Mod 6: Pulmonary Diseases And Pain

Front 1

1. Age related changes in pulmonary structure and physiology

Back 1

• Loss of elastic recoil
• Muscle endurance/strength reduced by as much as 20% by age 70.
• Alveolar wall tissue is lost resulting in decreased airway support and elasticity
• chest wall compliance decreases
• Stiffening of chest wall- ribs less flexible due to ossification, as the ribs become stiffer, chest wall unable to expand
• Changes in gas exchange
• Increase in flow resistance- Vital capacity decreases and residual volume increases (total lung volume remains unchanged)
• changes are gradual and usually do not result in problems for normally healthy persons.

Front 2

3. Pneumothorax: the presence of air or gas in the pleural space caused by:

Back 2

rupture in the

• visceral pleura [surrounds the lungs]
• or the parietal pleura and chest wall
  

Front 3

3. Primary (spontaneous) pneumothorax:

• occurs most often in what population?
  
• most often caused by?
  
• bleb rupture can occur during:
  
• ruptured blebs usually located in:
  

Back 3

• Occurs unexpectedly in healthy individuals, usually men, ages 20-40
  
• spontaneous rupture of blebs (blister-like formations) on the visceral pleura (although there may be underlying pleural disease with emphysema-like changes)
  
• sleep, rest or exercise
• apexes of lungs
  

Front 4

3. Clinical Manifestations of both Primary and Secondary Pneumothorax:

Back 4

• Sudden pleural pain
• Tachypnea
• Possibly mild dyspnea
• Manifestations depend on size of pneumothorax
• Poss. absent breath sounds, hyperresonance to percussion on affected side
• Dx by x-ray, US, CT
  

Front 5

3. Secondary (traumatic) pneumothorax

Caused by:

Back 5

• chest trauma (rib fracture, stab or bullet wounds,
• surgical procedure,
• rupture of bleb or bulla as occurs in COPD
• mechanical ventilation, particularly with PEEP)
  

Front 6

3. Iatrogenic pneumothorax is most commonly caused by:

Back 6

transthoracic needle aspiration

Front 7

3. Open (communicating) pneumothorax:

Air pressure in the pleural space = barometric pressure b/c:

Back 7

air drawn into pleural space during inspiration is forced back out during expiration

Front 8

3. Tension pneumothorax

• Site of rupture acts as:
• As more air enters pleural space, air pressure in pneumothorax begins to:
• Life threatening-->why?
• May be complicated by:
  

Back 8

• one-way valve, permitting air to enter on inspiration but preventing air escape by closing on expiration
• exceed barometric pressure
  
• compression atelectasis, compression and displacement of heart and great vessels
  
• severe hypoxemia, tracheal deviation away from affected lung, hypotension*
• Considered an emergency!

Front 9

4. Pulmonary edema

Back 9

Excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure or capillary permeability.

Front 10

4. Most common cause of pulmonary Edema

Back 10

#1-Left side heart disease-Left ventricle fails ----->increase pulmonary capillary hydrostatic

pressure.

*ARDs (injury to endothelium)-->increased capillary permeability---->movement of fluid & plasma protein into alveoli/interstitial space.

*Blockage of lymphatic vessels--->inability to remove fluid from interstitial space.

Front 11

4. Pulmonary Edema s/s

Back 11

dyspnea, orthopnea, hypoxemia, increased breathing work

Front 12

4. Acute respiratory distress system:

Back 12

Spectrum of acute lung inflammation and alveocapillary injury.

Most survivors have almost normal lung function one year after acute illness but may have other health problems including neurocognitive disorders up to five years later.

Front 13

4. Acute respiratory distress system:

Pathophysiology

Back 13

Alveoli capillary membrane producing massive pulmonary inflammation --->increases capillary permeability, severe pulmonary edema, surfactant inactivation, shunting, VQ mismatch, atelectasis and hypoxemia.

***Hallmark-Increased capillary permeability

Front 14

4. Acute respiratory distress system

3 phases 1st

Back 14

exudative-initial injury damages alveolar/capillary membrane-->inflammatory mediators--->cause damage--->increase capillary permeability-allow fluids, proteins and blood cells to leak into the alveoli--->pulmonary edema and loss of lung compliance

Front 15

4. Acute respiratory distress system

3 phases 2nd

Back 15

Proliferative-1-3 weeks after injury; edema resolution-->proliferation of pneumocysts, fibroblasts, and myofibroblasts.

Intra-Aveolar hemorrhagic exudate--->cellular granulation tissue appearing as hyaline membranes--->progressive hypoxemia.

Front 16

4. Acute respiratory distress system

3 phases 3rd

Back 16

Fibrotic-2-3 weeks after injury.

Remodeling and fibrosis occurs-obliterates the alveoli, respiratory bronchioles and interstitum

---->decreased functional residual capacity--->continuing VQ mismatch with sever R to L shunt--->acute respiratory failure.

Front 17

5a. Asthma

Back 17

Chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyper-responsiveness, constriction of the airways, and variable airflow obstruction that is reversible.

• Occurs at all ages, with approximately half of all cases developing during childhood, and another 3rd before age 40.
• Estimated that 24.6 million people have asthma
• Death rates are highest for female, black persons, and adults older than 65.
  

Front 18

5b. Athma- Etiology

Back 18

Familial disorder, more than 100 genes identified that may play a role in the susceptibility and pathogenesis

• Genes that influence production of IL-4, IL-5, and IL-13o IgEo Eosinophils, mast cells, adrenergic receptors, leukotrienes, nitric oxide, and transmembrane proteins in the endoplasmic reticulum.
• Specific gene expression may impart associated phenotypes, such as inflammation, sensitization to allergens, airway fibroblasts, airway remodeling, and responsiveness to asthma therapies.
• Other risk factors include: allergen exposure, urban residence, exposure to air pollution, tobacco smoke, environmental tobacco smoke, recurrent respiratory tract viral infections, esophageal reflux, obesity.
  

Front 19

5c. Asthma- Patho

Back 19

Epithelial exposure to antigen initiates both an innate and an adaptive immune response in sensitized individuals. Many cells and cellular elements contribute to persistent inflammation of the bronchial mucosa and hyper responsiveness of the airways: (macrophages, T helper2 lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, basophils)

Front 20

5d. Asthma - Clinical manifestations

Back 20

1. asymptomatic between attacks and pulmonary function tests are normal→
2. during remission no symptoms are present but pulmonary function tests will be abnormal
3. during attack: feels chest constriction, expiratory wheezing, dyspnea, nonproductive cough, prolonged expiration, tachycardia, tachypnea.
4. Severe attacks involve accessory muscles or respiration and wheezing is heard on inspiration and expiration. Pulsus paradoxus may be present ( decreased systolic blood pressure during inspiration or more than 10mgHg).

Front 21

5e. Chronic bronchitis

Back 21

Etiology: hyper-secretion of mucus and chronic productive cough that continues for at least 3 months of the year for 2 consecutive years

Pathophysiology: inspired irritants > airway inflammation with infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall. Continual bronchial inflammation > bronchial edema and increases the size and number of mucous glands and goblet cells in the airway epithelium. Thick mucous is produced and cannot be cleared because of impaired ciliary function.

Clinical manifestations: decreased exercise tolerance, wheezing, SOB. Typically have productive cough and evidence of airway obstruction shown by spirometry

Front 22

5f. Emphysema

Back 22

abnormal permanent enlargement of gas exchange airways accompanied by destruction of alveolar walls without obvious fibrosis

Front 23

5g. Emphysema - Etiology

Back 23

Primary emphysema :1-3% of all cases is commonly linked to an inherited deficiency of the enzyme a1-antitrypsin.

Secondary emphysema: major cause is inhalation of cigarette smoke, although air pollution, occupational exposures and childhood respiratory tract infections are known to be contributing factors.

Front 24

5h. Emphysema - Patho

Back 24

destruction of alveoli through the breakdown of elastin within the septa by an imbalance between proteases and anti-proteases, oxidative stress, and apoptosis of lung structural cells. Alveolar destruction also produces large air spaces within the lung. Air trapping causes hyper-expansion of the chest, this puts the muscles of respiration at a mechanical disadvantage. Results in increased work of breathing, hypoventilation and hypercapnia (CO2 retention, excessive CO2 in the blood.)

Front 25

5i. Emphysema - Clinical Manifestations

Back 25

• dyspnea on exertion that later progresses to marked dyspnea even at rest, little coughing and very little sputum are produced.
• Tachypnea with prolonged expiration and use of accessory muscles for ventilation.
• Barrel chest, chest has a hyper-resonant sound with percussion.
• Patient often leans forward with arms extended and braced on knees when sitting, pursed lip breathing.
  

Front 26

6.Pneumonia-

Back 26

Inflammatory reaction in the alveoli and interstitial.

Most pathogens that enter the lungs are expelled or immune system destroys.

Most important guardian of the lower respiratory tract is the alveolar macrophage- activating T-Cells and B-Cells.

Front 27

6.Pneumonia-Patho-

Back 27

*most common-aspiration of oropharyngeal sections in the lower respiratory tract.

*inhalation of microorganisms from sneezing, talking

*bacteria spreading from blood to lungs-bacteremia

Front 28

6.Pneumonia- Bacterial, atypical, viral

Back 28

Most common bacterial-streptococus PN;

gram+ staph and streph, gram neg- Klebsiella

Atypical-mycoplasma-small bacteria seen in summer and fall; school age children and young adults (dorms, colleges, barracks).

Viral-RSV, influenza (little mucous)

Front 29

6.Pneumonia- S/S-

Back 29

S/S-increased tactile fremitus, dull percussion, decreased breath sounds, CXR-consolidation

Bacterial-chills, fever, malaise, productive cough, purulent or blood tinged sputum

Viral-cold symptoms-preceded by URI, fever, non-productive cough, hoarseness, wheezing, fine rales,

Front 30

6.Pneumonia- Risk factors Community Acquired bacterial PN

Back 30

Young, old

Immunocompromised-(more likely to have opportunistic PN-fungal pneumocystic jerokeke-HIV, CA)

Underlying lung disease

ETOH

Smoker

Front 31

6. Tuberculosis

etiology

risk factors

tests

Back 31

Mycobacterium tb (acid fast aerobic bacilli)

-infect lungs but may infect other organs.

malnourished, immunosuppressed, living in crowded environments, incarcerated, elderly

Mantoux (tb skin test)-best, doesn't differentiate active from latent.

Blood tests interferon gamma release assays

-Quantiferon-TB GOLD

-T spot

Sputum culture-takes 3 weeks-definitive

CXR-Ghon tubercles- infiltrates in apex, lymph nodes

Front 32

6.Pathophysiology-TB

Back 32

droplet airborne (talk, sneeze, laugh) Lodges in the lungs---->mild puenocystics ----->bacilli migrate to lymph nodes----> T-cell mediated response-neutrophils & macrophages engulf and isolate bacilli. STOP the spread by trapping the bacilli in a granuloma called a ghon tubercle. It becomes dormant and will only show up with CXR or TB test. It may remain dormant for life or reactivation may occur d/t age, poor nutrition or reexposure which leads to active pulmonary disease.

Front 33

6. TB Clinical manifestations

Back 33

Latent TB-no s/s, can’t spread

Active TB-infective and sick

Bad cough-lasts 3 weeks or longer

Pain in chest, coughing up blood or sputum

Weakness, fatigue, anorexia, weight loss

Chills, diurnal fever, night sweats

Front 34

6. Acute Bronchitis

etiology

Risk Factors

Pathophysiology

Clinical manifestations

Back 34

etiology-viral

risk factors-Commonly follows a viral illness

Pathophysiology-acute infection or inflammation of airways or brochi. Self limited-tx with diet, good nutrition, cough syrup, fliuds, and rest.

Clinical manifestations-Nonproductive cough, occurs in paroxysms-cough, cough and cough and aggravated by cold, dry, dusty air. Mimics PN but no pulmonary consolidation.

Front 35

7a. Pulmonary embolism

Back 35

The occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or air bubble. Pulmonary emboli commonly arise (90%) from the deep veins in the thigh.

Front 36

7b. Virchow triad

Back 36

• Factors that cause a thrombi formation:
  
• Venous stasis (r/t immobility or heart failure),
• hyper-coagulability (pregnancy, oral contraceptives, cancer, inherited coagulation disorders, hormone replacement),
• injuries to the endothelial cells that line the vessels (from trauma or IV infusions)
  

Front 37

7c. Pulmonary Embolism - Clinical Manifestations

Back 37

In most cases the clinical manifestations are nonspecific. Depends on size of embolism: symptoms….

restlessness, apprehension, tachycardia, anxiety, dyspnea and then as it worsens=chest pain on inspiration and hemoptysis.

Front 38

7d. Pulmonary Embolism - Patho

Back 38

Depends on the size of extent of pulmonary blood flow obstruction, the size of the affected vessels, the nature of the emboli.

Pulmonary emboli can result in the following: Embolus with infarction (emboli causes death of lung tissue); Embolus without infarction; Massive occlusion (embolus that occludes a major portion of the pulmonary circulation); Multiple pulmonary emboli (may be chronic or recurrent).

The substance enters bloodstream or thrombus is dislodged by trauma, muscle action or changes in blood flow, amniotic embolism displaces blood in the vessel and causes immune response (release of neurohumoral substances such as serotonin, histamine, catecholamines, angiotensin II and inflammatory mediators such as endothelin, leukotrienes, thromboxanes, and toxic oxygen free radicals) that will lead to widespread vasoconstriction, shock, atelectasis, pulmonary edema and pulmonary htn, death. If the clot doesn’t cause infarction, the clot is dissolved by the fibrinolytic system and pulmonary function returns to normal. Risk of recurrent venous thromboembolism is 30% over the next 10 years.

Front 39

7e. COR PULMONALE

Back 39

Secondary to Pulmonary Artery Hypertension and will cause signs of right sided heart failure > Right ventricular enlargement…because right ventricle has to work harder to pump blood into the lung.

Front 40

7f. COR PULMONALE - Patho

Back 40

Develops as pulmonary hypertension, creating chronic pressure overload in the right ventricle will cause a back flow into the periphery which causes edema. Acute hypoxemia can exaggerate pulmonary HTN and dilate the ventricle. Right ventricular filling pressures are normal until failure occurs. Right ventricle usually fails when pulmonary artery pressure equals systemic blood pressure.

Front 41

7g. COR PULMONALE - Clinical manifestations

Back 41

Heart appears normal at rest. With exercise: Decreased cardiac output, chest pain. Electrocardiogram shows right ventricular hypertrophy.

Front 42

8a. Epiglottis - Etiology

Back 42

• 25% caused by H. influenza B
  
• Also caused by Strep A, B, C, F and G, strep pneumonia, candida, staph aureus and viruses
• Other causes include thermal injury, trauma and post transplant lymphoproliferative disorder

Front 43

8b. Epiglottis - Patho

Back 43

• Bacterial invasion
• Causes inflammation and epiglottis edema
• Causes upper airway obstruction
• Life threatening

Front 44

8c. Epiglottis - Clinical Manifestations

Back 44

• Ages 2-6 years
  
• Sudden onset high fever, irritability, sore throat, stridor and respiratory distress
• Develop drooling and dysphagia

Front 45

8d. Croup - Etiology

Back 45

• 6 months to 3 years (peak age 2 years)
• 85% viral cause (parainfluenza)
• Caused by influenza A, RSV, rhinovirus, adenovirus, rubella, mycoplasma pneumonia
• More common in fall and winter and in boys

Spasmodic croup - Sudden onset, usually at night, no viral prodrome, resolves quickly, occurs in older children, etiology is unknown and is thought to be associated with viral, allergy, asthma, and GERD.

Front 46

8e. Croup - Patho

Back 46

• Subglottic edema from infection
  
• Mucous membranes of larynx are tight to cartilage
• Subglottic space is looser and allows edema to develop

Front 47

8f. Croup - Clinical Manifestations

Back 47

• Rhinorrhea, sore throat and low grade fever
  
• Seal-like barking cough, hoarse voice and stridor.
• Most resolve spontaneously
• If upper airway obstruction develops this is urgent

Front 48

9. Tonsillar infections

Back 48

• Inflam. of tonsils/pharynx
• Peritonsillar abscess: unilateral complication of tonsillitis (must be drained & ATB tx)
• S/sx: fever, sore throat, dysphagia, muffled voice, pooling of saliva, trismus
• Cause: Group A staph aureus & MRSA

Front 49

9. Bacterial tracheitis

Back 49

• Acute upper airway obstruction
• Diffuse inflam. of the larynx/trachea/bronchi
• More common in children d/t narrow subglottic airway
• S/sx: barking cough, stridor, and fever (not to be confused with Croup)
• Cause: Group A staph aureus and often follows a recent viral upper respiratory infection

Front 50

10a. Bronchiolitis -Etilogy

Back 50

A common viral-induced lower respiratory tract infection of the small airways in children younger than 2 years of age. Most common pathogen is Respiratory syncytial virus (RSV), but may also be associated with adenovirus, rhinovirus (older children) influenza, strep, pneumococci, and human metapneumovirus.

Front 51

10b. Bronchiolitis - Etilogy

Back 51

Peak incidence is during winter (late December) and a spike in February, and tapers off in spring. Major reason for hospital admission of children younger than one and children of lower socioeconomic status. Healthy children usually have a complete recovery. Although about 50% of children who have RSV bronchiolitis before age one will have asthma diagnosed by age 6

Front 52

10c. Bronchiolitis - Pathophysiology

Back 52

• Agent causes inflammation and necrosis of the bronchial epithelium and destruction of ciliated epithelial cells.
• Infiltration of lymphocytes with lymphocytes around bronchioles and a cell mediated hypersensitivity to viral antigens with release of lymphokines causing inflammation, as well as activation of eosinophils, neutrophils, and monocytes.
  

Front 53

10d. Bronchiolitis - Pathophysiology

Back 53

• Submucosa becomes edematous, and cellular debris, and fibrin form plugs within bronchioles.
• Bronchospasm and mucous plugs cause narrowing of airways ( causes obstruction of airflow that is worse on expiration), air trapping, hyperinflation, and atelectasis which lead to ventilation-perfusion mismatch and hypoxemia.
  

Front 54

10e. Bronchiolitis - Pathophysiology

Back 54

• Airway resistance and hyperinflation result in decreased lung compliance and increased work of breathing and may cause hypercapnia in severe cases.
  

Front 55

10f. Bronchiolitis -Clinical Manifestations:

Back 55

• Symptoms vary child to child depending on the health of the child before illness and genetic predisposition.
• Symptoms may be mild or so bad that disease is fatal. Common symptoms start with rhinorrhea (runny nose), tight cough, poor feeding/decreased appetite, lethargy, and fever.
  

Front 56

10g. Bronchiolitis - Clinical Manifestations:

Back 56

• Infants may have tachypnea, expiratory wheezing, cough, rhinorrhea, mild fever, varying degrees of respiratory distress, and abnormal auscultatory findings of the chest.
• Severe cases: chest x ray reveal hyperexpanded lungs, patchy or peribronchial infiltrates, and atelectasis.
  

Front 57

10h. Bronchiolitis - Clinical Manifestations:

Back 57

• Severely affected infants appear anxious and distressed because of dyspnea and hypoxemia.
  
• Thoracic cage is overexpanded, particularly AP diameter.Infant takes rapid, short deep breaths, and wheezing, and rales are often heard on auscultation.
  

Front 58

10i. Bronchiolitis - Clinical Manifestations:

Back 58

• Overexpansion of lungs, the diaphragm is flattened, causing downward displacement of the liver and spleen.
• Abdominal distention results from air swallowingGenetics tendencies have been noted that correlate RSV bronchiolitis with asthma.
  

Front 59

11. SIDS

*Etiology

Back 59

• Unknown cause
  
• “Sudden death of an infant under 1 year which remains unexplained after a thorough case investigation including complete autopsy, exam of death scene, and review of clinical history”
  
• Probably due to immature ventilatory and arousal response to hypoxia
  

Front 60

11a. SIDS

*Theories on Etiology

Back 60

• Theory involving impaired autonomic regulation and failure of cardiovascular, ventilatory, and arousal responses (particularly those regulated by the hypoglossal nucleus (HGN) to hypoxemia or hypercarbia
• Other theories: airway obstruction events, increased vagal tone, sudden intrapulmonary shunting because of abnormalities of surfactant or pulmonary vessels, or exaggerated inflammation, eosinophil degranulation, and massive cytokine release causing pulmonary edema in response to bacterial or viral infections
  

Front 61

11b. SIDS

*Risk Factors

Back 61

• Genetic factors :10-20% may be caused by genetic variation in either ion channel or ion channel-associated proteins associated with primary electrical heart disease (like long QT and short QT syndrome)
• Preterm or low birth weight infants, multiple births, siblings of prior SIDS victims (4-6-fold increased risk), low or adverse socioeconomic status, large family size

Front 62

11c. SIDS

*Risk Factors

Back 62

• 75% have no predisposing risk factors
• Maternal factors- maternal smoking, young maternal age, unmarried, less prenatal care, poverty, illicit drug use or binge drinking
• Prone sleeping position, sleeping on soft bedding, overheating, bed sharing with an adult (particularly with a smoker)
  

Front 63

11e. SIDS

*Prevention

Back 63

• Back to sleep, firm sleep surface, room sharing without bed sharing, routine immunization, pacifier, avoidance of soft bedding, overheating, and exposure to tobacco smoke, alcohol, and drugs
• Breastfeeding
  

Front 64

12a. Pt c/o of having a nagging cough that just won’t go away. Can’t remember when it started. Productive. Having a hard time exercising and gets SOB easily.

Back 64

Chronic Bronchitis

Front 65

12b. Mother comes in with infant who is 8 months old, states infant has come down with a nasal cold and cough, has had a fever for several days now, cough is “barky”, hoarse cry, difficulty sleeping.

Back 65

Croup

Front 66

12c. healthy male, 32 years old. Exhibiting tachypnea and difficulty breathing. C/O pain in right side, “inside my ribcage”. On auscultation of right side, lung sounds diminished in UQ and absent in LQ.

Back 66

primary (spontaneous) pneumothorax

Front 67

12d. 4 year old presenting with severe respiratory distress. Temp is 103.6, sore throat, not been drinking or eating, positive for strep. Stridor present on inspiration.

Back 67

epiglottis

Front 68

12e. Pt complaining of difficulty breathing, “chest feels tight”, audible wheezing, heart rate and respirations are elevated, accessory muscles being used on inspiration.

Back 68

asthma

Front 69

12f. Pt was a smoker for 15 years but quit 5 years ago. Pt has a slight non productive cough with dyspnea and elevated respirations. State they used to only have trouble breathing when walking or climbing stairs but now it feels like it won’t go away and that they are always having trouble. Pt states it helps slightly to lean forward and rest arms on their knees.

Back 69

Emphysema

Front 70

12g. 14 year old girl comes into ER after falling off her horse and landing on a rock. Left side of rib cage is bruised, absent lung sounds, pt is tachpnic, severe trouble with breathing and in pain.

Back 70

Secondary (traumatic) pneumothorax

Front 71

12h. Mother brings in 15-month old child, with a “bad cold”, runny nose and cough. Exhibits tachypnea, wheezing, Temp is 100.2, dyspnea, O2 sats 90%, rales auscultated. Mother states child is not eating well and is lethargic.

Back 71

Bronchiolitis

Front 72

12i. Pt with a history of DVT comes in with difficulty breathing and is highly anxious, also c/o of mild chest pain. HR and resps are elevated.

Back 72

pulmonary embolism

Front 73

13a. Pain

Back 73

an unpleasant sensory and emotional experience with actual or potential tissue damage:

• A symptom is not a clinical sign, diagnosis or disease

• PAIN is always subjective

• The inability for an individual to communicate verbally does not negate the possibility that they are experiencing pain and have a need for pain relief

Front 74

13b. Specificity Theory

Back 74

• Amount of acute pain or specific injuries verses the amount of tissue injury (pin prick is less painful than a cut from a knife)

• The activation of specific pain receptors and fibers that project to the brain

• Doesn't explain chronic pain, cognitive or emotional elements that contribute to more complex types of pain

Front 75

13b. Specificity Theory

Back 75

Increase: use of alcohol, pain killers, hypnosis, warmth, distraction, and faith.

Decrease: repeated exposure to pain-killers

Front 76

13c. Patterning Theory

Back 76

• Explains the role of impulse intensity and re-patterning of the central nervous system.

• A limited theory, does not account for all pain experiences

Front 77

13c. Patterning Theory

Back 77

• It is a protective mechanism that alerts the individual to a condition or experience that is immediately harmful to the body.
• It is transient; it might last up to 3 months.
• Begins suddenly
• Physical manifestations include increased heart rate, hypertension, diaphoresis, dilated pupils and anxiety.
  

Front 78

13d. (1) Gate Control Theory (GCT)-integrates builds upon features of other Theories of Pain

Back 78

• Explains the complexities of the pain phenomenon
  
• Explains multidimensional aspects of pain perception and pain modulation
• Proposes that a neural mechanism of the dorsal horn root of the spinal cord acts like a gate that can increase or decrease the perception of pain that comes from the peripheral nerves to the CNS
• Pain is modulated by this “gate”

Front 79

13d. (2) Gate Control Theory GCT

Back 79

• Large myelenated A-delta fibers move the pain signals very rapidly and the brain perceives these signals as stinging and highly localized pain

• Small, un-myelinated C fibers move impulses more slowly. Pain transmission is poorly localized dull and aching in nature. Within the internal organs.

• Nociceptive transmissions on these fibers “open” the spinal gate and increase the perception of pain

Front 80

13d. (3) Gate Control Theory GCT

Back 80

• Closure or partial closure of the spinal gates occurs from non-nociceptive stimulation (from touch sensors in the skin).
• These signals are carried on non-nociceptive larger A-beta fibers and decrease pain perception (that is why rubbing a painful area may relieve some pain)
• Other efferent CNS pathways descent to the spinal cord and may close, partially close, or open the gate modulating the pain experience
• GCT gives understanding of neuronal pathways in PNS and CNS (Pain in paraplegics that do not “fit the theory”)

Front 81

13e. (1) Neuromatrix Theory

Back 81

• Grows out of the gate theory

• the brain produces patterns of nerve impulses drawn from various inputs- genetic, psychological and cognitive experiences

Front 82

13e. (2) Neuromatrix Theory

Back 82

• Last at least 3 months
• Ongoing (e.g., low back pain) or intermittent (e.g., migraine headaches).
• Changes in the peripheral and central nervous systems are thought to lead to chronic pain.
• normal heart rate and blood pressure.
• behavioral and psychologic changes often emerge, including depression, difficulty eating and sleeping, preoccupation with the pain, and avoidance of pain-provoking stimuli.
  

Front 83

13e. (3) Neuromatrix Theory

Back 83

• Pain is described as a multidimensional whole mind body spirit experience
• Explains how pain can be felt even with absence of inputs from the body (phantom limb)
• A stimulation like (stress, immune & sensory input, cultural factors, etc.) affect pain perception

Front 84

13e. (4) Neuromatrix Theory

Back 84

• Activation of sensory inputs from the periphery, can originate independently within the brain with no external input
• illustrates plasticity- (adaptable change in structure and function) of the brain

the Gate Theory idea that the body-self provides a holistic, integrated, dynamic consideration of pain

Front 85

13f. No single theory

Back 85

Adequately explains the complex dynamics of the many different types of pain or the pain experience

Front 86

14.The three portions of the nervous system responsible for the sensation and perception of pain are:

Back 86

1. The afferent pathway begins in the PNS, travels to the spinal gate in the dorsal horn and then ascends to higher centers in the CNS.

2. Interpretive centers located in the brainstem, mid-brain, diencephalon, and cerebral cortex.

3. The efferent pathways that descend from the CNS to the dorsal horn of the spinal cord modulate pain.

Front 87

14.The processing of potentially harmful (noxious) stimuli through a normally functioning nervous system is called....

Back 87

nociception

Front 88

14.Nociception involves four phases:

Back 88

transduction-stimulation of nociceptors

transmission-fast-delta A fibers (skin & muscles); slow-C-fiber (internal organs)

perception-pain awareness and interpretation

modulation-suppression or facilitation of pain

Front 89

14.Pain transduction begins ....

Back 89

when tissue is damaged by exposure to chemical, mechanical, or thermal noxious stimuli and is converted to electrophysiological activity.

This causes activation of nociceptors.

Front 90

14. Processing of pain

1st order neurons-nociceptors-

Back 90

bare nerve endings in the skin, joints, arteries and visera that respond to chemical, thermal, or mechanical stimulation.

Front 91

14. Processing of pain- 2nd order neurons

Back 91

Interneurons in the dorsal horn of the spinal column.

They cross over and ascend.

Excitatory or inhibitory-pain gate to regulate pain transmission

Front 92

14. Processing of pain- 3rd order neurons

Back 92

Afferent neurons in the spinothalamic tract.

Carry info to the sensory cortex and reticular/limbic systems to process and interpret pain.

Front 93

14. Endogenous Opiate Peptides

Back 93

Decrease the perception of pain-like opioids-bind with opioid receptors.

Enkephalins

Endorphins

Dynorphins

Endorphins

Front 94

14. Dynorphins

Back 94

Most potent

Front 95

14. Beta Endorphins

Back 95

Reside in the hypothalamus and pituitary and are released during stress, pain, emotion, eating chocolate, laughter, massage or acupuncture.

Reduce pain and produce sedation and euphoria.

Strong mu receptors agonists that provide natural pain relief.

Front 96

14. Endorphins

Back 96

Potent analgesics

GI and anti-inflammatory agents.

Front 97

15. Pain Threshold

Back 97

The point at which a stimulus is viewed as painful. This point does not tend to vary over the lifetime or between people.

Front 98

15. What causes perceptual dominance?

Back 98

Perceptual dominance is caused when pain is so intense in one location, that it tends to mask pain in another location.

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15. What factors can influence an individual's pain tolerance?

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Pain tolerance is the amount of pain, or length of time a person will endure pain before engaging in overt pain responses.

Influenced by:

Culture, expectations, mental and physical health, roles, gender, fatigue, anger, boredom, apprehension, and sleep deprivation.

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16. Somatic Pain

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• Superficial
  
• Arise from connective tissue, muscle or bone, and skin.
• It is either sharp and well localized (especially fast pain carried by Aδfibers) or dull, aching, throbbing, and poorly localized as seen in polymodal C fiber transmissions.
  

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16. Visceral Pain

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• Pain in internal organs and the lining of bodycavities with an aching, gnawing, throbbing, orintermittent cramping quality.
  
• Transmitted by sympathetic afferents and ispoorly localized
  
• Associated with nausea and vomiting,hypotension, restlessness, and,in some cases, shock.
  
• Radiates or is referred.
  

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16. Referred Pain

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• Felt in an area removed or distant from its point of origin
• The area of referred pain is supplied by the same spinal segment as the actual site of pain.
• Referred pain can be acute or chronic.
  

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16. Neuropathic Pain

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• Results from primary injury to the peripheral or central nervous system and is not the result of pain signaling from peripheral tissues or organs.
• The pathogenesis of neuropathic pain syndromes includes both peripheral and central mechanisms of pain sensitization.
  

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16. Peripheral Neuropathic Pain

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• Caused by peripheral nerve trauma, diabetic or alcohol abuse–induced neuropathy, carcinoma, nutritional deficiencies, and human immunodeficiency virus (HIV).
• Pain sensation can occur in the absence of a stimulus and may be evoked by movement (incident pain), and hyper sensitivity and/or allodynia may be present in the involved body part.
  

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16. Central neuropathic pain

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• Caused by a lesion or dysfunction in the CNS (brain or spinal cord).
• Alterations of the sensory pathways and impairment of descending inhibitory mechanisms contribute to the pain.
• Examples of central causes of neuropathic pain include brain or spinal cord trauma, tumors,vascular lesions, multiple sclerosis, Parkinson disease, postherpetic neuralgia(PHN), phantom limb pain, and reflex sympathetic dystrophy.
• Neuropathic pain is often paroxysmal with hyperesthesia and paresthesias (tingling sensations of pins and needles), burning, shooting, or stabbing sensations.
• Neuropathic pain is often described as “gnawing” and miserable.
  

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Back 106

.

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2. paroxysmal nocturnal dyspnea

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pt wakes up gasping for air

need to sit or stand

Associate with CHF or undx obstructive sleep apnea.

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2. orthopnea

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lying down SOB

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2. dyspnea

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flaring of nostrils

accessory use of muscles

retractions

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2. cough

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acute 2-3 weeks

chronic- > 3 weeks

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2. Kussmauls

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slightly increased ventilatory rate

Very large tidal volumes

No expiratory pause

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2. stridor

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high pitched sounds made during inspiration

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2. hyperventilation

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alveolar ventilation exceeds metabolic demands--->resp alkalosis from hypocapnia

Blowing off CO2

Caused by anxiety, head injuries and increased RR.

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2. hypoventilation

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alveolar ventilation inadequate to meet metabolic demands--->resp acidosis from hypercapnia

Caused by airway obstruction, chest wall restrictions, altered neurologic control of breathing

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2.central cyanosis

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Decreased arterial blood

Caused by Pulmonary disease or pulmonary/cardiac right to left shunts

Seen in lips of mucous membrane

Poor indication of respiratory failure.

Lack of cyanosis does not indicate normal 02

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2.Peripheral cyanosis

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Vasoconstriction of periphery

Seen in nails beds

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2.Clubbing

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Bulbous enlargement of the end of a digit -nailbed hypertrophy

Associated with cystic fibrosis, *pulmonary fibrosis, congenital heart disease, *bronchiectasis

Nonreversable

Painless

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4. ARDs S/S (progressive)

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Dyspnea/hypoxemia-poor response to 02 supplementation---->

Hyperventilation/Resp alkalosis--->

Decreased tissue perfusion, metabolic acidosis and organ dysfxn----->

Hypercapnia, resp acidosis and worsening

hypoxemia---->

Decreased cardiac output, hypotension and death

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17.PediatricPain

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*PediatricPain Pathways-functional preterm and newborn infants

*20-24 weeks gestations-nociceptors functional

*Infants, crying, facial expression, body language, lack of consolability

*5-18 years- lower pain threshold than adults

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17. S/S-infant Pain

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Brows-lowered, drawn together

Forehead-bulge between brows, vertical furrowsEyes-closed tightly

Cheeks-raised

Nose-broadened, bulging

Mouth-open, squarish

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17. Pain in Older Adults

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*Influenced by chronic disease

*Pain threshold increases d/t peripheral neuropathies, skin thickens, cognitive changes

*Pain tolerance decreases-women are more sensitive than men.

*Alterations in the metabolism of drugs and metabolites occur d/t decreased renal/liver function