Test #3

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Sarahs129
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266768
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Test #3
Updated:
2014-04-06 23:51:41
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Critical Care Test
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Description:
Shock States,Diabetes Crisis, Alterations in Metabolism and Nurtition
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  1. What is shock?
    • Mismatch between O2 delievery and O2 demand.
    • When oxygenation and tissue perfusion needs are not met.
    • Inability to adequately perfuse cells.
  2. Shock syndrome
    • Pattern of responses and symptoms related to inadequate tissue perfusion.
    • Involves a whole body response.
  3. Cardiogenic shock
    ie...
    • The inability of the heart to generate CO to perfuse tissues.
    • ie...Acute MI
  4. Hypovolemic shock
    ie...
    • Loss of intravascular volume imparing tissue perfusion.
    • ie...hemmorrhage, Burns, Dehydration
  5. Distributive shock
    -types of distributive shock
    • Impaired tissue perfusion from maldistribution of the vascular space.
    • (Does not fill vessels completly-no BP)
    • -Neurogenic, septic, anaphyactic
  6. Neurogenic shock
    Loss of sympathetic-mediated vascular tone
  7. Spetic shock
    Vasodilation from bacterial endotoxins
  8. Anaphyactic shock
    Vasodilation from histamine release
  9. Stages of shock
    • Inital (Early) stage
    • Compensatory stage
    • Progressive stage
    • Refractory stage
  10. Inital (Early) Stage of shock
    • Subtle symptoms - difficult to detect
    • Slight increase in HR and RR
    • Slight decrease in MAP (<10 mm Hg)
    • Mild anaerobic metabolism w/lactic acid production.
  11. Compensatory Stage of shock
    • Anaerobic metablolism with acidosis and increased K.
    • MAP decreased (10-15 mmHg)
    • Renal and hormonal compensatory mechanisms activated.
    • Increased HH, RR, thirst and anxiety.
    • Decreased BP, UO, SaO2
  12. How does the sympathetic response occur during shock?
    Pressure receptors detect low BP which will release catecholamines increasing CO and causing vasoconstriction which will increase HR and BP.
  13. Progressive Stage during shock
    • Compensitory mechanisms are no longer able to compensate.
    • MAP <20 mmHg
    • Hypoxia of vital organs
    • Oliguria/anuria
    • Rapid/weak pulse
    • CMS
  14. Refractory Stage of shock
    • Non-recoverable organ damage
    • LOC
    • pulse not palpable
    • SaO2 not measureable (very late sign)
    • Death
  15. General Clinical findins in all types of shock
    • BP <90/60
    • Tachycardia
    • Tachypnea
    • Oliguria/anuria
    • Altered mentation
  16. Lactate levels in shock
    • Increased = indication of poor perfusion and oxygenation.
    • Normal level - 0.6-202 mmol/L
    • Shock level - >4 mmol/L
  17. Base deficit in shock
    Base level increased d/t trying to compensate for acidosis.
  18. Goal in the management of shock
    • Improve tissue oxygenation and perfusion of tissues.
    • IV fluids 1st- NSS, fluid of choice
    • Vasoconstrictors 2nd - Neo, Levo, epi
    •    or Inotropes - Dubutomine, Milrinone
    • Vasodilators
    • Optimize nutrition
  19. Criteria for cardiogenic shock
    • Increased SVR
    • Decreased CO
  20. Main treatment of Cardiogenic shock
    Intra aortic balloon pump to reduce cardiac workload
  21. Intra aortic balloon pump
    • via femoral artery
    • placed in thorasic aorta
    • inflated and deflated with cardiac cycle:
    • -- inflated with diastole increasing coronary artery perfusion
    • -- deflated with systole decreasing workload and increasing CO
  22. Complications of Intra Aortic Balloon Pump
    • Femoral artery obstruction
    • Blood clots
    • Platelets destroyed
    • Balloon rupture
    • Infection
    • Bleeding
  23. Hypovolemic shock
    Decreased circulating volume, decreased tissue perfusion, decreased oxygenation.
  24. Assessment findings of hypovolemic shock
    • Hypotension
    • Orthostatic
    • Tachycardia/tachypnea
    • Decreased CO
    • Increased SVR
  25. Treatment of hypovolemic shock
    • Indentify source and stop fluid loss
    • Restore circulating volume
  26. Distributive shock states
    -Definition
    -Types
    • -Blood volume is not lost, it is not being distributed properly d/t vasodilation of the vessels.
    • -Neurogenic, Anaphylactic, Septic
  27. Neurogenic shock
    -Definition and cause
    -Manifestations
    • Caused by the sudden loss of the sympathetic nervous system - most common cause is SCI
    • -Massive vasodilation - very low BP
    • -Inhibition of baroreceptors - bradycardic
    • -Impaired thermoreulation - hypothermia
  28. Management and Treatment in Neurogenic shock
    • Stabilize spine
    • Improve preload to increase CO
    • Maintain BP with pressors
    • Correct bradycardia with atropine, dopamine or PPM
    • Correct hypothermia
    • DVT prophylaxis
  29. Anaphylactic shock
    • Severe antibody-antigen reaction.
    • Inital exposure causes antibody formation. Subsequent exposures release antibodies causing and allergic response.
  30. Manifestations of anaphylactic shock
    • Occur within minutes
    • Laryngeal edema
    • Decreased BP
    • vasodilation
    • bronchoconstriction
    • tachycardia
  31. Treatment of anaphylactic shock
    • Identify cause
    • Maintain airway- O2, intubation, Epi
    • Block histamine response- Benadryl, corticosteroids
  32. Septic shock
    • Most complex - Most common
    • Microorganisms which release endotoxins invade the body and enter bloodstream.
  33. Progression of sepsis
    Local infection - SIRS - Sepsis - Severe sepsis - Septic shock.
  34. Severe sepsis
    Sepsis with signs and symptoms of end organ failure
  35. Criteria of septic shock
    Signs and symptoms of severe sepsis PLUS persistant hypotension not responding to adequate fluid resiscitation
  36. Why are patients hypotensive in spetic shock?
    infection causes vasodilation
  37. Treatment of septic shock
    • Blood cultures prior to antibiotics
    • Fluid resuscitation or pressors
    • Maintain a PaO2 of >70% and a normal pH
    • Corticosteroids
    • Glucose control (<180)
    • Stress ulcer and DVT prophylaxis
  38. Goal CVP with septic patients
    • 8-12 mmHg
    • 12-15 mmHg if ventilated
  39. The nurse would assign which nursing diagnosis to any patient diagnosed with shock?
    1. Altered Tissue Perfusion
    2. Ineffective airway clearance
    3. Imbalanced Nutrition: Less than body requirements
    4. Impaired Gas Exchange
    1. Impaired tissue perfusion
  40. A patient presents with a 5-day history of n/v/d and fever. He has not been able to take fluids by mouth. The nurse provides care based on this patients risks for which problem?
    1. Obstructive shock
    2. Cardiogenic shock
    3. Hypovolemic shock
    4. Spetic shock
    3. Hypovolemic shock
  41. A patient presents to the ER with the report of being stung by a bee. the patient is experiencing dyspnea, edema and rash. Which medication would the nurse anticipate administering immediatly to help prevent progression to anaphylactic shock?
    1. Epi-
    2. Albuterol
    3. Prednisone
    4. Dopamine
    1. Epi-
  42. A patient who had abdominal surgery yesterday is cold, clamy and confused. Which additional assesement findings would support concern that this patient is in shock? (Select all that apply)
    1. Pulse is rapid and weak
    2. Arterial pH is 7.49
    3. Serum lactate level is 5.8 mmol/L
    4. base excess is 1 mmol/L
    5. Bp 92/50 mmHg
    • 1. Pulse is rapid and weak
    • 3. Serum lactate level is 5.8 mmol/L
  43. A patient is recieved in the ER from EMS after sustaining a brain injury in a fall. She is on a spineboard and has a cervical collar in place. She is not moving her lower extremities. What would alert the nurse to the possible development of neuroenic shock?
    1. The patient reports that she feels a tingling senation in her lower extermities.
    2. The patient's HR froms from 82 bpm to 52 bpm
    3. The patients gluose is 134 mg/dL
    4. The patients friend reports that the patient was unconscious for a few seconds after the fall.
    2. The patient's HR froms from 82 bpm to 52 bpm
  44. What effect does insulin have on metabolism?
    • Regulation of fats, cabs and protein metabolism.
    • Needed to transport glucose into the cells for uptake by the cells.
  45. In DM, what alterations occur with insulin?
    Both insulin deficiency and insulin release
  46. What metabolic problems occur because of insulin resistance?
    • Lipolysis
    • Lipidema
    • Elevated serum ketone levels
  47. What type of fluid and electrolyte imbalance occurs with insulin deficiency?
    • Increased plasma osmotic pressure
    • Shift of body fluids from the tissues and cells into the intravascular space
    • intracellular dehydration
  48. What effect does the state of hyperlycemia have on excretion?
    produces osmotic diuresis
  49. What electrolyte deficiency primarily occurs because of the osmotic diuresis that occurs with DM?
    Loss of K, Na, Cl, P
  50. What electrolyte deficiency that occurs in DM is primarily responsible for reported symptoms of weakness and fatigue?
    Hypokalemia and Hyponatremia
  51. What would the serum osmolality be in DM?
    Increased d/t increased fluid losses
  52. What would the urine osmolality be in DM?
    Decreased d/t copious amounts of dilute urine
  53. Why does polydipsia occur in DM?
    Dehydrate stimulates thirst center
  54. What effect does hyperglycemia have upon the cardiac output?
    Decreased CO d/t dehydration
  55. What effect does hyperglycemia have on tissue perfusion?
    • Decreased to the brain and vital organs.
    • Commonly results in ARF
  56. What would you expect the BP to be in an hyperglycemic state?
    Hypotensive d/t circulatory volume
  57. What is the most common complication of DM?
    hypoglycemic crisis
  58. What are some triggers of hypoglycemic crisis?
    • Exercise
    • Diet
    • Anti-hyperglycemic agents
  59. Manifestations of hypoglycemia
    • CMS
    • drowsiness
    • dizziness
    • death
    • sweatin
    • anxiety
    • clamminess
    • hyperventilation
  60. How miht hyperglycemia in older adults be overlooked or misdianosed?
    Cognitive alterations may be misdiagnosed as demetia or delirium
  61. Nursing action with alert patient with hypoglycemia
    • oral replacement of glucose: graham crackers, OJ, glucose tabs
    • Repeat q15
  62. Nursing action with unconscious patient with hypolycemia
    • Side-lying
    • 50% Dextrose IV push
    • BG q15
  63. If no IV access is available for use in the treatment of hypoglycemia in an unconscious patient, what is a critical nursing action?
    Administer IM glucagon as a substitute for IV Dextrose
  64. What is the most common hyperglycemic state?
    Diabetic Ketoacidosis
  65. What type of insulin alteration occurs in DKA?
    • Complete or absolute deficiency of insulin
    • NO insulin is available.
  66. What are the 3 classic clinical manifestations are seen in DKA?
    • Ketosis
    • Metabolic acidosis
    • Uncontrolled hyperglycemia
  67. What is the most common precipitating factor for the onset of DKA?
    Infection
  68. 2 ways that metabolic acidosis is detected in DKA.
    • pH imbalance
    • High anion gap (>18)
  69. 3 causes of an increased anion gap
    • DKA
    • Starvation
    • lactic acidosis
  70. Name a respiratory compensatory response to metabolic acidosis seen in DKA?
    kussmauls respitrations
  71. Describe kussmauls breathing.
    rapid to excrete carbonic acid - sweet smell
  72. What is the insulin alteration seen in HHS?
    • Insulin deficiency with insulin resistance
    • Produces enough insulin to prevent production of ketones
  73. Compare onset of HHS with onset of DKA.
    • HHS slower
    • DKS s/s occur rapidly
  74. Mortality of HHS vs. DKA
    HHS higher mortality d/t sever dehydration
  75. Most common precipitating factor contributing to the onset of HHS.
    Infection
  76. What medical condition is frequently associated with HHS?
    renal failure
  77. Lab data associated with HHS
    • Glucose >600
    • Decreased serum osmolality
    • pH >7.3
    • Negative ketones
    • No anion gap
  78. Diabetic populations that develop DKA or HHS.
    • Type I DM - DKA
    • Type II DM - HHS
  79. Priority medical and nursin management in DKA and HHS.
    • Restore intravascular volume.
    • Iso- or hypotonic
    • Change when BG in <200mg/dL, then with dextrose
  80. Correction of ketones in DKA?
    • Continuous IV infusion of insulin
    • IV volume replacement
    • Electrolyte replacement
  81. How do you not correct ketoacidosis too rapidly?
    Not giving IV push Na bicarb unless pH is <6.9
  82. What type of insulin and method of administration is given in DKA and HHS?
    • Short acting regular insulin
    • IV push then continuous infusion
  83. Anabolism
    Metabolic process that is best described as a  constructive tissue building process
  84. An example of when a patient is engaging in an anabolic metabolism.
    When they are nurished with nutrients
  85. What processes are occuring in the flow phase?
    • Hypermetabolism
    • Hyperglycemia
    • Increased O2 demands
    • Increased caloric needs
  86. What % of glucose is in TPN?
    10% glucose
  87. What IV classification is TPN?
    Hypertonic IV solution
  88. What would the nurse expect the anergy reaction to be when checking for a known antigen in a malnurished patient?
    No skin reaction occurs in a amlnurished state.
  89. What lab study is the most reliable indicator for the nurse to evaluate acute catabolic changes in the nutritional status of patients?
    Prealbumin
  90. What does loss of muscle mass indicate about the patients metabolic process?
    Ongoing catabolism
  91. What is the adrenal cortex response to metabolic stress?
    Increased cortisol resulting in hyperglycemia
  92. How will vital signs be altered by the adrenal medulla response to metabolic stress?
    Catecholamines will increase resulting in increased HR and BP
  93. What happens to glucose immediately upon physiologic stress?
    Glycogen stored become rapidly depleted causing hyperglycemia
  94. What is the preferred fuel source for cellular function?
    Carbs
  95. If carbs and fats are not available as fuel sources for cellular function, what does the body use?
    Proteins
  96. What hormone when secreted will enhance protein levels in the body?
    Growth hormone.
  97. What happens to insulin levels when the patient is in a catabolic state?
    • Low levels
    • Insulin deficiency occurs with low levels of proteins
  98. How does low levels of protein affect muscle mass?
    Loss of skeletal muscle mass
  99. How does low levels of protein affect the immune system?
    • Diminished resistance to infection.
    • Delayed wound healing.
  100. What is the metabolic effect on circulation volume when there is a metabolic stress induced stimulation?
    Volume increased because there is an increase in secretion of aldosterone.
  101. What is the name for the assessment measurements used to measure body mass and fat reserves?
    Anthropometric measurements
  102. Expected BMI for a malnourished patient.
    • <18
    • <16 indicated severe malnutrition
  103. What plasma protein is crucial for maintaining blood osmotic pressure and intravascular fluid volume?
    Albumin
  104. What factors can alter the accuracy of albumin levels?
    Hydration and renal or liver status.
  105. What factors can alter the accuracy of transferrin levels?
    • Low iron
    • Blood transfusions
    • Blood loss or anemia
  106. What is a nutritional goal for nitrogen balance in a high-acuity patient?
    Maintaining a positive nitrogen balance
  107. What would the expected TLC (total lymphocyte count) in malnutrition?
    Low - malnutrition causes immunosuppression
  108. What effect does overfeeding have upon the respiratory center?
    Can overburden the lungs
  109. Cachetic
    A patient who visibly looks like their fat stores are used up
  110. What effects does enteral nutrition have upon the health of the GI tract?
    • Maintains gut barrier function
    • Maintains gut immunologic function
  111. What micronutrient is particularly deficit in the malnourished alcoholic?
    thiamine
  112. When is TPN contraindicated?
    In patients with a functioning and usable GI tract.
  113. What are some administration measures that must be done when infusing lipid emulsion?
    • Infused in a separate line
    • Infuse on a pump
    • Connect lipids below the filter of the TPN line
  114. What is the most frequent complication of TPN?
    Hyperglycemia
  115. What type of metabolism occurs when there is respiratory acidosis?
    • Anaerobic metabolism
    • Because there is a lack of O2
  116. How is nitrogen balance measured?
    24 hour urine on ice -- measures urine urea nitrogen
  117. Kwashiorkor
    Severe catabolic protein malnutrition.
  118. Malnutritions effects on thyroid
    Decreased T3 and T4
  119. What is metabolism?
    • Transforming nutrients into energy by chemical professes
    • Converts food sources from its storage state into an energy source
  120. Anabolism
    • Building process
    • New cell growth
    • Requires energy
  121. Catabolism
    • Breakdown process
    • Exceeds anabolism
  122. Aerobic metabolism
    • Requires O2
    • Created energy from carbs, fats and proteins
  123. *Anaerobic metabolism
    • Where glycolysis is used for energy
    • Occurs with respiratory acidosis
    • Occurs when on a vent or hypoxic
  124. Preferred fuel source of cellular function
    Carbs
  125. Metabolic responses to stress
    • Glycogen stores become rapidly depleted
    • Body will use proteins if inadequate carbs and fats are available.
  126. Why is adequate levels of protein important?
    • Formation of cells, tissues and organs
    • Transmission of nerve impulses
    • Building blocks for genes, hormones, antibodies
  127. Effects of inadequate proteins
    • Malnourishment
    • Poor wound healing
    • Atrophy of gut
  128. ACTH and metabolism
    Targets adrenal cortex and regulates cortisol release which breaks down glycogen and lipids
  129. *Over feeding with Malnutrition
    DO NOT overfeed -- requires O2 and puts a burden on respiratory systems
  130. Lab assessments with malnutrition
    • Albumin - overall nutritional status, not presently
    • Prealbumin - most reliable as it's not altered by hydration
    • Nitrogen balance - calculated protein needed (what to have + nitrogen balance)
  131. Enteral feedings with malnutrition
    • Don't over feed
    • Have to give free water
  132. TPN
    • Thru a central line
    • Contraindicated in functioning GI tract
    • Has to given with a filter
    • Lipids get attached below the filter
  133. What if you run out of TPN?
    Hang D10 at the dame rate to prevent rebound hypoglycemia
  134. Metabolic response to stress
    Any response to stress can cause hyperglycemia
  135. Type I DM
    Beta cells not producing insulin
  136. Type II DM
    Glucose unable to get into cells
  137. Hypoglycemic crisis
    Can occur with any type of DM
  138. Thiazides and DKA
    Thiazides can cause DKA
  139. *Goal of DKA and HHS
    • Restore Fluid volume
    • Correct electrolytes
    • Normalize glucose
  140. Goal of the inflammatory response
    Limit the extent of injury and promote healing
  141. Cells involved in the inflammatory response
    • WBCs - primary
    • Mast cells
    • Endothelial cells
    • Platelets
  142. Patho of the inflammatory response
    Histamine is releases, allows leakage out of capillaries allowing WBCs out to work and causes leakage of fluid
  143. Phases of the inflammatory response
    • Inflammation
    • Coagulation
    • Fibrinolysis
    • **All must balance out
  144. C-reactive protein
    • Indicated inflammation
    • Increased with atherosclerosis
  145. S/S of systemic inflammatory response
    • *Must have 2 or more
    • Temp >100.9 or <96.8
    • Tachycardia >90
    • Tachypnea >20
    • PaCO2 >32 mm Hg
    • WBC <12,000 or >4,000 or <10% bands
  146. It is suspected that a patient is developing SIRS. Which assessment findings would the nurse interpret as supporting this suspicion? (Select all)
    1. Temp of 96.4 F (35.8 C)
    2. HR 108
    3. PaCO2 28 mmHg
    4. WBC 10,000
    5. RR 22
    1 - 2 - 3 - 5
  147. Examples of SIRS
    • Sepsis
    • Pancreatitis
    • Ischemia
    • Anaphylaxis
    • Central line infections
  148. SIRS
    Systemic inflammatory response syndrome
  149. What happens when SIRS is not contained?
    • Uncontrolled activation of inflammatory cells.
    • Damage to vascular endothelium (edema)
    • Disruption of immune cell function
    • Progresses to MODS
  150. Sepsis
    Systemic inflammatory response to an infection
  151. Severe sepsis/SIRS
    systemic inflammatory response plus hypoperfusion
  152. Septic shock/SIRS shock
    Sepsis induced shock
  153. S/S of septic shock
    • Hypotension despite fluid resuscitation
    • Presence of perfusion abnormalities
  154. Patho of Sepsis
    • Endothelium become inflamed and O2 and nutrients do not pass from vascular space to the cells.
    • Vascular permeability increases and capillaries leak fluids.
    • Coag cascade activated
    • Thrombin produced
    • Endothelial further damages
    • Fibrinolysis delayed due to APC deficit
    • Balance of clot formation and breakdown is disrupted
  155. Treatment goal of Sepsis
    • Decrease inflammation
    • Address coagulation
    • Restore Fibrinolysis
    • Maintain homeostatic
  156. Septic shock
    • Cause by endotoxins
    • Causes vasodilation resulting in decreased SVR, increased CO
  157. Sepsis resuscitation bundle
    • Measure serum lacate
    • Blood cultures prior to ABX
    • Broad spectrum ABX within 1 hr of ED admission
  158. Treatment of Sepsis
    • Fluid resuscitation
    • Vasopressors if not responding to fluids
    • Suport failing organs
    • Glycemic control (always hyperglycemic) Goal is <180
    • C&S
  159. A patient who has developed MODS has as a BG of 175 over the last 3 days. How would the nurse interpret this finding?
    Under adequate control -- Goal is to keep BG<180
  160. Risk factors for septic shock
    • Age
    • Coexisting diseases
    • Malnutrition
    • Invasive devices
    • Drug and fluid therapy
    • Surgical or traumatic wounds
  161. MODS
    • Multiple Organ Dysfunction Syndrome
    • 2 or more organ system failures
  162. High Risk for MODS
    • Trauma
    • Experienced a shock episode
    • >65
  163. Relationship between MODS and SIRS
    • All patients with MODS have SIRS
    • Not all patient with SIRS have MODS
  164. What statement about the pathogenesis of SIRS is accurate?
    1. It's not associated with MODS
    2. It is an abnormal generalized pro-inflammatory response.
    3. It is an attempt to limit inflammation
    4. It is associated with an excessive anti-inflammatory response.
    2. It is an abnormal generalized pro-inflammatory
  165. DIC
    • Disseminated Intravascular Coagulation
    • Accelerated clotting resulting in consumption of clotting factors
  166. Causes of DIC
    • Spillage of thromboplastin into circulation
    • Damage of vascular endothelium
    • Stagnant blood flow
    • Infectious agents
    • TBI
  167. S/S of DIC
    • Occult bleeding
    • Overt bleeding
    • Petechiae & ecchymosis
    • Decreased perfusion of tissues
  168. PTT and INR with DIC
    • Both will be elevated only in DIC -- unless converting from Heperain to Coumadin
    • --Will be a decrease in all things used to clot (Platelets)
    • -- Will be an increase in all things the represent bleeding time (PT/INR)
  169. Treatment for DIC
    • Initiating factor must be removed.
    • (If sepsis - must rid sepsis)
  170. The main cause of cardiogenic shock is...
    an inability of the heart to pump blood forward
  171. Which of the following parameters sports the diagnosis of cariogenic shock?
    1. Decreased RA pressure
    2. Decreased Wedge pressure
    3. Increased CO
    4. Decreased CI
    • 4. Decreased CI
    • --would be increased CVP, increased PA pressure
  172. With anaphylactic shock, which mechanism results in a decreased cardiac output?
    Histaminee release
  173. Which of the following drugs promotes bronchodilation and vasoconstriction?
    1. Solu-Medrol
    2. Gentamicin
    3. Atropine
    4. Epinephrine
    4. Epinephrine
  174. The patients at highest risk for neurogenic shock are those who have had...
    a SCI
  175. In septic shock, which of the following hemodynamic values would you expect to find?
    1. CO 10 L/min
    2. PA pressure 17 mmHg
    3. Wedge 23 mmHg
    4. SVR 1100
    • 1. CO 10 L/min
    • -- decreased SVR, decreased wedge, increased CO
  176. Which of the following is the pathophysiologic mechanism that results in septic shock?
    1. Bacterial endotoxins leads to vasodilation.
    2. Increased WBCs are released to fight invading bacteria
    3. Microorganisms invade organs such as the kidneys and heart
    4. Increase of ABCs leads to the decrease of RBC production and anemia.
    1. Bacterial endotoxins leads to vasodilation.
  177. The medical management of septic shock is aimed toward...
    Finding and eradicating the cause of infection.
  178. Signs of hypovolemia in the trauma patient include...
    1. Distended neck veins
    2. Decreased LOC
    3. Bounding radial and pedal pulses
    4. A widening pulse pressure
    2. Decreased LOC
  179. The net effect of the vascular phase of local inflammatory response is...
    The movement of blood cells and plasma proteins into the inflamed tissue.
  180. The goal of local inflammation is...
    Limit the extent of injury and promote healing.
  181. SIRS is an exaggerated systemic response to...
    1. Bacteria
    2. Sepsis
    3. Local infection
    4. Endotoxins.
    • 3. Local infection
    • **Not ALWAYS true in 1, 2, 4
  182. A patient has a temp of 35.5 C, HR 120 bpi, WBC of 3,000. This patient may have which of the following?
    1. MODS
    2. Bacteremia
    3. SIRS
    4. A local inflammatory response
    3. SIRS
  183. Which of the following clinical manifestations is NOT suggestive of the SIRS?
    1. Temp of 38.5
    2. HR 85
    3. RR 24
    4. WBC 15,000
    2. HR 85
  184. When SIRS is the results of an infection, it is called...
    Sepsis
  185. The difference between primary and secondary MODS is that primary NODS is the result of...
    Direct organ insult
  186. Prominent explanations for the pathologic changes that occur with NODS include:
    1. Uncontrolled systemic circulation
    2. Tissue hypoxia
    3. Unregulated apoptosis
    4. microvascular coagulation
    All of the above.
  187. The GI system is a common target organ for NODS related to...
    disruption of the mucosal barrier from hypoperfusion
  188. Which of the following is true about a definitive treatment for NODS? (Select all)
    1. There is no definitive treatment for MODS
    2. Current management is focused on supporting organ function
    3. Continuous renal replacement therapy must be used for patients with MODS
    4. Mechanical ventilation must be used for patients with MODS
    • 1. There is no definitive treatment for MODS
    • 2. Current management is focused on supporting organ function
  189. Clinical manifestations of ischemic hepatitis show up 1 to 2 days after insult. Which symptom below is indicative of hepatic insufficiency?
    1. Elevate serum creatinine
    2. Decreased bili
    3. jaundice
    4. Decreased serum transaminase
    3. Jaundice
  190. Ms. X is admitted to the ICU after she developed SIC following a vaginal delivery. What is the result of DIC?
    Depletion of clotting factors and excessive fibrinolysis, resulting in simultaneous microvascular clotting and hemorrhage.
  191. Lab values for DIC will show abnormalities in...
    Platelets
  192. 2 divisions of the nervous system
    • CNS
    • PNS
  193. Types of nerves
    • Voluntary
    • Involuntary
  194. Types of nerve cells
    • Neurons
    • Neuroglia (Glial cells)
  195. Neurons
    • Functional unit of the nervous system
    • DO NOT divide of replicate
    • Need O2 to survive
  196. Glial cells
    Provide support, nourishment and protection to the neurons
  197. 2 types of neurotransmitters
    • Excitatory - promote conduction
    • - Norepi-
    • Inhibitory - resists depolarization (slows down transmissions)
    • - Dopamine
  198. Cerebrum
    • Separated in (L) and (R) hemi-
    • Contains 4 lobes
    • Contains cerebral cortex - covering
  199. Brocca's area.
    Damage to it?
    • Within the frontal lobe of the cerebrum
    • Impaired motor speech
    • Expressive aphasia
  200. Wernicke's center.
    Damage to it?
    • Within the temporal lobe of the cerebrum
    • Inability to understand words and language
    • Receptive aphasia
  201. Global aphasia
    Inability to understand NOR able to speak
  202. Cerebellum responsibilities
    • Coordination of muscle movement
    • Maintenance of equilibrium and muscle tone
  203. Brain stem components
    • Medulla Oblongata
    • Pons
    • Midbrain
  204. Medulla Oblongata responsibilities
    • Involuntary functions
    • Decussation point (where impulses cross to opposite side of the body)
  205. Pons responsibilities
    Respiratory center
  206. Midbrain responsibilites
    Relay station
  207. Diencephalon contains....responsibilities
    • thalamus - sensory relay
    • hypothalamus - ANA and endocrine regulation, thermoregulation
  208. Limbic system
    Fight or flight
  209. Reticular formation
    Arousal and consciousness
  210. What does the subarachnoid space contain and what can a major complication be?
    • Contains BVs and CSF
    • If any part of the space gets clogged the fluid has no where to go.
  211. CSF
    • Should contain no RBCs or WBCs
    • Continuously produced
  212. Spinal tap
    • Between L4-5
    • NOT with ICP
  213. The tentorium cerebelli
    A fold in the Dura mater that separates the cerebrum and the cerebellum
  214. Cerbral arterial circulation
    • Carotids biforcate into internal and external.
    • Vertebral arteries
    • Circle of Wills at the base of the brain to ensure adequate blood flow to the brain.
  215. Cerebral verous circulation.
    • Unique as it contains no valves.
    • Important for maintaining any brain injury.
  216. Cranial Nerve III
    Occulomoter - constricts pupils
  217. Crainial Nerve IX
    Glossopharyngeal - gag reflex
  218. Cranial Nerve X
    Vagus - innervation to lungs
  219. ICP
    Hydrostatic force measured in the brain CSF fluid compartment.
  220. Normal ICP
    <15 mmHg
  221. Components of the brain
    • Brain tissue
    • Blood
    • CSF
  222. **Monro-Kellie Hypothesis**
    • An increase in the volume of 1 component in the brain mus be compensated by a decrease in 1 or both of the others.
    • If not, will result in ICP
    • ICV = H2O+CSF+CBV
  223. Bodys strongest incentive to breath?
    Increase PaCO2
  224. Manifestations of increased ICP
    • *Decreased LOC
    • Headache
    • Vomiting
    • Seizures
    • Change in V/S
    • Cushings Triad
    • Ocular changes
  225. Autoregulation and cerebral blood flow
    ie..HTN
    • Alteration in the diameter of the vessels to maintain constatnt blood flow to the brain over a wide range in systemic arterial pressure.
    • ie...HTN will increase pressure in the brain, autoregulation will decrease the diameter of the vessels to protect the brain.
  226. MAP for autoregulation
    MAP must be between 50 and 150mmHg for autoregulation.
  227. Calculating MAP
    MAP =  2(DBP) + SBP / 3
  228. Loss of autoregulation will cause...
    Inccreased ICP, d/t increase or decrease in BP, with or without brain injury.
  229. Cerebral Perfusion Pressure (CPP)
    Normal levels
    Goal levels
    • Pressure needed to maintain blood flow to the brain.
    • Normal is 70-100 mmHg
    • GOAL is to keep greater than 60 mmHg
  230. Goal of ICP treatment
    • Prevent secondary brain injury
    • Prevent herniation.
  231. Calculating CPP
    • CPP = MAP - ICP
    • CBF ceases when ICP=MAP
  232. CT scan
    • will determine bleed
    • If no bleed, may use contrast to enhance visualization
  233. MRI
    Superior to CT however, takes longer, no metal allowed and poor bone images
  234. Transcranial Doppler (TCD)
    • Used to detect blood flow in the brain
    • No blood flow = Brain death.
  235. Electroencephalography (EEG)
    • Electrical activity of the brain
    • Abnormal voltage could indicate malformations, aneurysms, vasospasms.
  236. MRA
    used in combination with MRI - evaluated carotid disease
  237. Lumbar puncture (LP)
    • Needle into subarachnoid space
    • Evaluate CSF for blood or infection
    • Not with increased ICP
  238. Circle of Wills
    Protective as it is the primary collateral pathway when major cerebral vessels are occluded.
  239. Venous circulation of the brain
    • Valveless
    • drain by gravity
    • low-pressure system
  240. The localized matching of CBF with cerebral metabolism occurs through...
    1. Autoregulation
    2. Anaerobic metabolism
    3. luxury perfusion
    4. CSF
    1. autoregulation
  241. According to the Monro-Kellie hypothesis, an increased in 1 intracranial compartment must be accompanied by...
    a decrease in another compartment
  242. ICP remains relatively stable and, under normal conditions, it is usually less than...
    15 mmHg
  243. ICP can be increase by anything that...
    increased intracranial volume
  244. CPP depends on all of the following except:
    1. cerebral blood volume
    2. brain volume
    3. CSF volume
    4.  cerebral medullary regulation.
    1. cerebral medullary regulation
  245. CPP must be greater than ____mmHg to ensure adequate cerebral oxygenation.
    60
  246. Your patient's MAP is 80 mmHg and the ICP is 25 mmHg. What is the CPP?
    55mmHg    (80 - 25 = 55)
  247. Which of the following is not associated with increased ICV?
    1. subdural hematoma
    2. hypotension
    3. subarachnoid hemorrhage
    4. meningioma
    2. hypotension
  248. Which of the following does not cause and increase in ICP?
    1. meningitis
    2. hypoglycemia
    3. subarachnoid hemorrhage
    4. brain tumor
    2. hypoglycemia
  249. Accumulation of CSF results in...
    hydrocephalus
  250. Hypoxemia and hypercapnia cause
    cerebral vasodilation
  251. As a compensatory mechanism, pressure regulation acts by constricting cerebral blood vessels in response to...
    1. elevated blood levels of O2
    2. decreased blood levels of O2
    3. elevated systemic BP
    4. decreased systemic BP
    3. elevated systemic BP
  252. The blood-brain barrier is permeable to all of the following except:
    1. H2O
    2. O2
    3. Lipid soluble compounds
    4. Most drugs
    4. Most drugs
  253. CCP at or below _____mmHg will results in a loss of autoregulation in inadequate cerebral oxygenation.
    60 mmHg
  254. What happens when ICP and MAP are equal?
    Brain perfusion ceases
  255. The net effect of a prolonged increased ICP is...
    Impaired cerebral tissue perfusion
  256. How does hypercapnia affect ICP?
    Cerebral vasodilation.
  257. Delirium
    • associated with arousal and unaware state
    • Most common
    • Acute confusion
  258. Management and prevention of delirium
    Identify and treat the underlying cause
  259. Dementia
    • aroused and aware
    • Slow onset
    • irreversible
  260. Coma
    • absence of arousal and awareness
    • unarousability for 6+ hours may mean brain injury
  261. Unconsciousness
    • Abnormal state where patient is unaware of self or enviornment
    • Can be brief fainting or prolonged coma
  262. Aspects to consciousness
    • Arousal - ability to awakes
    • Content - ability to think, reason and feel
    • *Both must occur*
  263. Persistant Vegetative State (PVS)
    • Wakefulness is present, awareness is not.
    • Brain stem functions - so abole to breath on own
  264. Brain Death
    • Complete irreversible cessation of function of the brain and brain stem.
    • HYPOTHERMIA must be absent as well as CNS DEPRESSANTS
  265. Neuro assessment
    Hourly neuro checks- Glascow, v/s
  266. When does a neuro assessment become unreliable
    • prior to intubation
    • no SCI
    • during sedation
  267. Glasgow Coma Scale
    • Measures eye opening, verbal response, motor response
    • Scores 3-15 -- 7-8 generall comatose
  268. Glasgow of 7-8
    Generally comatose
  269. Glasgow Coma Scale - Eye Response scoring
    • Opens spontaneously - 4
    • Open to verbal command - 3
    • Opens in response to pain - 2
    • No response - 1
  270. Glasgow Coma Scale - Verbal Response scoring
    • Talking/Oriented - 5
    • Confused speech/disoriented - 4
    • Inappropriate words - 3
    • Incomprehensible words - 2
    • No response - 1
  271. Glasgow Coma Scale - Motor Response scoring
    • Obeys commands - 6
    • Localizes pain - 5
    • Withdrawl - 4
    • Abnormal flexion - 3
    • Extension - 2
    • No response - 1
  272. Noxious Stimuli
    • Nail bed pressure
    • Tapezius pinch
    • Sternal rub
    • Supraorbital pressure
  273. Cushings triad
    • Increased systolic BP
    • Decreased diastolic BP
    • Bradycardia
  274. Oculocephialic reflex
    • "Dolls eyes"
    • Normal - (+) eyes stay fixed stright
    • Abnormal - (-) eyes move with head
  275. Oculoestibular reflex
    • Cold water into ear canal
    • Normal - (+) eyes shift to the side of the water
    • Abnormal - (-) eyes stay fixed
  276. Grasp reflex
    • Stimulation in palm produced grap
    • Normal (-)
  277. Babinski
    • Stroke lateral side of foot, big toe extends
    • Normal (-) flexion
    • Abnormal (+) extention
  278. Corneal reflex
    • stroke cornea with cotton
    • eyes should close
  279. Gag reflex
    gag when pharynx is touched
  280. Swallow reflex
    uvula elevates when touched
  281. Skull fractures
    • Can be open (more dangerous) or closed
    • Open - tears of the dura can cause CSF leakage (+ glucose)
  282. Concussion
    • cerebral damage at the microscopic level
    • Transient unconsciousness <20 min
  283. Signs and symptoms for concussions
    • amnesia
    • headache
    • vertigo
    • vomiting
    • slurred speech
  284. Postconcussion syndrome
    • symptoms same as initial ones
    • can continue for 3+ months after injury
  285. Contusion
    • Macroscopic soft tissue bruising
    • Unconsciousness more prolonged than concussion
  286. Diffuse Anoxal Injury
    • Movement of brain within the skull
    • Shearing of axons - neurnol death
  287. Mild diffuse anoxal injury
    • coma
    • minimal residual neuro damae
  288. severe diffuse anoxal injury
    • proloned coma
    • death
    • persistant vegetative state
  289. Epidural hematoma
    • outside of the dura
    • Usually ARTERIAL bleed - surgery
    • *Unconsciousness - rapid decline in LOC
  290. Subdural hematoma
    • Inside the dura
    • Usually VENOUS - if small, medicine. if large, surgery
  291. Acute, Subacute and Chronic subdural hematoma
    • Acute - immediate
    • Subacute - within 48 hrs
    • Chronic - after 10-14 days
  292. Subarachnoid hemorrhage (SAH)
    • "Worst headache of my life"
    • caused by aneurysm, AV malformation, HTN
    • precautions - QUIET environment
    • Treatment - clipping or coiling
  293. Complications of ASH
    • Vasospams - Triple H therapy (Hypervolemia, Hemodilution, hypertension) and intra-arterial nicardipine
    • Rebleeding - Clot lyses
    • Hydrocephalus - clogged from blood, no fluid can drain
  294. Brain tumors
    if not treated, will cause increased ICP
  295. Goal of controlling intracranial pressure
    • Prevent herniation
    • Prevent secondary brain injury
  296. Management of increased ICP
    • HOB 30 degrees
    • Head and neck in neutral plane
    • Avoid hip flexion
    • Do NOT cluster nursing activities
    • Avoid noxious stimuli (suctioning, bathing)
    • Prevent hypoxia
    • Prevent hypercabia
    • Control body temp
    • Prevent seizures (Ativan)
  297. Complications of increased ICP
    • Fluid and electrolyte imbalances (DI, SIADH)
    • Seizures
    • Hyperglycemia
    • Hyperthermia
    • CSF leak
    • venous thromboembolism
  298. Nursing responsibilities with increased ICP monitoring
    • Record pressures, waveforms and neurostatus
    • Record hourly pressures
    • Maintain aseptic technique
    • Monitor CSF leakage
  299. Burr hole
    hole into the skull
  300. Crainiotomy
    skull open
  301. Crainiectomy
    skull portion removed
  302. Stereotaxis
    pinpoint laser
  303. Keeping the head and neck in alignment in a patient with increased ICP will result in ...
    Increased venous outflow
  304. Your patient's MAP is 80mmHg and ICP is 15mmHg. What is the CPP?
    65mmHg
  305. Decorticate posturing is...and indicates...
    abnormal flexion and indicates cerebral hemisphere dysfunction.
  306. Which of the following GCS scores is consistent with coma?
    1. 8
    2. 10
    3. 12
    4. 15
    1. 8
  307. Cushing triad is evidenced by...
    • increase in systolic BP
    • decrease in diastolic BP
    • Bradycardia
  308. When administering mannitol to a patient, the nurse should monitor which of the following lab tests?
    1. Serum osmolality
    2. urine sodium
    3. serum calcium
    4. serum potassium
    1. serum osmolality
  309. Continuous EEG monitoring is useful for patients who receive...
    Barbituates
  310. A patient being treated for a traumatic brain injury is febrile with a temp of 100.  What is the priority nursing intervention?
    Administer the prn antipyretic
  311. A patient with a TBI is being treated for DI. Which finding would the nurse evaluate as indicated treatment is effective?
    1. K is decreased
    2. BP is decreased
    3. Serum Na is increased
    4. Output is decreased
    4. Urine output is decreased
  312. The nurse is caring for a patient recovering from surgery to evacuate an epidural hematoma. Which assessment finding would warrant immediate collaboration with he surgeon?
    1. Urine output has dropped from 100mL/hr to 60mL/hr
    2. The patient's hand grasps are weak bilaterally
    3. Fine crackles can be auscultated in the lung bases bilaterally
    4. The pupil on the side of the injury has become fixed and dilated.
    4. the pupil on the side of the injury has become fixed and dilated.
  313. A patient sustained a TBI is being sent to CT scan. Which nursing statements would help the patient's spouse understand the rationale for a CT vs. an MRI?
    1. CT scans are easier for patients with head injuries because movement is allowed.
    2. We can get results from a CT scan quicker than from an MRI.
    3. MRIs are more costly so the least expensive tests are always done first.
    4. ST scans show more detail than an MRI.
    2. We can get results from a CT scan quicker than from an MRI
  314. A patient was the unrestrained driver of a car that was struck head on by another vehicle. During initial assessment the nurse observes another nurse using supraorbital pressure to assess for the response. What nursing intervention is indicated?
    STOP the procedure
  315. A patient with a TBI has placement of an IVC. What interventions does the nurse perform regarding this catheter?
    • Assess color, and amount of CSF
    • Drain CSF
    • Monitor ICP
  316. A patient is admitted to the ED after sustaining injury in a fall. Which assessment finding would the nurse immediately communicate to the ED MD?
    1. The patient is taking sulfa drug for a UTI
    2. The patient has a bluish discoloration behind his ear
    3. The patients nose is running
    4. The patients smile is crooked
    5. The patients tongue is lacerated.
    • 2. The patient has a bluish discoloration behind his ear
    • 3. The patients nose is running
    • 4. The patients smile is crooked
  317. A patient comes into the ER with complaints of HA, lethargy and vomiting. He reports being hit in the head by a batted baseball during a company picnic "about 6 weeks ago." The nurse would ask additional assessment questions regarding which condition?
    Chronic subdural hematoma
  318. The nurse caring for a patient recovering  from surgery to evacuate an epidural hematoma. Which assessment finding would warrant immediate collaboration with the surgeon?
    Pupil on the side of the injury has become fixed and dilated.
  319. The family of a patient with a concussion is concerned that the patient continues to complain of and demonstrate ongoing neurological deficits even though the injury occurred 6 weeks ago, What information should the nurse provide?
    Symptoms of a concussion can last 3+ months.
  320. Manifestations of any GI bleeding
    • Hematemesis
    • Melena (black, tarry, foul smelling stool)
    • Hematochezia (bright red blood from rectum)
    • Occult bleeding
  321. *S/S of occult bleeding
    • loss of 100mL/day of blood
    • Anemia
    • Fatigue
  322. Peptic ulcer disease can be d/t
    • H. Pylori
    • NSAIDS
    • Smoking
    • Genetic predisposition
  323. #1 cause of GI bleed
    Peptic ulcer disease
  324. Most common place for peptic ulcers
    duodenal or stomach
  325. Classification of peptic ulcers
    by depth (erosion, acute, chronic) and location (gastric, duodenal)
  326. Manifestations of peptic ulcers
    • Gnawing pain in epigastric area
    • worse at night
    • 1-2 hrs after eating
    • hematemeisis
  327. diagnosis of peptic ulcers
    • presentation
    • labs
    • endoscopy
  328. *treatment of peptic ulcers
    • ABXs
    • PPIs
    • Carafate (coats ulcer)
    • Prostaglandins
    • * DRINK h2o after Carafate d/t constipation
  329. Esophageal varices
    UGI bleeding
  330. Treatment of esophageal varices with active bleeding
    • Central line (2 large bore IV sites)
    • ventilation
    • blood transfusions with FFP
    • Perssin to constrict vessels
    • Nitro to reduce resistance
    • Sengstaken-Blakemore tube
  331. Sengstaken-Blakemore tube
    contains 2 ballons - 1 esophageal one to press on the bleeding arteries and in the stomach to hold in place
  332. Priority for Sengstaken-Blakemore tube
    scissors in the room for respiratory distress
  333. Treatment for esophageal varices with controlled bleeding
    • Shunt
    • beta blockers
    • nitrated
    • sclerotherapy
  334. Endoscopic banding
    preferred treatment to occlude channels
  335. *Medications for GI bleeds
    • *Vasopressin - to constrict spanchnic circulation @ 20 units IV then .4-.6 units/min
    • Somatostatin
    • Octreotide
  336. Hemorrhagic gastritis
    transient inflammation of gastric mucosa
  337. Causes of hemorrhagic gastritis
    • NSAIDS
    • alcohol
    • stress
  338. Manifestations and diagnosis of hemorrhagic gastritis
    • hematemesis
    • slow bleed - "coffee grounds"
    • epigastric pain

    endoscopy
  339. *Prevention and treatment of hemorrhagic gastritis
    • PPIs
    • histamine
    • *early enteral feedings

    Keep pH above 4.0
  340. Mallory-Weiss Tears
    Tear in gastroesphageal junction caused by retching or vomiting
  341. *Causes of Mallory-Weiss tears
    *alcohol, gastritis, esophogitis
  342. Stress related mucosal disease
    Can be stress ulcers or diffuse erosions
  343. Causes of stress related mucosal disease
    • severe trauma
    • burns
    • head injuries
    • NSAIDS
    • criticall ill
  344. Risk factors for stress related mucosal disease
    • mechanical ventilation >48 hours
    • coagulopathy
    • GI ulcers
    • corticosteroids
  345. Treatment of stress related mucosal disease
    • prevention
    • assess for signs of hypoperfusion
    • monitor labs
    • avoid NSAIDs
    • discontinue vasopressors
    • initiate enteral feedings early
  346. Lower GI bleed
    bleeding distal to the ligament of Treitz
  347. Causes of lower GI bleeds
    most common?
    • diverticular disease - most common
    • AV malformations
    • colon and rectal lesions
    • IBD
  348. Ischemic bowel disease
    interruption of blood flow to the colon
  349. Manifestations of LGI bleed
    • melena
    • hematochezia
  350. Treatment of LGI bleed
    • Restore blood flow via...
    • fluid resuscitation
    • treat underlying cause
    • anx
  351. * Sudden drop in BP
    • Think GI bleed and perforation
    • Check H&H
    • Check othostatics
    • If uncontrolled - balloon tamponade
  352. *Ogilvie's syndrome
    • massively dilated colon
    • abdominal distention
    • no bowel sounds
    • no pain
    • - if not decompressed can cause perforation
    • *Found in bedridden patients
  353. Paralytic ileus
    • bowel obstruction d/t loss of intestinal peristalsis without physical obstruction.
    • Can occur anywhere along the GI tract
  354. *Hallmark sign of acute intestinal obstruction (paralytic ileus)
    *abdominal distention
  355. treatment of acute intestinal obstruction
    • ID patients at risk
    • *bedridden
    • NPO
    • electrolyte replacement
    • decompression
  356. Abdominal compartment syndrome
    • abnormally high pressures within the abdominal cavity
    • Causes impaired O2 delivery and compression on organs
  357. How does abdominal compartment syndrome cause ischemia?
    Releases cytokines -- cause free radicals -- causes ischemia
  358. Most common cause of abdominal compartment syndrome
    Blunt abdominal trauma
  359. Manifestations of abdominal compartment syndrome
    • abdominal pain
    • increasing abdominal girth
    • difficulty breathing
    • decreased output
  360. ACS/IAH
    -abdominal compartment syndrome/intra abdominal hypertension
  361. *Goal of Severe ACS
    *Keep pressures below 60mmHg

    -mean arterial pressure minus intraabdominal pressure = abdominal prefusion pressure
  362. What mmHg should the abdominal perfusion pressures be?
    >60 mmHg
  363. Functions of the liver
    • break down fats
    • Maintains normal BG
    • Converts ammonia to urea
    • Absorbs fat soluble vitamins
    • Stores iron
  364. Most common cause of acute liver failure
    Tylenol overdose
  365. Causes of acute liver failue
    • Tylenol overdose
    • Hepatitis
    • Herpes
    • Varicella
  366. Hallmark sign of acute liver failure
    • altered mentation
    • coagulopathy
  367. Heptaocellular dysfunction
    Minifestion
    • interrupts elimination of billirubin
    • Causes Jandice
  368. Most serious complication of acute liver failure
    cerebral edema = late sign of increased cerebral pressure
  369. *Treatment of cerebral edema
    • ICP monitoring
    • Maintain CPP >50-60
    • Keep ICP <20
    • HOB 30
    • Meds
    • *Hypothermia to decrease metablosm
  370. Pharmacology for cerebral edema
    • Propofol
    • Mannitol
  371. Asterixis
    hand flapping which occurs in acute liver failure
  372. Hepatic encephalopathy
    unable to clear amonia
  373. *Pancreas
    • common bile duct drains bile from liver to pancreatic duct
    • *Had endocrine and exocrine functions
  374. Acute pancreatitis
    auto-digestion of gland
  375. *Manifestations of hemorrhagic pancreatitis
    *necrotizing, irreversible, poor prognosis
  376. *Manifestations of acute pancreatitis
    • abdominal pain
    • serum amylase an lipase 3x normal
    • CT confirmation
    • fever and tachy
    • + Cullen or Turner sign
  377. Cullen's sign
    brusing on abdomen
  378. Turners sign
    brushing on flanks
  379. Pain meds for acute pancreatitis
    Morphine -- NO DEMEROL
  380. An elderly patient presents with fever, leukocytosis, LLQ pain and diarrhea alternating with constipation. This concludes that these are frequently seen in clients with...
    Diverticulitis
  381. The client says to the nurse, "My doctor told me that my ulcer may have been caused by bacteria. I though ulcers were caused by diet and too much stress." Which of the following responses is best?
    1. If it were caused by bacteria, you would have a fever as a result of the inflammation.
    2. We know that ulcers can be spread easily, so be careful not to spread them to your children.
    3. Diet and stress have nothing to do with developing an ulcer.
    4. Even though the bacteria H. Pylori causes inflammation, other factors may cause increase acid.
    4. Even though the bacteria H. Pylori causes inflammation, other factors may cause increase acid.
  382. Which of the clients would be most at risk for an intestinal obstruction?
    1. A client who smokes and consumes large amounts of caffeine
    2. An elderly client who is on bedrest because of post-op abdominal surgery
    3. An individual eating low-fiber, high-fat diet
    4. An adult diagnosed with cirrhosis of the liver
    2. An elderly client who is on bedrest
  383. An elderly client is worried about bright red blood in his stool along with feeling tired. The nurse determines that these symptom's are characteristic of...
    1. Ascending (R side) colon cancer
    2. Descending (L side) colon cancer
    3. Gallbladder disease
    4. Gastric ulcers
    2. Descending (L side) colon cancer
  384. What food should be avoided with clients with PUD?
    chocolate -- caffeine
  385. Which of the clients are most likely to develop pancreatitis?
    1. a 59 yo male with a history of occasional alcohol use
    2. A client with renal problems and hypocalcemia
    3. A client recovering from an MI
    4. A client with a stone lodged in the pancreatic duct.
    4. a client with a stone lodged in the pancreatic duct
  386. A nurse caring for a patient with liver cirrhosis. Which complication should warrant the highest consideration?
    1. vasicose veins
    2. constipation
    3. bleeding tendencies
    4. intermittent claudication
    3. bleeding tendencies
  387. Priority initial nursing interventions for a patient with hemorrhagic pancreatitis are...
    Assessing for shock and starting IV fluids
  388. Autograft
    • From one part of a persons body to another
    • ie...skin graft, bypass
  389. Heterograft
    • transplant between different species
    • ie...valves
  390. Allograft
    • transplant between member of the same species
    • ie...organs/tissues
  391. Isograft
    transplant between identical twins
  392. Living donors
    • persons who volunteer to have an organ removed from transplantation
    • blood relatives are the best d/t increased histocompatibility
  393. Complications of donating an organ
    • surgical risks
    • family pressure to donate
    • financial
    • future need of the organ
  394. Deceased donor
    organs and tissue recovered after death
  395. Cardiac death
    • cessation of cardiac and respiratory function
    • Can only donate tissues
    • Must be recovered within 12-24 hours
  396. Brain death
    • Cessation of function of entire brain and brainstem
    • Can donate solid organs as well as tissues
  397. Uniform Anatomical Gift Act
    Uniformity of donation in all states
  398. Required-Request Legislation
    Hospital responsibility for identifying potential donors
  399. National Organ Transplant Act
    Set up Organ and Transplantation Network
  400. Uniform Determination of Death Act
    Guideline for stats to establish legal definition of death
  401. Determination of Cardiac death
    • Listen to heart and lungs
    • Check BP
    • Check for pupillary response
  402. Determination of Brain death
    Must have: coma, absence of brain stem reflexes, failed apnea test
  403. Coma r/t brain death
    reversible causes must be r/o - drugs, neuromuscular blockade, hypothermia
  404. Absence of brain stem reflexes r/t brain death
    • GSC of 3
    • no response to verbal or painful stimuli
    • Check: pupillary light response, dolls eyes, oculocephalic, corneal and cough reflexes
  405. Apnea r/t brain death
    • test respiratory drive with increased PCO2
    • *If any respiratory effort - back on vent, they are not brain dead
    • Check ABGs after 10 minutes
    • *If PCO2 is >60, patient is apnic, patient is brain dead
  406. Time of death
    If all cardinal signs of death are interpreted as consistesnt with brain death then patient is dead. A death certificate can be issued.
  407. Stability for donation
    Must not have HIV or active metastatic cancer
  408. Consenting for organ donation
    Always obtained by OPO
  409. #1 problem with organ transplantation
         and why?
         prevention?
    • Rejection
    • immune system is activated and recognized as "non-self"
    • Immunosuppressants for life
  410. Hyperacute rejection
    • Minutes to hours
    • Rare with tissue typing
  411. Acute rejection
    • Days to months
    • Prompt recognition and treatment to save the organ
  412. Chronic rejection
    happens after years
  413. Immunosuppressant complications
    • Infection
    • organ dysfunction
    • malignancy
    • DM
    • steroid-induced complications
  414. Renal transplantation
    • d/t ESRD caused by HTN, DM, glomerulonephritis
    • keep bad kidney and attach transplant below
  415. Cardiac transplantion
    d/t cardiomyopathy, CAD, Heart failure
  416. Denervation of heart after transplantation
    • the back wall of the heart remains intact when the bad heart is removed.
    • *Alters the ability to respond to hypovolemia, hypotension, exercise and certain drugs
    • *May not experience any ischemic chest pain
  417. Thermal burns
    Caused by flame, flash, scald or contact burns
  418. Extent of thermal burn damage depends on...
    • Temperature of the agent
    • Concentration of the heat
    • Duration of contact
  419. Jackson's Theory of Thermal Wounds
    • Zone of Coagulation - center of the burn
    • Zone of Stasis - around coagulation area, decreased blood flow, whitish in color
    • Zone of Hyperemia - peripheral area with increased blood flow, red and inflammed
  420. Patho of thermal burns
    • Capillary disrupted by secretion of histamine and serotonin
    • Can cause burn edema
  421. Burn edema
    • Creates massive fluid shifts
    • Can cause fluid loss by evaporation
  422. Thermal burns at risk for...
    Hypovolemic shock/Burn shock d/t fluid loss
  423. Chemical burns
    From exposure to a corrosive agent (acids, alkalis)
  424. Extent of chemical burns depends on...
    • Amount and concentration
    • length of exposure
    • Mechanism of chemical action
  425. Tissue destruction by acids
    • Self-limiting
    • Forms mass at area on contact causing necrosis and eschar
  426. Tissue destruction from alkalis
    • Destroys cell membrane through liquefaction necrosis.
    • Deeper tissue penetration
  427. Electrical burns
    Current travels from once point to another
  428. Complication of electrical burns
    • Outer skin may not appear too bad, but it burns from the inside out.
    • Cardiac dysrhythmias
  429. Radiation burns
    From the transfer of radiant energy to the body
  430. Area at risk for radiation burns
    • tissues that multiple at a continuous rate
    • ie...skin, BVs, intestinal lining, bone marrow
  431. Extreme cold burns
    • Exposure to severe cold temps, mircovascular occlusion
    • Reperfusion causes additional tissue damage
  432. System-wide complications of burns
    • Vascular permeability and edema
    • Immunosuppression
    • Decreased renal blood flow
    • Altered hemodynamics
    • Hypermetabolism
    • Increased gut mucosal permibility
  433. Initial emergency management of burn wounds
    • Stop the burning process - cold water, NOT ice.
    • Protect the airway, breathing and circulation
  434. Superficial burns
    • Top layer of skin
    • Sunburn
    • May have blistering and peeling
    • Heals 3-5 days
  435. Superficial partial-thickness burns
    • into the dermis
    • *Blisters
    • Heals 10-14 days
    • Do not break blisters, provide comfort, will be sore underneath
  436. Deep partial-thickness burns
    • deep into the dermis
    • No blisters
    • Heals 2-3 weeks
    • May scar and may need skin graft
  437. Full-thickness burns
    • Into the subcutaneous layer
    • Yellow-leathery appearance
    • *No pain
    • Will need skin grafts
  438. Deep full-thickness burns
    • Deep into the subcutaneous layer
    • Can involve muscle, bone, tendons
    • May require amputation
  439. Lund and Browder Chart
    Percentage of body burned determined by Total BSA
  440. Rule of Nines
    • Body divide into areas of 9% and 18% to determine extent of body damage
    • Hand and genitals = 1% each
    • Head and arms = 9% each
    • Legs, chest and back = 18% each
  441. #1 cause of death from burns
    Infection
  442. Resusciative phase
    • Begins at time of injury
    • Lasts 48-72 hours
    • Maintain CV and Pulm. stabilization
  443. Cardiovascular effects of burns >40%
    • *Decreased CO
    • hypovolemic shock
    • Vasoconstriction
    • Increased capillary permeability
    • Massive fluid and electrolyte shifts
  444. Parkland formula
    • 4ml of Ringers x TBSA % burned x wt
    • 1/2 given in 1st 8 hours - 1/2 in the next 16 hours
  445. Patient weighing 68kg with 50% TBSA burn
    How much fluid should he get?
    • 4 x 50 x 68 = 13,600
    • 6,800 during first 8 hours
    • 6,800 during next 16 hours
  446. Peripheral vascular effects of burns
    blood flow is compromised by eschar and compartment syndrome
  447. Signs of limb ischemia
    • Pain
    • Reduced sensation
    • Weakness
    • Swelling?
  448. Eschar
    • stiff, non-elastic
    • Tough, dead tissue
    • Requires emergency escharotomy
  449. Escharotomy
    opening of the eschar to relieve pressure
  450. Carbon Monoxide poisoning
    • Chemical inhalation
    • CO attaches to Hbg and does not allow O2 to attach
  451. Confirmation of CO exposure confirmed by...
    serum carboxyhemoglobin level
  452. S/S of CO poisoning
    • HA
    • nausea
    • dizziness
    • LOC
    • hypoxemia
    • death
  453. Treatment of CO poisoning
    • 100% O2
    • Aggressive hypobaric O2 therapy
  454. SaO2 with CO poisoning
    not accurate -- must use COH levels
  455. lyisMetabolic effects of burns >40% TBSA
    • Hyper
    • -glycolysis
    • -proteolysis
    • -lipolysis
    • -hypermetabolism
  456. Nutritional needs of burn patients
    increased calories and protein to maintain immune system and wound healing
  457. Renal effects of burns
    Risk for myoglobinuria d/t the release of myoglobin from muscle damage
  458. Myoglobinuria s/s and treatment
    • red to reddish brown urine -- signs of ARF d/t clogged tubules
    • flush kidneys to maintain output of 75-100mL/hr
  459. Inflammatory stage of wound healing
    • lasts 2 weeks
    • vasodilation - increased blood flow, increased O2 and increased nutrients
  460. Proliferative phase of wound healing
    • last up to a month
    • collagen synthesis - skin repair
  461. Maturation phase of wound healing
    • Lasts 6-18 months
    • Collage strengthens
    • hypertrophic collage can become rigid and decrease mobility
  462. Goal of acute rehabilitative phase of burns
    • Prevent and control infection
    • Preserve viable tissue
    • Promote wound closure
    • Minimize complications

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