failure - Coughing every morning: Bronchitis. - Coughing in supine position: Rhinitis. - Coughing after intake of food: Indicates aspiration. - **Production of sputum:** Actions of the lings in presence of irritants: - Purulent sputum (yellow, brown, green, mutt): Bacterial infection. - Thin mucoid sputum: Viral bronchitis. - Pink tinged sputum: Lung tumor - Frothy: Pulmonary edema - Mucoid: Pulmonary edema - **Chest pain:** Can be sharp/stabbing - **Wheezing** - **Hemoptysis** ## 2. Obstructive Lung Disease - Elimination of CO2, causing overexpansion of the lungs: - COPD - Pneumonia - Bronchitis ## 3. Ventilation Lung Disorder (alveoli) - accumulation of fluids in the lungs. - Disease: Pneumonia, Pulmonary edema, pleural effusion ## 4. Perfusion - Capillaries blockage: Disease: Pulmonary embolism ## Lung Volume and Capacities: - **Tidal Volume (TV):** Inhalation and exhalation; Volume of air in a normal quiet respiration. (MV: 500 mL / 0.5 L) - **Inspiratory reserve volume (IRV):** Volume of air containing in your lungs after you forcibly inspire it (MV: 2700 mL/ 2.5 L) - **Expiratory reserve volume (ERV):** Forceful expiration; Amount of IRV (MV: 1,000 mL / 1.5 L) - **Residual volume (RV):** Volume of air that you can’t expire forcefully. - IRV + TV = Inspiratory capacity (capacity of the lungs to inhale oxygen). - ERV + RV: Functional residual capacity (capacity of the paren to eliminate CO2) - **Total lung capacity:** Sum of TV, IRV, ERV, RV (air your lungs can hold (VL) - **FiO2:** Fraction of inspired oxygen (normal: 21%-24%) ## Breathing Patterns: - **Eupnea:** Normal breathing rate/pattern. - **Tachypnea:** Increased respiratory rate - **Bradycardia:** Decreased respiratory rate. - **Apnea:** Absence of breathing. - **Hyperpnea:** Increased depth and rate of breathing - **Cheyne-Stokes:** Gradual increases and decreases in respirations with periods of apnea - **Biot’s:** Abnormal breathing patterns with groups of rapid respiration at equal depth and regular apnea persists - **Kussmaul:** Tachypnea and hyperpnea with a prolonged inspiratory phase. - **Apneustic:** Prolonged inspiratory phase with a prolonged expiratory phase. ## Overview of Different Types of Lung Disorder: 1. **Restrictive Lung Disorder:** Restriction in the inhalation of oxygen. - Amyloidosis: Accumulation of protein in the lungs. Common in old age and rheumatoid arthritis. - Fibrosis: Thickening of the lungs. - Asbestosis: Accumulation of asbestos. ## Diaphragm - Inhale (contracts). - Exhale (relaxes). ## Normal Lung Sound: - **Bronchial:** High pitch sound. - **Bronchovesicular:** Moderate pitch. - **Vesicular:** Low pitch, heard on the lower lobe of the lungs (if you hear high pitch sounds, it indicates pneumonia). ## Adventitious sounds: - **Wheezing:** Asthma, COPD. - **Rhonchi:** Gurgling moist sound heard in patients with chronic bronchitis and lobar fibrosis. - Indicates upper airway obstruction - **Stridor:** - Indicates upper airway obstruction. - **Fine crackles and coarse crackles:** There’s accumulations of fluids. ## Diminished breath sounds: - **Pleural effusion**: Accumulation of fluid in the pleural cavity - **Pneumothorax**: Air in the thoracic cavity. ## Condition: Lung Sound, Vibration, Percussion, Mediastinal Shift -**Normal:** Normal, Normal, Resonance, none. - **Pneumonia:** Crackles, Normal, Dull, none. - **Pleural effusion:** Diminished, Decreased, Dull, yes, if large - **Pneumothorax:** Diminished, Decreased, Hyper resonance, yes. - **COPD:** Wheezing, Normal, Hyper resonance, none ## Pharynx (throat) - Oro: (throat) - Naro: (oval cavity) - Larynx: (adjacent to larynx) ## Epiglottitis: - Cause: Infection caused by Hib virus - Vaccine: HIB vaccine - Treatment: Tracheostomy, medication: Corticosteroids (ex.bethamethavone) - Endotracheal tube position: Tripod ## Larynx: - True vocal cords. - Glottis (above the vocal cords). - Plays a role in coughing: Most fundamental defense mechanism of the lungs - G: where O2 and CO2 goes in and out w/o gas exchange. ## Trachea - “Tracheomalacia: Collapse trachea.” - Wind pipe - Cartilage - Capillary pressure: 25 mmHg - Cause: Trauma, chronic respiratory infection, prolonged endotracheal tube usage. ## Right and left bronchi: - Begins at carina - Shorter and more vertical: - "Bomohiaku": No cartilage - **Alveoli:** Functional unit of gas exchange. - Has alveolar cell “pneumocytes." - Epithelium type 1 & 2. - Surfactant: Type II - Anti-trypsin: Inhibits elastase - It can cause collapse of the lungs - ## COPD: - Causes deficiency of anti-trypsin - Anti-trypsin: Reduces inflammatory cells (WBC) - Causes accumulation of elastin - Elastin (collagen fiber) - Elastin: Holds elastin for expansion and recoil of the lung. ## Respiratory system: - System responsible for gas exchange, inspiration of 02 and expiration of CO2. ## Secondary functions: - Facilitates sense of smell. - Produces sound (larynx) - Maintains acid-base balance (respiratory rate regulates carbonic acid balance in the blood). - Maintains body water level: Breathing rapidly inhales more CO2, If there is a loss of CO2, causes reduction of carbonic acid in blood. Respiratory rate adjusts. - Plays a role in maintaining water in the body. - Release water vapor - Heat balance. - Respiratory warms the air to match our body temperature. ## Upper Respiratory tract (URT) - Nasal cavity, nostril, oral cavity, pharynx, larynx, trachea ## Lower Respiratory tract (LRT) - Right main bronchus, left main bronchus, right lung, diaphragm ## Nasal Sinuses - **Function:** Humidification: Warm and humidified inspired air - **Maxillary:** - **Ethmoid:** - **Frontal:** - **Sphenoid:** - Turbinates: Warms and humidifies inspired. - Vibrivae: Nasal hair - Mucus: Traps and filters organism (lysozyme) - plays a role in neutralizing microorganisms, pathogens that are entering our airway. - **Note:** Cold air makes the system lose moist air. ==End of OCR==