WGU pathophysiology D236 exam with
| | | | |
verified answers |
What |is |Starling's |Law |of |Capillary |forces? |
How |does |this |explain |why |a |nutritionally |deficient |child |would |have |edema? |- |correct |answer |
Starling's |Law |describes |how |fluids |move |across |the |capillary |membrane. |There |are |two |major |
opposing |forces |that |act |to |balance |each |other, |hydrostatic |pressure |(pushing |water |out |of |the
|capillaries) |and |osmotic |pressure |(including |oncontic |pressure, |which |pushes |fluid |into |the |
capillaries). |
Both |electrolytes |and |proteins |(oncontic |pressure) |in |the |blood |affect |osmotic |pressure, |high |
electrolyte |and |protein |concentrations |in |the |blood |would |cause |water |to |leave |the |cells |and |
interstitial |space |and |enter |the |blood |stream |to |dilute |the |high |concentrations. |
On, |the |other |hand, |low |electrolyte |and |protein |concentrations |(as |seen |in |a |nutritionally |
deficient |child) |would |cause |water |to |leave |the |capillaries |and |enter |the |cells |and |interstitial |
fluid |which |can |lead |to |edema.
How |does |the |RAAS |(Renin-Angiotensin-Aldosterone |System) |result |in |increased |blood |volume |
and |increased |blood |pressure? |- |correct |answer |A |drop |in |blood |pressure |is |sensed |by |the |
kidneys |triggers |prodcution |of |renin
Renin |triggers |the |liver |to |produce |angiotensinogen, |and |converts |it |into |Angiotensin |I |and |
angiotensin |II |by |the |enzyme |
Angiotensin-converting |enzyme |(ACE). |Angiotensin |II |stimulates |peripheral |arterial |
vasoconstriction |which |raises |BP. |
,Angiotensin |II |stimulate |the |adrenal |gland |to |release |aldosterone, |which |acts |to |increase |
sodium |and |water |absorption |increasing |blood |volume, |while |also |increased |potassium |
secretion |in |urine.
How |can |hyperkalemia |lead |to |cardiac |arrest? |- |correct |answer |Normal |levels |of |potassium |are
|between |3.5 |and |5.2 |mEq/dL. |Hyperkalemia |refers |to |potassium |levels |higher |that |5.2
|mEq/dL. |
A |major |function |of |potassium |is |to |conduct |nerve |impulses |in |muscles. |Too |low |causes |
muscle |weakness |too |much |can |cause |muscle |spasms. |
This |is |especially |dangerous |in |the |heart |muscle |and |an |irregular |heartbeat |can |cause |a |heart |
attack
The |body |uses |the |Protein |Buffering |System, |Phosphate |Buffering |System, |and |Carbonic |Acid-
Bicarbonate |System |to |regulate |and |maintain |homeostatic |pH, |what |is |the |consequence |of |a |
pH |imbalance |- |correct |answer |Any |increase |or |decrease |in |blood |pH |can |alter |the |structure |of
|the |protein |(denature), |thereby |affecting |its |function |as |well
Describe |the |laboratory |findings |associated |with |metabolic |acidosis, |metabolic |alkalosis, |
respiratory |acidosis |and |respiratory |alkalosis. |(ie |relative |pH |and |CO2 |levels). |- |correct |answer |
Normal |ABGs |(Arterial |Blood |Gases) |Blood |pH: |7.35-7.45 |PCO2: |35-45 |mm |Hg |PO2: |90-100 |
mm |Hg |HCO3-: |22-26 |mEq/L |SaO2: |95-100% |
Metabolic |acidosis |ph |less |than |7.35 |and |low |HC03. |Metabolic |alkolosis |ph |greater |than |7.35 |
and |so |is |hco3 |both |of |these |can |be |caused |my |dka. |if |the |ph |and |pco2 |levels |are |going |in |the |
same |direction |it |is |metabolic |if |they |are |going |in |a |different |direction |it |is |respiratory
Respiratory |alkolosis |ph |greater |than |7.35and |pco2 |is |decreased. |repsiratory |acidosis |is |ph |less
|than |7.35 |and |pco2 |greater |than
The |anion |gap |is |the |difference |between |measured |cations |(Na+ |and |K+) |and |measured |anions
|(Cl- |and |HCO3-), |this |calculation |can |be |useful |in |determining |the |cause |of |metabolic |acidosis.
|
,Why |would |an |increased |anion |gap |be |observed |in |diabetic |ketoacidosis |or |lactic |acidosis? |- |
correct |answer |The |anion |gap |is |the |calculation |of |unmeasured |anions |in |the |blood. |
Lactic |acid |and |ketones |lead |to |the |production |of |unmeasured |anions, |therefore |leads |to |an |
increase |in |the |AG.
Why |is |it |important |to |maintain |a |homeostatic |balance |of |glucose |in |the |blood |(ie |describe |the
|pathogenesis |of |diabetes)? |- |correct |answer |Insulin |is |the |hormone |responsible |for |initiating |
the |uptake |of |glucose |by |the |cells. |Cells |use |glucose |to |produce |energy |(ATP). |
In |a |normal |individual, |when |blood |glucose |increases, |the |pancreas |is |signaled |to |produced |in |
insulin, |which |binds |to |insulin |receptors |on |a |cells |surface |and |initiates |the |uptake |of |glucose. |
Glucose |if |left |in |the |blood, |can |to |bind |to |proteins |and |lipids, |which |can |lead |to |loss |of |
function. |leading |to |damage |in |the |heart |and |kidneys.
Compare |and |contrast |Type |I |and |Type |II |Diabetes |- |correct |answer |Type |I |diabetes |is |caused |
by |lack |of |insulin. |With |out |insulin |signaling, |glucose |will |not |be |taken |into |the |cell |and |leads |
to |high |blood |glucose |(hyperglycemia). |Type |I |is |usually |treated |with |insulin |injections. |
Type |II |diabetes |is |caused |by |a |desensitization |to |insulin |signaling. |The |insulin |receptors |are |no
|longer |responding |to |insulin, |which |also |leads |to |hyperglycemia. |
Type |II |is |usually |treated |with |drugs |to |increase |the |sensitization |to |insulin |(metformin), |
dietary |and |life-style |changes |or |insulin |injections.
Describe |some |reasons |for |a |patient |needing |dialysis |- |correct |answer |AEIOU-acidosis. |
Electrolytes, |Intoxication/Ingestion, |overload, |uremia. |Patients |with |kidney |or |heart |failure. |
A |build |up |of |phosphates, |urea |and |magnesium |are |removed |from |the |blood |using |a |semi-
permeable |membrane |and |dialysate. |
, AEIOU: |
A—acidosis; |
E—electrolytes |principally |hyperkalemia; |
I—ingestions |or |overdose |of |medications/drugs; |
O—overload |of |fluid |causing |heart |failure; |
U—uremia |leading |to |encephalitis/pericarditis
Compare |and |contrast |hemodialysis |and |peritoneal |dialysis. |
What |are |some |reasons |for |a |patient |choosing |one |over |the |other? |- |correct |answer |
Hemodialysis |uses |a |machine |to |pump |blood |from |the |body |in |one |tube |while |dialysate |(made
|of |water, |electrolytes |and |salts) |is |pumped |in |the |separate |tube |in |the |opposite |direction. |
Waste |from |the |blood |diffuses |through |the |semipermeable |membrane |separating |the |blood |
from |the |dialysate. |
Peritoneal |Dialysis |does |not |use |a |machine, |but |instead |injects |a |solution |of |water |and |glucose
|into |the |abdominal |cavity. |The |peritoneum |acts |as |the |membrane |instead |of |dialysis |tubing. |
The |waste |products |diffuse |into |the |abdominal |cavity |and |the |waste |solution |is |then |drained |
from |the |body. |
Peritoneal |dialysis |offers |continuous |filtration |and |is |less |disruption |to |the |patient's |daily |
routines. |However, |it |does |require |some |training |of |the |patient |and |is |not |recommended |for |
individuals |who |are |overweight |or |have |severe |kidney |failure. |
Hemodialysis |provides |medical |care, |but |3 |times |a |week |for |several |hours |sitting |at |a |hospital |
or |clinic. |Individuals |with |acute |kidney |failure |are |recommended |to |use |hemodialysis.
How |does |homeostasis |and |maintaining |optimal |physiological |health |impact |your |wellbeing? |- |
correct |answer |Homeostasis |acts |to |create |a |constant |and |stable |environment |in |the |body |
despite |internal |and |external |changes. |Proteins |and |other |cellular |processes |require |optimal |
conditions |in |order |to |carry |out |their |functions. |
| | | | |
verified answers |
What |is |Starling's |Law |of |Capillary |forces? |
How |does |this |explain |why |a |nutritionally |deficient |child |would |have |edema? |- |correct |answer |
Starling's |Law |describes |how |fluids |move |across |the |capillary |membrane. |There |are |two |major |
opposing |forces |that |act |to |balance |each |other, |hydrostatic |pressure |(pushing |water |out |of |the
|capillaries) |and |osmotic |pressure |(including |oncontic |pressure, |which |pushes |fluid |into |the |
capillaries). |
Both |electrolytes |and |proteins |(oncontic |pressure) |in |the |blood |affect |osmotic |pressure, |high |
electrolyte |and |protein |concentrations |in |the |blood |would |cause |water |to |leave |the |cells |and |
interstitial |space |and |enter |the |blood |stream |to |dilute |the |high |concentrations. |
On, |the |other |hand, |low |electrolyte |and |protein |concentrations |(as |seen |in |a |nutritionally |
deficient |child) |would |cause |water |to |leave |the |capillaries |and |enter |the |cells |and |interstitial |
fluid |which |can |lead |to |edema.
How |does |the |RAAS |(Renin-Angiotensin-Aldosterone |System) |result |in |increased |blood |volume |
and |increased |blood |pressure? |- |correct |answer |A |drop |in |blood |pressure |is |sensed |by |the |
kidneys |triggers |prodcution |of |renin
Renin |triggers |the |liver |to |produce |angiotensinogen, |and |converts |it |into |Angiotensin |I |and |
angiotensin |II |by |the |enzyme |
Angiotensin-converting |enzyme |(ACE). |Angiotensin |II |stimulates |peripheral |arterial |
vasoconstriction |which |raises |BP. |
,Angiotensin |II |stimulate |the |adrenal |gland |to |release |aldosterone, |which |acts |to |increase |
sodium |and |water |absorption |increasing |blood |volume, |while |also |increased |potassium |
secretion |in |urine.
How |can |hyperkalemia |lead |to |cardiac |arrest? |- |correct |answer |Normal |levels |of |potassium |are
|between |3.5 |and |5.2 |mEq/dL. |Hyperkalemia |refers |to |potassium |levels |higher |that |5.2
|mEq/dL. |
A |major |function |of |potassium |is |to |conduct |nerve |impulses |in |muscles. |Too |low |causes |
muscle |weakness |too |much |can |cause |muscle |spasms. |
This |is |especially |dangerous |in |the |heart |muscle |and |an |irregular |heartbeat |can |cause |a |heart |
attack
The |body |uses |the |Protein |Buffering |System, |Phosphate |Buffering |System, |and |Carbonic |Acid-
Bicarbonate |System |to |regulate |and |maintain |homeostatic |pH, |what |is |the |consequence |of |a |
pH |imbalance |- |correct |answer |Any |increase |or |decrease |in |blood |pH |can |alter |the |structure |of
|the |protein |(denature), |thereby |affecting |its |function |as |well
Describe |the |laboratory |findings |associated |with |metabolic |acidosis, |metabolic |alkalosis, |
respiratory |acidosis |and |respiratory |alkalosis. |(ie |relative |pH |and |CO2 |levels). |- |correct |answer |
Normal |ABGs |(Arterial |Blood |Gases) |Blood |pH: |7.35-7.45 |PCO2: |35-45 |mm |Hg |PO2: |90-100 |
mm |Hg |HCO3-: |22-26 |mEq/L |SaO2: |95-100% |
Metabolic |acidosis |ph |less |than |7.35 |and |low |HC03. |Metabolic |alkolosis |ph |greater |than |7.35 |
and |so |is |hco3 |both |of |these |can |be |caused |my |dka. |if |the |ph |and |pco2 |levels |are |going |in |the |
same |direction |it |is |metabolic |if |they |are |going |in |a |different |direction |it |is |respiratory
Respiratory |alkolosis |ph |greater |than |7.35and |pco2 |is |decreased. |repsiratory |acidosis |is |ph |less
|than |7.35 |and |pco2 |greater |than
The |anion |gap |is |the |difference |between |measured |cations |(Na+ |and |K+) |and |measured |anions
|(Cl- |and |HCO3-), |this |calculation |can |be |useful |in |determining |the |cause |of |metabolic |acidosis.
|
,Why |would |an |increased |anion |gap |be |observed |in |diabetic |ketoacidosis |or |lactic |acidosis? |- |
correct |answer |The |anion |gap |is |the |calculation |of |unmeasured |anions |in |the |blood. |
Lactic |acid |and |ketones |lead |to |the |production |of |unmeasured |anions, |therefore |leads |to |an |
increase |in |the |AG.
Why |is |it |important |to |maintain |a |homeostatic |balance |of |glucose |in |the |blood |(ie |describe |the
|pathogenesis |of |diabetes)? |- |correct |answer |Insulin |is |the |hormone |responsible |for |initiating |
the |uptake |of |glucose |by |the |cells. |Cells |use |glucose |to |produce |energy |(ATP). |
In |a |normal |individual, |when |blood |glucose |increases, |the |pancreas |is |signaled |to |produced |in |
insulin, |which |binds |to |insulin |receptors |on |a |cells |surface |and |initiates |the |uptake |of |glucose. |
Glucose |if |left |in |the |blood, |can |to |bind |to |proteins |and |lipids, |which |can |lead |to |loss |of |
function. |leading |to |damage |in |the |heart |and |kidneys.
Compare |and |contrast |Type |I |and |Type |II |Diabetes |- |correct |answer |Type |I |diabetes |is |caused |
by |lack |of |insulin. |With |out |insulin |signaling, |glucose |will |not |be |taken |into |the |cell |and |leads |
to |high |blood |glucose |(hyperglycemia). |Type |I |is |usually |treated |with |insulin |injections. |
Type |II |diabetes |is |caused |by |a |desensitization |to |insulin |signaling. |The |insulin |receptors |are |no
|longer |responding |to |insulin, |which |also |leads |to |hyperglycemia. |
Type |II |is |usually |treated |with |drugs |to |increase |the |sensitization |to |insulin |(metformin), |
dietary |and |life-style |changes |or |insulin |injections.
Describe |some |reasons |for |a |patient |needing |dialysis |- |correct |answer |AEIOU-acidosis. |
Electrolytes, |Intoxication/Ingestion, |overload, |uremia. |Patients |with |kidney |or |heart |failure. |
A |build |up |of |phosphates, |urea |and |magnesium |are |removed |from |the |blood |using |a |semi-
permeable |membrane |and |dialysate. |
, AEIOU: |
A—acidosis; |
E—electrolytes |principally |hyperkalemia; |
I—ingestions |or |overdose |of |medications/drugs; |
O—overload |of |fluid |causing |heart |failure; |
U—uremia |leading |to |encephalitis/pericarditis
Compare |and |contrast |hemodialysis |and |peritoneal |dialysis. |
What |are |some |reasons |for |a |patient |choosing |one |over |the |other? |- |correct |answer |
Hemodialysis |uses |a |machine |to |pump |blood |from |the |body |in |one |tube |while |dialysate |(made
|of |water, |electrolytes |and |salts) |is |pumped |in |the |separate |tube |in |the |opposite |direction. |
Waste |from |the |blood |diffuses |through |the |semipermeable |membrane |separating |the |blood |
from |the |dialysate. |
Peritoneal |Dialysis |does |not |use |a |machine, |but |instead |injects |a |solution |of |water |and |glucose
|into |the |abdominal |cavity. |The |peritoneum |acts |as |the |membrane |instead |of |dialysis |tubing. |
The |waste |products |diffuse |into |the |abdominal |cavity |and |the |waste |solution |is |then |drained |
from |the |body. |
Peritoneal |dialysis |offers |continuous |filtration |and |is |less |disruption |to |the |patient's |daily |
routines. |However, |it |does |require |some |training |of |the |patient |and |is |not |recommended |for |
individuals |who |are |overweight |or |have |severe |kidney |failure. |
Hemodialysis |provides |medical |care, |but |3 |times |a |week |for |several |hours |sitting |at |a |hospital |
or |clinic. |Individuals |with |acute |kidney |failure |are |recommended |to |use |hemodialysis.
How |does |homeostasis |and |maintaining |optimal |physiological |health |impact |your |wellbeing? |- |
correct |answer |Homeostasis |acts |to |create |a |constant |and |stable |environment |in |the |body |
despite |internal |and |external |changes. |Proteins |and |other |cellular |processes |require |optimal |
conditions |in |order |to |carry |out |their |functions. |
