NURS 6501 – Advanced Pathophysiology Modules 1-4 –
Walden University – 2025-2026 Study Guide with Verified
Questions & Answers
Why |is |HDL |considered |good |cholesterol? |- |answersIt's |able |to |remove |cholesterol |from |artery |
plaques |and |recycle |it |back |to |the |liver.
Why |is |HDL |consider |good |cholesterol |- |answersHDL |is |considered |good |cholesterol |because |it |
collects |excess |cholesterol |in |the |body |cells |and |transports |it |to |the |liver |where |it |is |excreted. |HDL |
carries |20 |to |25% |of |total |plasma |cholesterol.
Explain |the |role |inflammation |has |in |the |development |of |atherosclerosis |- |answersInflammation |in |the
|heart |muscle |caused |by |chronic |inflammatory |processes |leads |to |mitochondrial |damage |that |results |
in |an |increased |free |radical |production |that |further |activates |the |chronic |inflammatory |vicious |cycle
Explain |the |role |inflammation |has |in |the |development |of |atherosclerosis |- |answersActivated |mast |
cells |recruit |inflammatory |cells |that |provoke |plaque |formation |and |lead |to |atherosclerosis. |Chronic |
inflammatory |infiltrates |occupy |layers |of |arteries |were |stable |plaques |are |formed |and |associated |with
|atherosclerosis.
Explain |the |role |inflammation |has |in |the |development |of |atherosclerosis |- |answersAdditionally |active |
inflammation |involves |a |thinning |at |the |fibrous |Of |atherosclerotic |plaque |which |predisposes |
vulnerable |plaque |to |rupture.
Why |does |the |APRN |recognize |as |the |result |of |the |pleural |friction |rub? |- |answersThe |inflammation |of |
the |pericardium |due |to |either |the |underlying |autoimmune |disease |or |a |post |viral |syndrome |causes |
roughening |of |the |pericardium. |This |causes |the |classic |rug |which |can |be |best |heard |at |the |Apex |of |
the |heart |and |left |sternal |border.
Explain |how |a |positive |strep |test |has |caused |the |patient's |symptoms |- |answersRheumatic |heart |
disease |RHD |only |develops |after |a |pharyngeal |infection |with |group |a |beta |hemolytic |streptococcus. |It |
is |an |abnormal |response |to |humoral |and |cell |mediated |response |to |M |proteins. |Inflammation |causes |
proliferative |and |exudative |lesions |in |connective |tissue.
Explain |how |a |positive |strep |test |has |caused |the |patient's |symptoms |- |answersInflammation |causes |
scarring |of |the |valve |tissue. |Inflammation |usually |affects |the |endocardium |which |contains |the |valves. |
Endocardial |inflammation |causes |swelling |of |leaflets |in |the |valves.
Describe |the |factors |that |could |have |contributed |to |the |development |of |a |DVT |in |this |patient |and |
explain |how |each |of |the |factors |could |cause |DVT |- |answersVirchow's |Triad |caused |damage |to |the |
walls |of |the |vessels. |Injury |to |the |intimal |layer |of |the |vessel, |antiplatelet |substances |such |as |nitric |
oxide |and |prostacyclin, |along |with |the |expression |of |collagen |on |the |vessel |wall, |causes |adherence |to
|the |platelets |to |the |vessel |wall.
, Describe |the |factors |that |could |have |contributed |to |the |development |of |a |DVT |in |this |patient |and |
explain |how |each |of |the |factors |could |cause |DVT |- |answersPlatelets |become |activated, |then |
aggregate, |forming |clots. |Venous |stasis |is |a |result |of |obesity, |patients |advanced |age, |and |inability |to |
perform |physical |therapy |therapy.
Explain |why |large |pulmonary |embolus |interferes |with |oxygenation |- |answersThe |embolus |lodges |
somewhere |in |the |pulmonary |circulation |and |causes |a |ventilation/perfusion |mismatch |V/Q. |
Ventilation |perfusion |mismatch |or |V/Q |defects |are |defects |in |total |long |ventilation |perfusion |ratio.
Explain |why |large |pulmonary |embolus |interferes |with |oxygenation |- |answersIt |is |a |condition |in |which |
one |or |more |areas |of |the |lung |receive |oxygen |but |no |blood |flow, |or |they |receive |blood |flow |but |no |
oxygen |due |to |obstruction |somewhere |in |the |pulmonary |circulation. |This |causes |a |decreased |area |for
|oxygen |exchange.
Explain |why |a |large |pulmonary |embolism |causes |right |ventricular |strain |- |answersThe |V/Q |mismatch |
causes |release |of |neurohumeral |substances |and |inflammatory |mediators |that |cause |vasoconstriction |
of |the |pulmonary |vasculature |further |impeding |oxygenation.
Explain |why |a |large |pulmonary |embolism |causes |right |ventricular |strain |- |answersHemodynamically |
this |vasoconstriction |results |in |pulmonary |hypertension, |making |it |difficult |for |the |right |ventricle |to |
pump |blood.
Explain |why |a |large |pulmonary |embolism |causes |right |ventricular |strain |- |answersThe |V/Q |mismatch |
also |creates |decreased |production |of |surfactant |causing |atelectasis |that |further |decreases |surface |
area |available |for |oxygen |exchange.
Explain |early |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersWhen |there |is |
an |initial |airway |exposure |to |an |antigen, |an |innate |and |adaptive |immune |response |is |initiated.
Explain |early |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersCells |that |can |
initiate |the |inflammation |of |the |bronchial |mucosa |and |hyperresonance |of |the |airways |include |Dedrick
|cells, |T-helper |2 |cells, |lymphocytes, |B |lymphocytes, |mast |cells, |neutrophils, |eosinophils, |and |
basophils.
Explain |early |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersEarly |asthmatic |
response |is |a |phase |of |bronchospasm |that |peaks |at |about |30 |minutes |and |usually |resolves |after |
about |3 |hours.
Explain |late |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersLate |asthmatic |
responses |are |mediated |by |earlier |exposure |in |early |phase |that |causes |a |latent |release |of |
inflammatory |mediators. |These |mediators, |leukotrienes |and |prostaglandin |D, |cause |bronchospasm, |
edema, |and |mucus |secretions |that |obstruct |airflow.
Explain |late |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersAirway |
obstruction |creates |resistance |to |airflow |and |causes |air |trapping. |Continued |air |trapping |increases |
intrapleural |and |alveolar |gas |pressure, |decreases |ventilation |and |perfusion |leading |to |uneven |and |
variable |ventilation/perfusion |in |the |lung.
Walden University – 2025-2026 Study Guide with Verified
Questions & Answers
Why |is |HDL |considered |good |cholesterol? |- |answersIt's |able |to |remove |cholesterol |from |artery |
plaques |and |recycle |it |back |to |the |liver.
Why |is |HDL |consider |good |cholesterol |- |answersHDL |is |considered |good |cholesterol |because |it |
collects |excess |cholesterol |in |the |body |cells |and |transports |it |to |the |liver |where |it |is |excreted. |HDL |
carries |20 |to |25% |of |total |plasma |cholesterol.
Explain |the |role |inflammation |has |in |the |development |of |atherosclerosis |- |answersInflammation |in |the
|heart |muscle |caused |by |chronic |inflammatory |processes |leads |to |mitochondrial |damage |that |results |
in |an |increased |free |radical |production |that |further |activates |the |chronic |inflammatory |vicious |cycle
Explain |the |role |inflammation |has |in |the |development |of |atherosclerosis |- |answersActivated |mast |
cells |recruit |inflammatory |cells |that |provoke |plaque |formation |and |lead |to |atherosclerosis. |Chronic |
inflammatory |infiltrates |occupy |layers |of |arteries |were |stable |plaques |are |formed |and |associated |with
|atherosclerosis.
Explain |the |role |inflammation |has |in |the |development |of |atherosclerosis |- |answersAdditionally |active |
inflammation |involves |a |thinning |at |the |fibrous |Of |atherosclerotic |plaque |which |predisposes |
vulnerable |plaque |to |rupture.
Why |does |the |APRN |recognize |as |the |result |of |the |pleural |friction |rub? |- |answersThe |inflammation |of |
the |pericardium |due |to |either |the |underlying |autoimmune |disease |or |a |post |viral |syndrome |causes |
roughening |of |the |pericardium. |This |causes |the |classic |rug |which |can |be |best |heard |at |the |Apex |of |
the |heart |and |left |sternal |border.
Explain |how |a |positive |strep |test |has |caused |the |patient's |symptoms |- |answersRheumatic |heart |
disease |RHD |only |develops |after |a |pharyngeal |infection |with |group |a |beta |hemolytic |streptococcus. |It |
is |an |abnormal |response |to |humoral |and |cell |mediated |response |to |M |proteins. |Inflammation |causes |
proliferative |and |exudative |lesions |in |connective |tissue.
Explain |how |a |positive |strep |test |has |caused |the |patient's |symptoms |- |answersInflammation |causes |
scarring |of |the |valve |tissue. |Inflammation |usually |affects |the |endocardium |which |contains |the |valves. |
Endocardial |inflammation |causes |swelling |of |leaflets |in |the |valves.
Describe |the |factors |that |could |have |contributed |to |the |development |of |a |DVT |in |this |patient |and |
explain |how |each |of |the |factors |could |cause |DVT |- |answersVirchow's |Triad |caused |damage |to |the |
walls |of |the |vessels. |Injury |to |the |intimal |layer |of |the |vessel, |antiplatelet |substances |such |as |nitric |
oxide |and |prostacyclin, |along |with |the |expression |of |collagen |on |the |vessel |wall, |causes |adherence |to
|the |platelets |to |the |vessel |wall.
, Describe |the |factors |that |could |have |contributed |to |the |development |of |a |DVT |in |this |patient |and |
explain |how |each |of |the |factors |could |cause |DVT |- |answersPlatelets |become |activated, |then |
aggregate, |forming |clots. |Venous |stasis |is |a |result |of |obesity, |patients |advanced |age, |and |inability |to |
perform |physical |therapy |therapy.
Explain |why |large |pulmonary |embolus |interferes |with |oxygenation |- |answersThe |embolus |lodges |
somewhere |in |the |pulmonary |circulation |and |causes |a |ventilation/perfusion |mismatch |V/Q. |
Ventilation |perfusion |mismatch |or |V/Q |defects |are |defects |in |total |long |ventilation |perfusion |ratio.
Explain |why |large |pulmonary |embolus |interferes |with |oxygenation |- |answersIt |is |a |condition |in |which |
one |or |more |areas |of |the |lung |receive |oxygen |but |no |blood |flow, |or |they |receive |blood |flow |but |no |
oxygen |due |to |obstruction |somewhere |in |the |pulmonary |circulation. |This |causes |a |decreased |area |for
|oxygen |exchange.
Explain |why |a |large |pulmonary |embolism |causes |right |ventricular |strain |- |answersThe |V/Q |mismatch |
causes |release |of |neurohumeral |substances |and |inflammatory |mediators |that |cause |vasoconstriction |
of |the |pulmonary |vasculature |further |impeding |oxygenation.
Explain |why |a |large |pulmonary |embolism |causes |right |ventricular |strain |- |answersHemodynamically |
this |vasoconstriction |results |in |pulmonary |hypertension, |making |it |difficult |for |the |right |ventricle |to |
pump |blood.
Explain |why |a |large |pulmonary |embolism |causes |right |ventricular |strain |- |answersThe |V/Q |mismatch |
also |creates |decreased |production |of |surfactant |causing |atelectasis |that |further |decreases |surface |
area |available |for |oxygen |exchange.
Explain |early |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersWhen |there |is |
an |initial |airway |exposure |to |an |antigen, |an |innate |and |adaptive |immune |response |is |initiated.
Explain |early |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersCells |that |can |
initiate |the |inflammation |of |the |bronchial |mucosa |and |hyperresonance |of |the |airways |include |Dedrick
|cells, |T-helper |2 |cells, |lymphocytes, |B |lymphocytes, |mast |cells, |neutrophils, |eosinophils, |and |
basophils.
Explain |early |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersEarly |asthmatic |
response |is |a |phase |of |bronchospasm |that |peaks |at |about |30 |minutes |and |usually |resolves |after |
about |3 |hours.
Explain |late |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersLate |asthmatic |
responses |are |mediated |by |earlier |exposure |in |early |phase |that |causes |a |latent |release |of |
inflammatory |mediators. |These |mediators, |leukotrienes |and |prostaglandin |D, |cause |bronchospasm, |
edema, |and |mucus |secretions |that |obstruct |airflow.
Explain |late |asthmatic |responses |in |the |cells |responsible |for |the |responses |- |answersAirway |
obstruction |creates |resistance |to |airflow |and |causes |air |trapping. |Continued |air |trapping |increases |
intrapleural |and |alveolar |gas |pressure, |decreases |ventilation |and |perfusion |leading |to |uneven |and |
variable |ventilation/perfusion |in |the |lung.
