Pulmonology 5

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HuskerDevil
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94464
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Pulmonology 5
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2011-07-18 16:59:09
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DPAP2012 Pulmonology
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Pulmonology flashcards made by previous students
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  1. Cleanses, warms, & moistens air
    LUNGS: Airway Tree
  2. Distributes air to deeper parts of the lung
    LUNGS: Airway Tree
  3. Dilation/constriction of smooth muscle determines ease of air flow; Defense – mucociliary transport system
    LUNGS: Airway Tree
  4. Site of Gases Exchange
    Alveoli/Capillary
  5. Defined as the exchange of air between the atmosphere and the alveoli.
    Ventilation
  6. occurs in three stages: inhalation & gas exchange (between alveoli-capillaries & blood-tissues); oxidative metabolism (in cells) generates CO2 & ATP; Tissue-blood gas exchange & exhalation to remove CO2
    Respiration
  7. is the airflow in the lungs
    Ventilation
  8. inhalation & gas exchange (between alveoli-capillaries & blood-tissues).
    Respiration
  9. - oxidative metabolism (in cells) generates CO2 & ATP
    Respiration
  10. Tissue-blood gas exchange & exhalation to remove CO2
    Respiration
  11. resides in Brainstem
    Autonomic Respiration
  12. originates in cerebral cortex and can override autonomic control.
    Voluntary ventilation
  13. Diaphragm and accessory muscles; Coordinated through phrenic, intercostal, cranial and cervical nerves; Chemoreceptors and mechanoreceptors
    Respiration
  14. blood is 100% saturated
    Arterial blood
  15. blood is typically 75% saturated
    Venous blood
  16. 0-60mmHg -slope
    Binding Cooperativity: Steep slope
  17. 60-100mmHg -slope
    Binding Cooperativity: Flat slope
  18. provides an inexpensive, noninvasive alternative means of monitoring hemoglobin saturation with oxygen.
    Oximetry
  19. Affected by: Severe anemia, Abnormal hemoglobin, Presence of intravascular dyes & Lack of pulsatile arterial blood flow
    Pulse oximetry is affected by
  20. falls with increasing altitude.
    Normal arterial Po2
  21. Shape and Symmetry: anterior and posterior chest
    Inspection
  22. Assesses airflow through the tracheobronchial tree
    Auscultation
  23. soft, low-pitched. Heard over most of lung fields.
    Vesicular breath sounds
  24. medium pitched. Heard over main bronchus & (R) upper posterior lung.
    Bronchovesicular breath sounds
  25. loud, high-pitched. Only heard over trachea.
    Bronchotracheal breath sounds
  26. Inspiration > expiration
    Vesicular breath sounds
  27. Inspiration = expiration
    Bronchovesicular breath sounds
  28. Expiration slightly > inspiration
    Bronchotracheal breath sounds
  29. Added or extra sounds; Are always abnormal and usually indicate underlying respiratory and/or cardiac pathology
    Adventitious Lung Sounds
  30. discontinuous; heard more often in inspiration; not usually cleared by coughing; dry or wet; fine, medium or coarse
    Crackles
  31. small airways forced open in disruptive fashion
    Crackles physiology:
  32. continuous; fog horn or snoring quality usually clear with coughing
    Rhonchi
  33. air passing through an obstructed airway. thick secretions, tumor
    Rhonchi physiology:
  34. continuous, musical, high-pitched sound (tea kettle); most commonly heard in asthma and is diffuse and usually bilateral
    Wheezes
  35. forceful air flow through a constricted airway
    Wheezes physiology:
  36. in a pediatric patient suggests foreign body aspiration
    unilateral wheezing
  37. Inflamed pleural surfaces rubbing together
    Rub
  38. Pleural sound; Like leather rubbing together; Evanescent and depend on amount of fluid in pleural space
    Rub
  39. transmitted voice sounds
    Vocal resonance
  40. Assess anywhere on chest where adventitious sounds are heard; Normally voice sounds on auscultation are muffled & unclear
    Vocal resonance
  41. Increased transmission of voice sounds indicate
    airless lung
  42. E” is heard as “A”
    Egophony:
  43. “99” sounds louder, clearer
    Bronchophony:
  44. whispered sounds are clear
    Whispered pectoriloquy:
  45. An uncomfortable awareness of breathing, not appropriate to the level of exertion
    Dyspnea
  46. Chest “tight”; “Can’t get enough air in”; “Wake up in middle of night short of breath”; “Short of breath”; ask for Scale of zero to ten
    Dyspnea
  47. Dyspnea onset minutes or hours
    Dyspnea Acute
  48. Dyspnea develops over weeks to months
    Dyspnea Chronic
  49. Acute MI; Congestive heart failure, Cardiac tamponade
    Causes of acute dyspnea: Cardiovascular system
  50. Bronchospasm, Pulmonary infection – bronchitis, pneumonia, Pulmonary embolism Pulmonary edema, Pneumothorax, Upper airway obstruction
    Causes of acute dyspnea: Respiratory system
  51. Asthma, COPD, Interstitial lung disease, Cardiomyopathy
    Causes of chronic dyspnea
  52. History and physical exam lead to accurate diagnoses in approx 2/3 of patients
    Dyspnea – Evaluation
  53. Oximetry/ABG; CXR; Spirometry; CBC; ECG
    Dyspnea – Evaluation
  54. Treat the cause; Oxygen; Pulmonary rehab; Treat anxiety
    Dyspnea - Treatment
  55. Clears the tracheobronchial tree of mucus, foreign particles, and noxious aerosols
    Cough
  56. One of the most common reasons for outpatient visits; May impair sleep and social functioning
    Cough
  57. Cough < 3 weeks
    Cough Acute
  58. Cough >3 weeks
    Cough Persistent
  59. women > men to develop
    chronic Cough
  60. Stimulated cough centers in resp tract send impulses to cough center in
    medulla
  61. Most commonly associated with URI; Other causes pneumonia, aspiration, pulmonary embolism, pulmonary edema
    Acute cough
  62. Low-grade chronic bronchitis; Increased intensity and intractability of pre-existing cough – think lung cancer
    Persistent cough in Smokers
  63. Upper airway cough syndrome (postnasal drip); Asthma; Gastroesophageal reflux (GERD)
    Persistent cough in Nonsmokers
  64. ACE inhibitor-induced cough
    Persistent cough
  65. Fatigue, Insomnia, Headache, Urinary incontinence, Rib fractures (ribs 5-7)
    Cough - Complications
  66. History and physical exam [Timing of cough, Sputum production, Nasal discharge, Frequent throat clearing, Wheezing] Chest x-ray esp in smokers or fever/wt loss patients
    Cough - Evaluation
  67. Treat underlying cause; Eliminate irritant exposures; Smoke, occupational agents;
    Cough - Treatment
  68. Persistent cough after URI (think)
    asthma
  69. Expectoration of blood originating below the vocal cords
    Hemoptysis
  70. Most likely from bronchial arteries (under more pressure than pulmonary circulation)
    Hemoptysis
  71. upper resp tract bleeding and upper GI bleed
    mimics of Hemoptysis
  72. Bronchitis; Bronchogenic carcinoma; Pneumonia
    Hemoptysis - Most common causes in U.S.:
  73. Infection (TB most common cause of hemoptysis worldwide); Goodpasture’s syndrome, Wegener’s granulomatosis, Auto-immune (e.g., lupus pneumonitis), Iatrogenic (drug-induced, radiation), Cocaine-induced
    Hemoptysis -Parenchymal diseases
  74. A-V malformation; Pulmonary embolism; Elevated pulm cap pressure (mitral stenosis or LVH); Iatrogenic (Swan-Ganz catheter)
    Hemoptysis- Pulmonary vascular disorders
  75. History and physical exam; Chest radiograph; Hematocrit; U/A and renal function; Coag profile; Further eval – bronchoscopy/HRCT
    Hemoptysis - Evaluation
  76. Treat underlying cause; Risk factors for tumor - aggressive workup [ >40 yo, >40 pack yr history of smoking, > 1 week of hemoptysis]
    Hemoptysis - Treatment
  77. substance that can donate a H+ ion (Lowers pH)
    ACID
  78. substance that can accept a H+ ion (Raises pH)
    BASE
  79. Metabolism of carbohydrates & fats generates 15,000 mmol of CO2; CO2 combines w/ water to form H2CO3
    CARBONIC ACID
  80. Metabolism of proteins forms 50-100 mmol of acid which the kidney must excrete
    NONCARBONIC ACID
  81. oxidation of sulfur-containing amino acids generates
    H2SO4
  82. compound that binds H+ when the [H+] rises and releases it when the [H+] falls. The body buffers are primarily weak acids (HPO4-2 + H+ H2PO4-)
    BUFFER
  83. HA
    ACID
  84. H+=
    CATION
  85. A¯=
    ANION
  86. Help in Diagnosis; Measure Respiratory Function; Make Changes in Treatment, Ventilator Settings, Monitor Acid Base Balance, For Example DKA
    Arterial Blood Gas
  87. pH Measures
    Percent of H+ Concentration
  88. pCo2 Measures
    Pressure of Carbon Dioxide
  89. pO2 Measures
    Pressure of Oxygen
  90. HCO3 Measures
    Bicarbonate
  91. SaO2 Measures
    Oxygen Saturation
  92. BE Measures
    Base Excess
  93. Arterial Blood Gas Measures
    pH, pCo2, pO2, HCO3, SaO2, BE
  94. Normal Value: pH
    7.35 - 7.45
  95. Normal Value: pCo2
    35-45
  96. Normal Value: pO2
    80-100
  97. Normal Value: HCO3
    24
  98. Normal Value: SaO2
    80-100%
  99. Normal Value: BE
    +/- 2
  100. CO2 is an acid and reflects lung function; causes
    respiratory disorder
  101. HCO3 is a base and reflects Kidney function; causes
    metabolic disorder
  102. exerting opposite effect on pH
    CO2 and HCO3
  103. are highly reactive especially with proteins
    H+ ions
  104. There is a change in charge distribution that leads to a change in molecular configuration which leads to a change in protein function
    When proteins gain or lose H+ ions
  105. The H+ concentration varies little from 40 nanomol/L & is regulated by:
    Chemical buffering by IC & EC buffers
  106. Control of partial pressure of carbon dioxide is by
    ventilation changes (pulmonary)
  107. Control of plasma bicarbonate concentration is by changes in
    renal excretion of H+
  108. maintain the correct balance of substances in the body including H+ and HCO3-
    Kidneys and Lungs
  109. The vast majority of the acid produced per day is buffered and removed when
    CO2 is exhaled. (CARBONIC ACID)
  110. Kidneys excrete acid via
    titratable acid and ammoniagenesis
  111. Kidneys excrete acid via
    titratable acid and ammoniagenesis
  112. BICARBONATE BUFFERING SYSTEM: Under the control of the kidneys:
    metabolic
  113. BICARBONATE BUFFERING SYSTEM: Under the control of the lungs:
    respiratory
  114. + =hydrogen ion concentration in nmol/L
    H+
  115. #NAME?
    Pco2
  116. #NAME?
    HCO3-
  117. Compare Bicarb from
    Chem7
  118. The pH must be defended and maintained near
    7.4
  119. HOW DOES THE KIDNEY REGENERATE BICARBONATE?
    IT ACIDIFIES THE URINE (pH 5-6)
  120. URINARY ACIDIFICATION
    AMMONIAGENESIS
  121. normal pH
    7.4
  122. normal CO2
    40
  123. normal HCO3
    24
  124. decrease pH; decrease HCO3, decrease CO2
    Metabolic Acidosis
  125. decrease pH, increase HCO3, increase CO2
    Respiratory Acidosis
  126. increase pH, increase HCO3, increase CO2
    Metabolic Alkalosis
  127. increase pH, decrease HCO3, decrease CO2
    Respiratory Alkalosis
  128. causes Anion Gap METABOLIC ACIDOSIS (AGMA)[MUDPILERS]
    Methanol, Uremia, Diabetic/Starvation Ketoacidosis, Paraldehyde/Phenformin Isopropyl Alcohol, Isoniazid, Lactic Acidosis, Ethylene Glycol/Ethyl Alcohol Rhabdomyolysis, Salicylates, Other Causes: Hyperalbuminemia, iatrogenic
  129. Anion Gap =
    Na – (Cl +HCO3)
  130. Diarrhea, lose
    NAGMA
  131. Acid w/o Cl added; H+ buffered HCO3; Anion is added to non measured pool to inc AG
    AGMA
  132. Uretero sigmoidoscopy, Small Bowel Fistula, Excess Chloride & Diarrhea(Most Common), Carbonic Anhydrase Inhibitor/CRF, Renal Tubular Acidosis, Addison’s Disease, Pancreatic Fistula
    METABOLIC ACIDOSIS: Non Anion Gap (NAGMA)
  133. HYPERCHLOREMIC METABOLIC ACIDOSIS=
    NONANION GAP METABOLIC ACIDOSIS
  134. IF YOU GET ACIDOTIC FROM DIARRHEA, WHAT DOES THE KIDNEY DO?
    MAKE MORE BICARB!
  135. How does the kidney make more bicarb?
    INCREASE NH4+ URINARY EXCRETION
  136. to differentiate between renal and extrarenal causes of NAGMA.
    Calculate Urine Anion Gap (UAG)
  137. U[Na] + U[K] – U[Cl]
    Urine Anion Gap (UAG)
  138. Normal Urine Anion Gap (UAG)
    -10 to +10
  139. Decreased UAG < -10
    Extrarenal NAGMA
  140. Increased UAG > +10
    Renal NAGMA
  141. Kussmaul’s respirations
    METABOLIC ACIDOSIS
  142. decreased LOC leads to Coma; Weakness, decreased DTRs, Tachycardia( increased CO to decreased CO that leads to Hypotension and Dysrhythmia; Kussmaul’s respirations; Warm, flushed skin & mucous membranes; Anorexia, Nausea and Vomiting, increased K+
    METABOLIC ACIDOSIS: Signs and Symptoms
  143. Hydration, Correct the underlying cause: Insulin, Antidiarrheal medications, Dialysis. Note: Sodium Bicarb is not routinely given
    METABOLIC ACIDOSIS: Treatment
  144. Lungs fail to eliminate CO2
    ACUTE RESPIRATORY ACIDOSIS
  145. CNS Depression: Sedatives, CVA, Head trauma
    ACUTE RESPIRATORY ACIDOSIS
  146. Neuromuscular Disease: Myasthenia, GBS, Polio, Muscular dystrophy, hypokalemia
    ACUTE RESPIRATORY ACIDOSIS
  147. Impaired Lung Mechanics: Pleural effusion, pneumothorax, crush injury
    ACUTE RESPIRATORY ACIDOSIS
  148. Acute airway Obstruction: Foreign body aspiration, tumor, laryngospasm, bronchospasm
    ACUTE RESPIRATORY ACIDOSIS
  149. Acute Respiratory Disease: Severe Pneumonia, Pulmonary Edema
    ACUTE RESPIRATORY ACIDOSIS
  150. Lungs fail to eliminate CO2
    CHRONIC RESPIRATORY ACIDOSIS
  151. COPD, Pickwickian Syndrome, Thoracic Cage, Limitations: Kyphoscoliosis, Scleroderma, Chronic Neuromuscular diseases
    CHRONIC RESPIRATORY ACIDOSIS
  152. decreased LOC, Weakness, decreased DTRs, Ineffective respiratory efforts, increased [K+] if acute; Tachycardia leads to increased CO to decreased CO to Hypotension and Dysrhythmia
    RESPIRATORY ACIDOSIS Signs and Symptoms:
  153. Maintain patent airway with enhanced gas exchange: Meds, O2, Pulmonary toilet, ventilatory support, monitor ABGs to make appropriate adjustments in therapy; Assess LOC frequently; Modify diet to Low carbohydrate and high fat
    RESPIRATORY ACIDOSIS Treatment:
  154. A PRIMARY INCREASE IN HCO3
    METABOLIC ALKALOSIS
  155. THE PATHOGENESIS OF CHRONIC METABOLIC ALKALOSIS INVOLVES TWO DISTINCT PHYSIOLOGICAL DERANGEMENTS
    GENERATION & MAINTENANCE
  156. by either an addition of bicarbonate /a loss of acid or /a loss of a fluid containing proportionally more chloride than bicarbonate
    A PRIMARY INCREASE IN HCO3 in METABOLIC ALKALOSIS
  157. H+ loss from ECF space, HCO3- retention, Contraction alkalosis
    GENERATION
  158. Decreased ECF/Chloride depletion, Persistent mineralocorticoid excess, Hypercapnia, Potassium depletion(profound)
    MAINTENANCE
  159. Urine Chloride < than 15 mEq/L; Extracellular Fluid Contraction; Saline responsive (corrects volume contraction)
    Chloride Responsive Metabolic Alkalosis
  160. Urine Chloride > 15 mEq/L; Associated with excess mineralocorticoid; Associated with Hypokalemia; Saline unresponsive
    Chloride Resistant Metabolic Alkalosis
  161. Saline responsive (corrects volume contraction)
    Chloride Responsive Metabolic Alkalosis
  162. Saline unresponsive
    Chloride Resistant Metabolic Alkalosis
  163. Gastrointestinal Causes: Vomiting, NG suction, Chloride wasting diarrhea, Villous Adenoma
    Chloride Responsive Metabolic Alkalosis
  164. Renal Causes: Diuretic use, Carbenicillin, Penicillin, Sulfate, Phosphate, Post- hypercapnia
    Chloride Responsive Metabolic Alkalosis
  165. Exogenous Alkali: Sodium Bicarb, Sodium Citrate, Lactate, Gluconate, Acetate, Transfusion, Antacid
    Chloride Responsive Metabolic Alkalosis
  166. Cystic Fibrosis & Achlorhydria
    Chloride Responsive Metabolic Alkalosis
  167. Hypertensive Patient: Adrenal Disease: 1° Hyperaldosteronism, Cushing Syndrome, Liddle Syndrome
    Chloride Resistant Metabolic Alkalosis
  168. Hypertensive Patient: Exogenous Steroids: corticoids, licorice, carbenoxalone, glycyrrhizic acid, chewing tobacco
    Chloride Resistant Metabolic Alkalosis
  169. Normotensive Patient: Bartter or Gitelman Syndrome, Hypokalemia, Milk- alkali syndrome, Refeeding alkalosis, excessive alkali administration
    Chloride Resistant Metabolic Alkalosis
  170. Hallmark sign: increased bicarbonate level with rising PCO2
    METABOLIC ALKALOSIS
  171. Shallow slow breathing, Anxiety and irritability, (+)Chvostek’s sign (+)Trousseau’s sign, decreased [K+] & [Ca+]; Paresthesias, muscle cramping and weakness; Tetany and seizures; Tachycardia, may be hypotensive, palpitations; increased bicarb & PCO2
    METABOLIC ALKALOSIS Signs and Symptoms:
  172. Antiemetic medications; Monitor electrolytes and replace as indicated - Potassium sparing diuretic; Seizure Precautions
    METABOLIC ALKALOSIS: Treatment:
  173. Lungs eliminate Too much of CO2
    RESPIRATORY ALKALOSIS
  174. Increased Central Respiratory Drive: Anxiety, CNS infection, CVA, Brain tumor, Head trauma Medications: Salicylates, Nicotine, Aminophylline, progesterone, catecholamines, fever, sepsis, pregnancy, liver failure, hyperthyroidism
    RESPIRATORY ALKALOSIS
  175. Increased Chemoreceptor Stimulation: Anemia, CO poisoning, pulmonary edema, pneumonia, PE, high altitude, restrictive lung disease
    RESPIRATORY ALKALOSIS
  176. Iatrogenic: faulty settings with the mechanical ventilator
    RESPIRATORY ALKALOSIS
  177. CNS, Hypotension, Excess mechanical ventilation, Atelectasis, Pain, Cirrhosis Hypermetabolic State, Insufficient, Oxygenation, Psychogenic, Salicylates/Sepsis
    RESPIRTORY ALKALOSIS
  178. Rapid deep respirations, Anxiety and irritability, + Chvostek’s sign + Trousseau’s sign; decreased [K+] & [Ca+]; Paresthesia, muscle cramping and weakness; Tetany and seizures; Tachycardia, may be hypotensive, palpitations
    RESPIRATORY ALKALOSIS: Signs and Symptoms:
  179. Monitor ABGs periodically; Decrease respiratory rate: - focused breathing, decrease breaths per minute on ventilator settings, O2 therapy; Antianxiety medications
    RESPIRATORY ALKALOSIS: Treatment
  180. Acidemia
    pH < 7.4
  181. Alkalemia
    pH > 7.4
  182. For every increase in pCO2 of 10mm, pH decreases by .08
    Acute Respiratory Acidosis:
  183. For every increase in pCO2 of 10mm, pH decreases by .03
    Chronic Respiratory Acidosis
  184. For every decrease in pCO2 of 10mm, pH increases by .08
    Acute Respiratory Alkalosis:
  185. For every decrease in pCO2 of 10mm, pH increases by .03
    Chronic Respiratory Alkalosis:
  186. Anion Gap normal
    12
  187. change in anion Gap (AG)
    Patient’s AG – Normal AG (12)
  188. Corrected HCO3
    change in AG + patient’s HCO3
  189. If corrected HCO3 = 24
    Pure AGMA
  190. If corrected HCO3 = <24
    AGMA + NAGMA
  191. If corrected HCO3 = >24
    AGMA + Additional Metabolic Alkalosis

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