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CRRAB II Week 4 - WLB > PBL #4 > Flashcards

Flashcards in PBL #4 Deck (14):

How does anatomy and physiology describe the coupling of the lungs and thorax?

The lungs are not directly attached to the chest wall but they change their volume and shape according to the changes in shape and volume of the thoracic cavity. Pleura covering the surfaces of the lungs (visceral) or the thoracic cavity (parietal) together with a thin (20 μ m) layer of liquid between them create a liquid coupling.


What is the quick & dirty pathophysiology of a pneumothorax?

  • Degradation of pulmonary elastic fibers leads to → formation of subpleural bullae
  • Presence of bullae induces → inflammation → producing small airway obstruction
  • Alveolar pressure > intrapleural pressure, resulting in intrapleural air and lung deflation


What are the mechanisms of normal ventilation?

  • Expansion of the chest by mechanical stimulation (muscles: Diaphragm, anterior scalenes, external intercostals, pectoralis minor) → fluid in the pleural spaces maintains lung viscera link to the parietal pleura → lung expands in response, creating a pressure vacuum (decreased intrathoracic pressure) → passive filling of the increased lung volume from atmospheric gasses (flow of air).
  • Compression of the thoracic cavity (muscles: internal intercostals, abdominus rectus, etc) → increased thoracic pressure → air expelled from lung (flow of air).


What are the three types of chest pain?

  • Nociceptive pain
  • Cardiac ischemic pain
  • Pleuritic/Visceral pain


What is the mechanism underlying nociceptive chest pain?

  • Inflammatory cytokines come rushing to injury spot → 
  • release of bradykinins, cytokines, H+ ions and other mediators → 
  • activate the terminals of Aδ and C fibers →
  • TRPV1 or TRPV2 receptors activated → 
  • ascend up spinal cord → spinothalamic and dorsal columns/medial lemniscus → 
  • to VPL nucleus → primary somatosensory cortex


What is the mechanism underlying cardiac/ischemic chest pain?

  • Low O2 getting to the heart triggers local chemoreceptors →
  • adenosine and bradykinin release → 
  • stimulates sensory ends of vagal and sympathetic afferent fibers →
  • fibers traverse upper 5 thoracic (sympathetic) ganglia → signals transmitted to the thalamus
  • In spinal cord: cardiac sympathetic nerve impulses may converge with somatic thoracic structure impulses → referred pain you get in your chest


What is the mechanism underlying pleuritic/visceral chest pain?

  • Primary afferents in vagus nerve will be triggered 
  • respond to the increased pressure in the lungs during inspiration
  • message travels up both traditional spinothalamic pathways (the contralateral ventrolateral quadrant) as well as by ipsilateral and dorsal spinal pathways
  • trigger somatosensory cortex
  • The pain will then be referred to the ipsilateral side as it comes back down
    •  In our case, the apex of the lung was collapsed → referred pain to T1 or T2 regions. Worse with inspiration due to the increased intrathoracic pressure from the air unable to escape.
    • Nociceptive C fibers in the lungs/trachea will travel up with the vagus nerve to the spinal cord → head up to the NTS of the medulla


What are the physiologic mechanisms for dyspnea?

  • Respiratory sensations are the consequence of interactions between efferent motor output from brain →  ventilatory muscles (feed-forward) and afferent incoming sensory input from receptors throughout the body (feedback).
  • Mismatch between central ventilatory drive and the magnitude of ventilation produced (called neuromechanical dissociation) →  dyspnea.
    • In other words, dyspnea is the result of dissociation between ongoing motor signals to the respiratory muscles and incoming afferent information. ­
    • Bigger mismatch = ­increased intensity of dyspnea


What is the A-a gradient and its role in respiratory pathophysiology?

  • A-a gradient is the difference in partial pressure of oxygen (PO2) between the alveolar PO2 (PAO2) and arterial pO2 (PaO2).
  • Normally there is a mismatch between ventilation and perfusion in the lungs
    • i.e. PAO2 and PaO2 are not the same
    • normal is 10-15 mmHg
  • Hypoxemia due to pulmonary cause increases the A-a gradient
  • Hypoxemia due to an extrapulmonary cause does not increase the A-a gradient


What is the relationship between Birt-Hogg-Dube syndrome and pneumothorax?

  • Birt-Hogg-Dube Syndrome:
    • Autosomal dominant syndrome characterized by benign skin follicle tumors, multiple renal cell neoplasms and spontaneous pneumothorax.
      • Rare mutation in Exon 11 of the BHD gene encoding folliculin protein (tumor suppressor gene)
  • Spontaneous pneumothorax can occur as the result of ruptured pulmonary cysts:
    • Lung lesions = pulmonary cysts
    • Pulmonary cysts are found in 24% of patients with BHD syndrome


How does the starvation response and explain an elevated blood glucose?

Increased sympathetics → norepinephrine binds beta-2 receptors in the liver → glycogenolysis is increased → increased blood glucose


How does how malnutrition, specifically a vitamin C deficiency, contribute to the development of a pneumothorax?

  • Vitamin C (ascorbic acid) → enzyme used to make collagen from procollagen
    • (by way of hydroxylating proline and lysine)
  • Without the production/maintenance of collagen → weakening of pulmonary elastic fibers → formation of a subpleural bullae
  • Macrophage and neutrophil influx causes inflammation → inflammation-induced obstruction of the small airways increases alveolar pressure, resulting in an air leak into the lung interstitium
  • Mediastinal pressure increases, causing rupture of the mediastinal parietal pleura → Pneumothorax


How is a Cohort study different from a Cross-sectional study?

  • Cohort: 
    • Compares a group with a given exposure or risk factor to a group without such exposure.
    • Measures relative risk of disease. Asks the question, “Who developed the disease?”
    • Longitudinal study!
  • Cross-sectional: 
    • Collects data from a group of people to assess frequency of disease and related risk factors at a particular point in time.
    • Measures disease prevalence.
    • Asks the question “What is happening?”


What is the best approach for addressing/treating resistant Anorexia Nervosa?

Cognitive behavioral therapy - enhanced (CBT-E)

  • addresses factors which predispose an individual to the illness
  • factors that maintain the illness (especially the obsessive-compulsive components of eating disorders)
  • Rely on extensive psychoeducational, interpersonal, and belief system restructuring.  
  • Also address the role of starvation in brain functioning
  • 60 week program = typical for those with resistant AN