NURS 6620 exam 1 practice question
review with correct answers
During |cell |injury |caused |by |hypoxia, |why |does |an |increase |in |the |osmotic |pressure |within |the |
cell |occur? |- |CORRECT |ANSWER✔✔-b.Sodium |chloride |enters |the |cell.
In |hypoxic |injury, |movement |of |fluid |and |ions |into |the |cell |is |associated |with |acute |failure |of |
metabolism |and |a |loss |of |ATP |production. |Normally, |the |pump |that |transports |sodium |ions |out
|of |the |cell |is |maintained |by |the |presence |of |ATP |and |ATPase, |the |active |transport |enzyme. |In |
metabolic |failure |caused |by |hypoxia, |reduced |ATP |and |ATPase |levels |permit |sodium |to |
accumulate |in |the |cell, |whereas |potassium |diffuses |outward. |The |increase |of |intracellular |
sodium |increases |osmotic |pressure, |which |draws |more |water |into |the |cell. |(Transport |
mechanisms |are |described |in |Chapter |1.) |The |remaining |options |do |not |accurately |describe |
the |cell |injury |that |results |in |increased |osmotic |pressure |caused |by |hypoxia.
A |healthcare |professional |is |caring |for |four |patients. |Which |patient |should |the |professional |
assess |for |hyperkalemia |or |hypermagnesmia? |- |CORRECT |ANSWER✔✔-c.Renal |failure
Hyperkalemia |should |be |investigated |when |a |history |of |renal |disease, |massive |trauma, |insulin |
deficiency, |Addison |disease, |use |of |potassium |salt |substitutes, |or |metabolic |acidosis |exists. |
Hyperparathyroidism |might |lead |to |hyperphosphatemia. |Vomiting |is |frequently |associated |
with |potassium |depletion. |Hyperaldosteronism |also |can |lead |to |potassium |wasting.
Renal |failure |usually |causes |hypermagnesemia, |in |which |magnesium |concentration |is |greater |
than |2.5 |mEq/L. |Hypermagnesemia |is |not |a |result |of |the |other |options.
A |major |determinant |of |the |resting |membrane |potential |necessary |for |the |transmission |of |
nerve |impulses |is |the |ratio |between |what? |- |CORRECT |ANSWER✔✔-Intracellular |and |
extracellular |K+
The |ratio |of |K+ |in |theICF |to |K+ |in |the |ECF |is |the |major |determinant |of |the |resting |membrane |
potential, |which |is |necessary |for |the |transmission |and |conduction |of |nerve |impulses, |for |the |
maintenance |of |normal |cardiac |rhythms, |and |for |the |skeletal |and |smooth |muscle |contraction. |
This |is |not |true |of |the |other |options.
, How |do |free |radicals |cause |cell |damage? |- |CORRECT |ANSWER✔✔-a.Giving |up |an |electron, |
which |causes |injury |to |the |chemical |bonds |of |the |cell |membrane
A |free |radical |is |an |electrically |uncharged |atom |or |group |of |atoms |having |an |unpaired |
electron. |Having |one |unpaired |electron |makes |the |molecule |unstable; |thus |to |stabilize, |the |
molecule |gives |up |an |electron |to |another |molecule |or |steals |one. |Therefore |it |is |capable |of |
forming |injurious |chemical |bonds |with |proteins, |lipids, |or |carbohydrates-key |molecules |in |
membranes |and |nucleic |acids. |Free |radical |damage |is |not |caused |by |hypoxia, |lysosomal |
enzymes, |or |transferring |atoms.
Physiologic |pH |is |maintained |at |approximately |7.4 |because |bicarbonate |(HCO3) |and |carbonic |
acid |(H2CO3) |exist |in |what |ratio? |- |CORRECT |ANSWER✔✔-b.20:1
The |relationship |between |HCO3 |and |H2CO3 |is |usually |expressed |as |a |ratio. |When |the |pH |is |
7.4, |this |ratio |is |20:1 |(HCO3:H2CO3). |The |other |options |do |not |accurately |identify |physiologic |
pH |by |the |correct |ratio |of |HCO3 |and |H2CO3.
Removal |of |part |of |the |liver |leads |to |the |remaining |liver |cells |undergoing |which |compensatory
|process? |- |CORRECT |ANSWER✔✔-c.Hyperplasia
Compensatory |hyperplasia |is |an |adaptive |mechanism |that |enables |certain |organs |to |
regenerate. |For |example, |the |removal |of |part |of |the |liver |leads |to |hyperplasia |of |the |
remaining |liver |cells |(hepatocytes) |to |compensate |for |the |loss. |The |other |options |do |not |
accurately |identify |the |compensatory |process |described |in |the |question.
What |causes |the |rapid |change |in |the |resting |membrane |potential |to |initiate |an |action |
potential? |- |CORRECT |ANSWER✔✔-Sodium |gates |open, |and |sodium |rushes |into |the |cell, |
changing |the |membrane |potential |from |negative |to |positive.
When |a |resting |cell |is |stimulated |through |voltage-regulated |channels, |the |cell |membranes |
become |more |permeable |to |Na+. |As |Na+ |moves |into |the |cell |the |membrane |potential |
decreases, |or |moves |forward, |from |a |negative |value |(in |millivolts) |to |zero. |The |Na+ |gates |
open, |and |Na+ |rushes |into |the |cell, |causing |the |membrane |potential |to |reduce |to |zero |and |
then |become |positive |(depolarization).
review with correct answers
During |cell |injury |caused |by |hypoxia, |why |does |an |increase |in |the |osmotic |pressure |within |the |
cell |occur? |- |CORRECT |ANSWER✔✔-b.Sodium |chloride |enters |the |cell.
In |hypoxic |injury, |movement |of |fluid |and |ions |into |the |cell |is |associated |with |acute |failure |of |
metabolism |and |a |loss |of |ATP |production. |Normally, |the |pump |that |transports |sodium |ions |out
|of |the |cell |is |maintained |by |the |presence |of |ATP |and |ATPase, |the |active |transport |enzyme. |In |
metabolic |failure |caused |by |hypoxia, |reduced |ATP |and |ATPase |levels |permit |sodium |to |
accumulate |in |the |cell, |whereas |potassium |diffuses |outward. |The |increase |of |intracellular |
sodium |increases |osmotic |pressure, |which |draws |more |water |into |the |cell. |(Transport |
mechanisms |are |described |in |Chapter |1.) |The |remaining |options |do |not |accurately |describe |
the |cell |injury |that |results |in |increased |osmotic |pressure |caused |by |hypoxia.
A |healthcare |professional |is |caring |for |four |patients. |Which |patient |should |the |professional |
assess |for |hyperkalemia |or |hypermagnesmia? |- |CORRECT |ANSWER✔✔-c.Renal |failure
Hyperkalemia |should |be |investigated |when |a |history |of |renal |disease, |massive |trauma, |insulin |
deficiency, |Addison |disease, |use |of |potassium |salt |substitutes, |or |metabolic |acidosis |exists. |
Hyperparathyroidism |might |lead |to |hyperphosphatemia. |Vomiting |is |frequently |associated |
with |potassium |depletion. |Hyperaldosteronism |also |can |lead |to |potassium |wasting.
Renal |failure |usually |causes |hypermagnesemia, |in |which |magnesium |concentration |is |greater |
than |2.5 |mEq/L. |Hypermagnesemia |is |not |a |result |of |the |other |options.
A |major |determinant |of |the |resting |membrane |potential |necessary |for |the |transmission |of |
nerve |impulses |is |the |ratio |between |what? |- |CORRECT |ANSWER✔✔-Intracellular |and |
extracellular |K+
The |ratio |of |K+ |in |theICF |to |K+ |in |the |ECF |is |the |major |determinant |of |the |resting |membrane |
potential, |which |is |necessary |for |the |transmission |and |conduction |of |nerve |impulses, |for |the |
maintenance |of |normal |cardiac |rhythms, |and |for |the |skeletal |and |smooth |muscle |contraction. |
This |is |not |true |of |the |other |options.
, How |do |free |radicals |cause |cell |damage? |- |CORRECT |ANSWER✔✔-a.Giving |up |an |electron, |
which |causes |injury |to |the |chemical |bonds |of |the |cell |membrane
A |free |radical |is |an |electrically |uncharged |atom |or |group |of |atoms |having |an |unpaired |
electron. |Having |one |unpaired |electron |makes |the |molecule |unstable; |thus |to |stabilize, |the |
molecule |gives |up |an |electron |to |another |molecule |or |steals |one. |Therefore |it |is |capable |of |
forming |injurious |chemical |bonds |with |proteins, |lipids, |or |carbohydrates-key |molecules |in |
membranes |and |nucleic |acids. |Free |radical |damage |is |not |caused |by |hypoxia, |lysosomal |
enzymes, |or |transferring |atoms.
Physiologic |pH |is |maintained |at |approximately |7.4 |because |bicarbonate |(HCO3) |and |carbonic |
acid |(H2CO3) |exist |in |what |ratio? |- |CORRECT |ANSWER✔✔-b.20:1
The |relationship |between |HCO3 |and |H2CO3 |is |usually |expressed |as |a |ratio. |When |the |pH |is |
7.4, |this |ratio |is |20:1 |(HCO3:H2CO3). |The |other |options |do |not |accurately |identify |physiologic |
pH |by |the |correct |ratio |of |HCO3 |and |H2CO3.
Removal |of |part |of |the |liver |leads |to |the |remaining |liver |cells |undergoing |which |compensatory
|process? |- |CORRECT |ANSWER✔✔-c.Hyperplasia
Compensatory |hyperplasia |is |an |adaptive |mechanism |that |enables |certain |organs |to |
regenerate. |For |example, |the |removal |of |part |of |the |liver |leads |to |hyperplasia |of |the |
remaining |liver |cells |(hepatocytes) |to |compensate |for |the |loss. |The |other |options |do |not |
accurately |identify |the |compensatory |process |described |in |the |question.
What |causes |the |rapid |change |in |the |resting |membrane |potential |to |initiate |an |action |
potential? |- |CORRECT |ANSWER✔✔-Sodium |gates |open, |and |sodium |rushes |into |the |cell, |
changing |the |membrane |potential |from |negative |to |positive.
When |a |resting |cell |is |stimulated |through |voltage-regulated |channels, |the |cell |membranes |
become |more |permeable |to |Na+. |As |Na+ |moves |into |the |cell |the |membrane |potential |
decreases, |or |moves |forward, |from |a |negative |value |(in |millivolts) |to |zero. |The |Na+ |gates |
open, |and |Na+ |rushes |into |the |cell, |causing |the |membrane |potential |to |reduce |to |zero |and |
then |become |positive |(depolarization).
