Patho unit 7 ch. 26

  1. Pulmonary Disease: Signs and Symptoms 
    • Also known as shortness of breath
    • Breathlessness, air hunger, labored breathing
    • Caused by increased airway resistance
    • symptoms: breathing is uncomfortable
    • Signs: Flared nostrils and use of accessory muscles (shoulders and arms)
  2. Pulmonary Disease: Signs and Symptoms 
    • A protective reflex that cleans airways with an explosive expiration to remove foreign particle
    • Should it be suppressed? Not usually only for severe discomfort
  3. Pulmonary Disease: Signs and Symptoms 
    Abnormal sputum
    • Sputum is mucus mixed with substances in lower respiratory tract (passenger on the mucociliary escalator)
    • Changes (color, consistency, odor, and amount) provide information about a disease and disease progression
  4. Pulmonary Disease: Signs and Symptoms 
    Hemoptysis (Blood/coughing)
    • Coughing up blood or bloody secretions 
    •   -usually bright red (mixing air and red blood cells  keeps them oxygenated)
    •   -Localized infection or alveolar-capillary membrane
  5. Kussmaul Respiration
    • Decrease in blood pH (increase in plasma [H+]) causes hyperventilation 
    • Results in :
    •   -Increased respiratory rate
    •   -Large increase in tidal volume
    •   -no expiratory pause
  6. Cheyne-Stokes Respiration
    • Breathing Fuctuates
    •   -periods of apnea or hypopnea alternating with period of hyperpnea
    • Occurs in about half of patients with congestive heart failure or neurological disease including stroke
    • More common during sleep
  7. Hypoventilation
    • alveolar gas exchange insufficient for metabolic demands
    •   -increased PCO2
    •   -respiratory acidosis
  8. Hyperventilation
    • alveolar gas exchange greater than metabolic demands
    •  -decreased PCO2
    • respiratory alkalosis
    • causes: anxiety, head injury, pain, decreased PCO2
  9. Pulmonary Disease: Signs and Symptoms 
    • Bluish discoloration of mucous membranes and skin caused by increased amounts of deoxygenated hemoglobin 
    •   -O2 saturation is a measure of how many oxygen binding sites on hemoglobin are occupied 
    •   -Normal:
    •    -O2 saturation 97-99% in arterial blood
    •    O2 saturation 75% in venous blood
    •   -Cyonosis
    •    -O2 saturation <85% in arterial blood
  10. Pulmonary Disease: Signs and Symptoms 
    • Increased connective tissue and vasculature in fingers/toes because of chronic anoxia
    • Mechanism unclear
    •   -probably due to some sort of chemical signaling 
    •   -prostiglandins, ferritin, bradykinin, estrogen, platelet derived growth factor, hepatocyte growth factor and growth hormone have been suggested
  11. Pulmonary Disease: Signs and Symptoms 
    Pleuritic Pain
    • Sharp stabbing pain associated with breathing (like being stabbed with an ice pick)
    •   -From disorders affecting the pleurae, airways, and chest walls
  12. Ventilation-Perfusion Coupling
    • Pulmonary ventilation (V.): amount of air in liters entering the lungs per minute
    •   -V.A: amount of air ( in liters) entering alveoli per minute
    • Perfusion (Q.): amount of blood that flows through the lung capillaries each minute
    • Ventilation-Perfusion Coupling: The matching of pulmonary blood flow to oxygen
    •   -under hypoxic conditions pulmonary blood vessels constrict
    •   -forces or shunts blood to areas of higher oxygen
  13. Ventilation-Perfusion Coupling
    • In healthy individuals:
    •   -V.A= 4.5L/min
    •   -Q. =5.0 L/min
    • Ideally, the ventilation/perfusion ratio is about 1
    • If no air enters the lungs, V.A/Q.=zero
    •   -blood flows but no gas exchange takes place
    • If air enters  the lungs but blood does not flow, V.A/Q.=oo
    •   -For example, if blood clot lodges in lung (pulmonary embolism)
    •   -Blood is not oxygenated ad cannot release waste CO2
  14. Hypercapnia
    Blood [CO2] too high
    • Depression of respiratory center by drugs
    • Diseases of the medulla
    •   -respiratory centers of brainstem affected by infection or trauma
    • Problem with phrenic nerve innervation 
    •   -polio, amyotyrophic lateral sclerosis, spinal cord injury
    • Diseases of the neuromuscular junction
    •   -myasthenia gravis, muscular dystrophy 
    • Thoracic cage trauma or congenital deformity 
    • Large airway obstruction
    •   -Tumors, apnea
    • Physiologic dead space
    •   -emphysema 
  15. Hypoxemia
    Blood [O2] too low
    • Problem with oxygen delivery to alveoli
    •   -reduced PO2
    •   -reduced ventilation of alveoli (V.A)
    • Problem with oxygen moving across the alviolar-capillary membrane
    •   -V.A/Q. mismatch
    •   -Blocage in alveolar-capillary  (A-C) membrane
    • Problem with blood arriving to be oxygenated
  16. Pnuemothroax
    • if air can leak into the plural cavity, then thoracic cavity cannot develop a pressure difference
    • No pressure difference , and surface tension (even with sufactant) takes over and causes the delicate alveolar-capillary membrane to collapse in on itself 
    • When this happens all over the lung, the entire lung collapses and pneumothorax results 
    • This is a special case of the more genera term atelectasis, any abnormal structure in the alveoli of the lung
  17. Atelectasis
    • any abnormal structure in the alveoli
    • If the alveoli resemble a bunch of grapes then atelectasis is what happens when the grapes are smashed
    • External respiration depends critically in the normal structure of alveoli
    • Obviously, atelectasis interferes with gas exchange
  18. Pleural Effusion
    • Any abnormal or excessive liquid in the alveoli interferes with external respiration - dyspnea
    • Transudative efusion 
    •   -increase in hydrostatic pressure or decreasein oncotic pressure in capillary (i.e starling forces that promote edema)
    •   -This is the mechanism of pulmonary edema in congestive heart failure
    • Exudative effusion
    •   -increase in capillary permeability that allows blood cells and/or plasma proteins to leak into alveoli
    •   -Empyema 
    •    -pus (i.e neutrophils and dead invaders)
    •   -Hemothorax
    •    -blood
    •   -Chylothorax
    •    -chyle (lymph and fats) 
  19. Bronchiectasis
    • Remodeling of the bronchi due to chronic inflammation 
    • Bronchial smooth muscle replaces with connective tissue 
    • This increases the width of bronchi, but mucus narrows the lumen and makes it difficult to pass air through the conducting portion of the airways
  20. Bronchiolitis
    • chronic inflammation of the bronchioles
    • Like bronchiectasis, fibrous connective tissue replaces functional tissue (such as smooth muscle)
    • Narrowing of bronchiole lumen
  21. Pulmonary Edema
    see slides on p.295
  22. Pulmonary Edema :
    Heart Disease
    • Valvular dysfunction, Coronary artery disease, Left ventricular dysfunction
    • These cause increased pressure in left atrium
    • Which causes increased pulmonary capillary hydrostatic pressure
    • Resulting in Pulmonary edema
  23. Pulmonary Edema:
    Injury to Capillary Endothelium
    • Increased capillary permeability &decreased surfactant produciton
    • causes fluids and proteins to leak into interstitial space and into alveoli
    • Resulting in Pulmonary edema
  24. Pulmonary Edema:
    Blockage of lymphatic vessels
    • Fluid not removed from interstitial space
    • Causes fluid to accumulate in interstitial space
    • Resulting in Pulmonary edema
  25. Acute Respiratory Distress syndrome (ARDS)
    • ARDS is the most severe manifestation of acute lung injury in adults
    •   -also occurs in children
    • All disorders that result in ARDS acutely injure the alveolar-capillary (A-C) membrane, causing severe pulmonary edema and markedly reduced compliance (elastic properties) of the lung
  26. ARDS: Step 1
    • Neutrophils release a battery of inflammatory mediators
    •   -Proteolytic enzymes, O2 free radicals, and pro-inflammatroy cytokines
    • This leads to pulmonary vasoconstriction, vascular occlusion, and pulmonary hypertension
  27. ARDS: Step 2
    The damaged alveolar epithelial barrier breaks, allowing flooding of the alveolar space and making it difficult or impossible for oxygen to diffuse into the capillaries
  28. ARDS: Step 3
    • Edema overwhelms type ll alveolar cells (septal cells)
    •   -these cells make surfactant to reduce lung surface tension
    •   -now they cannot make enough surfactant to compensate for the huge amounts of liquid 
    •   -surface tension of liquid causes the delicate alveoli to collapse
  29. ARDS: Step 4
    • See slide on p. 296
    • Protein and enzymes make a jelly-like substance called the hyaline membrane
    • The figure below shows alveoli filled with hyaline membrane
    •   -not much gas exchange can take place
    • ARDS requires treatment with mechanical ventilation
  30. Asthma
    • More common in the young
    • Manifestations
    •   -Dyspnea, prolonged expiration with eiratory wheezing, early nonproductive cough, tachycardia, tachypnea and acidosis
    • Treatment
    •   -Inhaled bronchodilators
    •    -decrease smooth muscle spasm
    •   -Anti-inflammatory agents (glucocotgicoids and leukotriene receptor blockers)
    •    -decrease production, release or binding of inflammatory mediators 
  31. Chronic Obstructive Pulmonary Disease (COPD)
    • Signs/symptoms and treatments of chronic bronchitis and emphysema are very similar
    • Therefore, both called COPD
    • Signs/symptoms of COPD
    •   -exercise intolerance, dyspnea, whezzing, productive cough, hypoxemia causing polycythemia and cyanosis, pulmonary hypertension, and congestive heart failure
  32. Emphysema Part 1
    • Enlargement and destruction of alveoli (lung remodeling), loss of elasticity , and trapping of air
    • Cigarette smoking always results in emphysema
    •   -Chemicals in cigarette smoke inhibit a key lung enzyme called a1-antitrypsinase
    •   -this blocks neutrophil elastase and prevents it from breading down elastin 
    •   -In the absense of a1-antitrypsinase, elastase breaks down the elastic connective tissue of the alveolar wall, replacing it with non-elastic , fibrous connective tissue(alveolar remodeling)
    •   -patients with a mutation causing a1-antitrypsinase deficiencey (1/1500 persons of European descent) have syndrome where this occurs spontaneously, in absence of cigarette smoke
  33. Emphysema part 2
    • Sign and symptoms
    •   -Dyspnea
    •   -Late developing cough
    •   -Tachypnea
    •   -Prolonged expiration
    •   -Pulmonary hypertension
    •   -Barrel chest
    • Ironically, inspiration is intact, but ability to expire is reduced 
    •   -Loss of elstin makes lungs less elastic 
    •   -Lungs become over-inflated 
    •   -Muscles in chest wall forced to work harder to expel air
  34. Chronic Bronchitis
    • In chronic Bronchitis, the obstruction is caused by inflammation and thickening of the respiratory mucus membranes, ciliary impairment, accumulation of mucus and pus
    • We don't see lung remodeling unless emphysema is also present 
    • Causes: cigarette smoking, air pollutants, infections
  35. Treatment of COPD
    • Treatment is virtually the same for emphysema and chronic bronchitis 
    •   -smoking cessation 
    •   -Antibiotics:
    •    -given prophylactically because of patient's susceptibility to infection 
    •   -Bronchodilators
    •   -Anti-inflammatory drugs: glucocorticoids
    •    -Leukotriene inhibitors (e.g. Singulair) less effective
    •   -O2 administration
  36. Pneumonia
    • Acute infection of the lower respiratory tract
    •   -Caused by rickettsiae, mycoplasma, and other bactieria;fungi and viruses are also implicated
    • Commonly-acquired
    •   -Steptococus pneumoniae
    •   -Mycoplasma pneumoniea ("walking pneumonia")
  37. Pneumonia part 2
    • Hospital acquired (nosocomial infection)
    •   -Staphylococcus aureus and Kiebsiella pneumoniae
    •   -Occurs in patients with COPD or patients with a viral respiratory illness
    • Pneumonia of immunocompromised individuals
    •   -Fungi pneumonia (pneumocystis jiroveci) often seen in AIDS patients
    •    -old name pneumocystis carinii
    •    -Often still called PCP (
  38. Pneumonia part 3
    • Organisms reach the lungs by:
    •   -Inspiration or aspiration of oropharyngeal secretions
    •   -Via the circulation (systemic infection, sepsis, or needle contamination)
    • Normal lung degense(cough reflex, mucocillary clearance and phagocytosis) become inadequate or compromised
    •   -e.g. cilia or the mucociliary escalator paralyzed by chemical in cigarette smoke or preexisting COPD
  39. Pneumonia par 4
    • In most individuals susceptibility, not exposure . is the overriding factor
    •   -the pathogen is not contained 
    •   -Toxins are released that damage bronchial mucus membranes and alveolar capillary membranes
    •   -Exudative edema and dibris fill the bronchioles and ventilation/perfusion (V.A/Q.) mismatch results in shunting
  40. Signs and symptoms of Pneumonia
    • Often a productive cough
    • Pleuritic chest pain, chills, malaise
    • Inpiratory crackles
    • Evidence of infiltrates on x-ray is the key diagnostic feature
  41. Pneumonia treatment
    • treatment depends on where the disease was acquired, the causative organism, and the severity of the disease
    •   -Antibiotics ,supplemental oxygen, and in severe cases mechanical ventilation 
  42. Tuberculosis
    • Infection caused by Mycobacterium tuberculosis, and acid-fast bacillus that affects the lungs
    • Incidence is increasing due to drug resistant strains and possibly related to HIV infections
    • Emigration, crowded institutional settings, substance abuse and poor access to medical c are also contribute
Card Set
Patho unit 7 ch. 26
Patho unit 7 ch. 26