NU 672 Final

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NU 672 Final
2013-04-30 22:46:54
boston college CRNA bc

for the final test!
Show Answers:

  1. Where do peptic ulcer diseases occur?
    • Upper GI tract
    • (stomach and first few centimeters of duodenum)
  2. What are some things that are associated with PUD?

    • Corticosteroids
    • H. pylori
    • EtOH
    • NSAIDS
    • Smoking
  3. What are Curling's Ulcers?
    Ulcers in the duodenum caused by burns;  decreased plasma volume (blood flow) to stomach results in ischemia–sloughing of gastric cells results

    curling iron = burn
  4. What are Cushing's ulcers?
    • Ulcers caused by brain injury... 
    • ↑ICP → vagal stimulation → gastric acid
  5. What are some complications of PUD?
    • Hemorrhage
    • Obstruction
    • Perforation
  6. What causes GERD?
    ↓ LES tone

    fatty foods, smoking, obesity, alcohol, meds, immaturity of LES in infants, neurological disease (CP), things that delay gastric emptying (pyloric stenosis, hiatal hernias)
  7. What are S&S of GERD?
    • esophagitis (inflammation of the esophagus),
    • pain, ulcerations, obstructions (stricture)
  8. Is GERD common in infancy?
  9. What children suffer more complications with GERD, such as esophagitis, malnutrition, and respiratory problems?
    Those with neurologic disorders
  10. T/F: You want to feed a child with GERD more volume less often.
    False. Small frequent feeds of thickened formula are recommended.
  11. Regarding Crohn's & UC, which one is primarily of the rectum or sigmoid?

    large intestine is typically the only affected site
  12. Regarding Crohn's and UC, which one can affect any part of the GI tract (from mouth to anus)
  13. The pathophysiology of Crohn's & UC involves:
    a) an environmental trigger such as microbial flora
    b) a failure of immune regulation
    c) a genetic predisposition
    d) all of the above
    D) all of the above
  14. Granulomas (inflammed cells that become lumped together to form a lesion) are present in _______
    Crohn's disease
  15. In ___________ the ulceration is deeper and may extend into all the layers of the bowel wall.
    Crohn's disease

    In ulcerative colitis, these ulcers do not extend beyond this inner lining of the large intestine
  16. In ______, narrowed lumen and obstruction are not uncommon complications. These conditions are less frequently found in cases of ______.
    In Crohn's disease, narrowed lumen and obstruction are not uncommon complications. These conditions are less frequently found in cases of ulcerative colitis.
  17. Ulcerative colitis has a genetic link to:
    HLA DR2
  18. genetic link to these is found in ______:
    HLA DR1 and
    HLA-DQw5 alleles,
    IBD1 locus on chromosome 16,
    NOD2 mutations,
    chromosome 5q (IBD5), IBD3
    Ulcerative colitis
  19. Which disease (UC vs. Crohn's) has continuous
    involvement of the colon, beginning with the rectum
  20. What is hepatitis?
    Inflammation of the liver due to drugs, toxins like Etoh & bacterial or viral infections
  21. What is another name for Hepatitis B Virus?
    Serum Hepatitis
  22. How is serum hepatitis / HBV transmitted?
    infected blood, sex, needles, rectal
  23. What disease is associated with hepatocellular carcinoma?
    HBV/"Serum Hepatitis"
  24. Is there a vaccine for Hep B?
  25. This disease is an abnormal immune response to otherwise normal intestinal flora:
    Crohn's Disease
  26. High V/Q is...
    Dead space

    (V/Q > 0.9)
  27. Low V/Q is...

    (V/Q < 0.8)
  28. Relating to V/Q, supplemental oxygen is relatively ineffective for...
    • low V/Q - aka shunt
    • (V/Q < 0.8)
  29. What are some early responses for asthma?
    • Release of mediators (induce bronchospasm, edema, mucous secretion)
    • IgE binding to antigen - first 15 minutes
    • Mast cell degranulation - first 15 minutes

  30. When does the epithelial damage of asthma occur?
    4-8 hours to days after exposure
  31. What do mast cells release?
    histamine, leukotrienes, interleukins, and prostaglandins
  32. Late responses of asthma...
    • epithelial damage
    • inflammatory changes

  33. How much fluid is normally between the visceral and parietal plura?
    3-4 teaspoons
  34. T/F: All pleural effusions cause symptoms.
  35. What is a Chylothorax?
    pleural effusion caused by lymph fluid

    "direct extravasation"
  36. How does malignancy cause pleural effusion?
    incrased capillary permeability due to obstruction
  37. T/F: Rheumatoid arthritis can be a cause of pleural effusion
  38. T/F: Tuberculosis can be a cause of pleural effusion.
  39. How does CHF lead to pleural effusion?
    ↑ hydrostatic pressure
  40. What is the normal V/Q ratio?
  41. Describe the patho of ARDS leading to pulmonary edema.
    • endothelial damage → inflammation → 
    • ↑ capillary permeability → PE & lung hemorrhage
  42. What is the less severe form of ARDS called?
    ALI (acute lung injury)
  43. T/F: ARDS is life threatening and often lethal.
    True. By definition, it is a serious condition (the less acute version is called ALI).

    Mechanical ventilation and critical care are usually required.

    • 90% death rate in untreated patients
    • 50% death rate in treated patients
  44. Inflammation of ARDS is a problem because
    gas exchange impairment, hypoxemia
  45. ARDS is a condition that affects only the lungs.
    False. It can result in multiple organ failure
  46. Is the cause of ARDS direct or indirect?
    • could be both
    • ie - trauma, infection
  47. What are some inflammatory processes related to ARDS?
    • Complement activation
    • Platelet aggregation
    • Release of neutrophil mediators
  48. What type of WBC is activated in ARDS?

    activated neutrophils release a variety of products that damage the alveolar cells and lead to edemasurfactant inactivation, and formation of a hyaline membrane.
  49. What are the 3 stages or ARDS?
    • 1. Exudative stage
    • 2. Fibroproliferative stage
    • 3. Resolution & Recovery
  50. Describe the Exudative stage of ARDS. When does it begin?
    Characterized by accumulation of excessive fluid, protein and inflammatory cells in that alveoli from the capillaries. 

    The exudative phase unfolds over the first 2 to 4 days after onset of lung injury.
  51. Describe the Fibroproliferative stage of ARDS.
    • Connective tissue and other structural elements in the lungs proliferate in response to the initial injury. Under a microscope, lung tissue appears densely cellular.
    • Also, at this stage, there is a danger of pneumonia, sepsis, and rupture of the
    • lungs causing leakage of air into surrounding areas.
  52. How long can lung function improve in the resolution and recovery stage of ARDS?
    6-12 months, or longer
  53. This layer of lung tissue wraps directly around the lung.
    visceral pleura
  54. This layer of lung tissue is closest to the outer chest wall.
    Parietal pleura
  55. What does MODS always involve?
    • inflammatory mediators which damage endothelium throughout the body
    • (cytokines such as TNF, IL1, endotoxins from gram negative bacterial infection)
  56. What is MODS?
    Progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury
  57. The "respiratory failure" stage of MODS occurs when?
    first 72 hours
  58. The "liver failure" stage of MODS occurs when?
    5-7 days
  59. The "GI bleeding" stage of MODS occurs when?
    10-15 days
  60. The "kidney failure" stage of MODS occurs when?
    11-17 days
  61. Is MODS a primary or a secondary disease?
    can be either
  62. Which organs are most commonly involved in MODS?
    lungs, spleen, liver, kidneys
  63. MODS used to be called
    MOF (multiple organ failure)
  64. What systems are activated in MODS?
    • kinin
    • complement
    • coagulation
    • fibrinolytic

    DIC may occur
  65. What is a proposed cause of MODS?
    gram - bacteria

    ischemia and structure changes → gut permeability → gram – escapes from gut and runs rampant
  66. What WBCs are involved in MODS?
    neutrophils - they are attracted to the damaged endothelium
  67. What is released from damaged endothelial cells and what does it do?
    nitric oxide - it increases permeability and causes vascular leakage
  68. What ultimately leads to the organ failure in MODS?
    acidosis and uneven distribution of blood flow
  69. What is the treatment for MODS?
    supportive...ventilation, fluid/electrolyte balance, control infection, TPN...
  70. What type of genetic transmission occurs in CF?
    autosomal recessive
  71. T/F: CF is a rare disease.
    False, it is common. 1000 new cases are diagnosed each year.
  72. Which disease has the manifestation of "salty sweat?"
  73. What is the genetic cause of CF?
    chromosome 7 gene mutation (CFTR gene, "cystic fibrosis transmembrane regulator")

    results in chloride ion channel problem: defective chloride ion secretion with excessive sodium and water absorption
  74. What are the manifestations of CF?
    • thick & viscid respiratory tract secretions
    • micro-environment protects microbial agents
    • defective mucociliary clearance
    • neutrophil influx with release of elastase & inflammatory mediators
    • chronic airway obstruction and bacterial infection; development of chronic bronchitis, bronchiectasis, respiratory failure
  75. T/F: CF is more common in Asians.
    False. Caucasians.

    Cystic fibrosis is less common in other ethnic groups, affecting about 1 in 17,000 African Americans and 1 in 31,000 Asian Americans
  76. Why are CF pt's skinny?
    Thick and sticky mucous blocks ducts in the pancreas and causes malnutrition of the patient
  77. Patho of CF?
  78. What is another name for RDS?
    Hyaline membrane disease
  79. What is the result of RDS on the respiratory system?
    deficiency in alveolar surface area for gas exchange

    results in atelectasis, shunting, persistence of fetal circulation
  80. Describe a hyaline membrane
    composed of cellular debris, red blood cells, neutrophils, and macrophages. Appears as amorphous material, lining or filling the alveolar spaces and blocking gas exchange
  81. When does RDS begin?
    shortly after birth
  82. S&S for RDS?
    tachypnea, chest wall retractions, expiratory grunting, flaring of the nostrils, cyanosis, hypercarbia, prolonged apnic periods, ventilatory failure
  83. How long is the clinical course for RDS?
    • 2 to 3 days.
    • Day 1-worsens
    • Day 2-may be stable
    • Day 3- resolution
  84. What is a clinical sign that RDS is resolving?
  85. What is the most common single cause of death in the first month of life?
  86. Treatment for RDS could include:
    • maternal glucocorticoid administration
    • surfactant to infant via ET tube
    • ventilatory support
    • inhaled nitric oxide
  87. What causes RDS?
    developmental insufficiency of surfactant production and structural immaturity in the lung
  88. When do type II pneumocytes mature?
    23-28 weeks gestation

    type II cells secrete surfactant
  89. Is it possible to have RDS in a term infant?
    Yes, it can also result from a genetic problem with the production of surfactant
  90. T/F: RDS is less likely in babies delivered by C-section due to less stress on the baby during birth.
    False. The stess is thought to help with glucocorticoids which help lung maturation
  91. What is the key presenting factor in compartment syndrome?
    Pain out of proportion to physical findings
  92. What is compartment syndrome?
    Increased pressure in muscle compartment that leads to muscle and nerve damage
  93. T/F: Pathologic fractures do not occur with normal activities, but increased stress can cause bones to break more easily.
    False. Pathologic fractures can be caused by normal activities.
  94. What is the most common metabolic disease?
  95. T/F: The patho of osteoporosis involves osteoblast activity > osteoclast activity.
    • False. 
    • OsteoBlasts Build bone.
    • OsteoClasts Cut bone.

    So, in osteoporosis, osteoclast activity is > osteoblast activity
  96. Which med is antiosteoclastic?

    Fosamax cuts the cutting!
  97. Which med is pro-osteoblastic?

    Forteo builds that bone fort!
  98. Which hip is most often involved in developmental dysplasia of the hip?
  99. Which gender is more likely to have developmental dysplasia of the hip?
    Females (80% of cases)
  100. T/F: The first born is at greatest risk of developmental dysplasia of the hip.
  101. T/F: Hip formation is not completed until 24 weeks gestation.
    False, it is largely complete by 11 weeks
  102. What are some conditions associated with developmental dysplasia of the hip?
    • oligohydramnios (low amniotic fluid)
    • down syndrome
    • spina bifida
  103. Which type of birth increases the risk for developmental dysplasia of the hip?
  104. Osteoporosis is a skeletal disorder characterized by loss of bone mass and deterioration of the architecture of ________ bone with a subsequent increase in bone fragility and susceptibility to fractures
  105. What types of things cause osteoporosis?
    • endocrine disorders
    • malignancy
    • aging
  106. T/F: a low protein diet increases your risk of osteoporosis
    False. High protein diet is a risk factor
  107. What are some risk factors for osteoporosis?
    • White
    • Aging
    • Small bone structure
    • Postmenopausal (female)
    • Smoking, alcohol, caffeine
    • Sedentary
    • Calcium Deficient
    • More...
  108. T/F: RA usually has a gradual onset.
  109. Is RDS more of a dead space or shunt problem?
  110. T/F: MODS is easy to treat if diagnosed early.
    False. Prevention is more valuable, as it is hard to reverse.

    "UNCONTROLLED inflammatory response"
  111. What is the most important cell contributing to inflammation?
  112. Why is it so hard to increase the PO2 in ARDS?
    diffusion impairment (hyaline membrane)
  113. Can ARDS develop in babies?
  114. How long does it take for CK to become elevated after an MI?
    6-12 hours
  115. When does the peak CK level occur?
    18-24 hours after the MI, then it gradually returns to baseline
  116. When is troponin detectable in serum after MI?
  117. T/F: Troponin returns to baseline levels 2 days after the MI.
    False. It remains elevated at low levels for 5-7 days
  118. When damaged cells release potassium, it contributes to decreased
  119. What type of HF does Paget's disease produce?
    High output HF
  120. What type of HF does throtoxicosis produce? (high vs. low)
    High output HF
  121. Conditions that cause AV shunt cause which type of HF? (high vs. low)
    High output
  122. Ischemic heart diseases results in _______ output HF. (high vs. low)
  123. Cardiomyopathy results in _______ output HF. (high vs. low)
  124. Sepsis causes which type of HF? (high vs. low)
    low output
  125. Where do fatty streaks form?
    between the endothelium and internal elastic lamina
  126. What do fatty streaks contain?
    atherogenic lipoproteins and macrophage foam cells
  127. What is the fibrous cap made of?
    layers of smooth muscle and connective tissue matrix
  128. Where is the autonomic control center for the cardiac function and blood pressure located?
    bilaterally in the medulla oblongata
  129. What does the vasomotor center control?
    sympathetic-mediated acceleration of heart rate and blood vessel tone
  130. What does the cardioinhibitory center control?
    parasympathetic-mediated slowing of heart rate