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WGU D236 pathophysiology: Objective Assessment Questions and Verified Answers | Latest 2026/2027 GRADED A+

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WGU D236 pathophysiology: Objective Assessment Questions and Verified Answers | Latest 2026/2027 GRADED A+ WGU D236 pathophysiology: Objective Assessment Questions and Verified Answers | Latest 2026/2027 GRADED A+ WGU D236 pathophysiology: Objective Assessment Questions and Verified Answers | Latest 2026/2027 GRADED A+ WGU D236 pathophysiology: Objective Assessment Questions and Verified Answers | Latest 2026/2027 GRADED A+ WGU D236 pathophysiology: Objective Assessment Questions and Verified Answers | Latest 2026/2027 GRADED A+ WGU D236 pathophysiology: Objective Assessment Questions and Verified Answers | Latest 2026/2027 GRADED A+

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WGU D236 Pathophysiology
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WGU D236 pathophysiology

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WGU D236 pathophysiology: Objective
Assessment Questions and Verified
Answers | Latest 2026/2027 GRADED A+

What is Starling's Law of Capillary forces?


How does this explain why a nutritionally deficient child would have edema?


- DDStarling'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?

,WGU D236 pathophysiology OA Exam Study Guide 2026 Questions and Answers



- DDA drop in blood pressure is sensed by the kidneys by low perfusion, which in turn begins to

secrete renin.




Renin then triggers the liver to produce angiotensinogen, which is converted to Angiotensin I in the

lungs and then angiotensin II by the enzyme




Angiotensin-converting enzyme (ACE). Angiotensin II stimulates peripheral arterial vasoconstriction

which raises BP.




Angiotensin II is also stimulating the adrenal gland to release aldosterone, which acts to increase

sodium and water reabsorption increasing blood volume, while also increased potassium secretion in

urine.




How can hyperkalemia lead to cardiac arrest?


- DDNormal levels of potassium are between 3.5 and 5.2 mEq/dL. Hyperkalemia refers topotassium

levels higher that 5.2 mEq/dL.




A major function of potassium is to conduct nerve impulses in muscles. Too low and muscle weakness

occurs and too much can cause muscle spasms.

,WGU D236 pathophysiology OA Exam Study Guide 2026 Questions and Answers



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


- DDProteins contain many acidic and basic group that can be affected by pH changes. 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).


- DDNormal 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%




Respiratory acidosis and alkalosis are marked by changes in PCO2. Higher = acidosis and lower =

alkalosis




Metabolic acidosis and alkalosis are caused by something other than abnormal CO2 levels. This could

include toxicity, diabetes, renal failure or excessive GI losses.

, WGU D236 pathophysiology OA Exam Study Guide 2026 Questions and Answers



Here fare fthe frules fto ffollow fto fdetermine fif fis frespiratory for fmetabolic fin fnature. f-If fpH fand

fPCO2 fare fmoving fin fopposite fdirections, fthen fit fis fthe fpCO2 flevels fthat fare fcausing fthe

fimbalance fand fit fis frespiratory fin fnature.




-If fPCO2 fis fnormal for fis fmoving fin fthe fsame fdirection fas fthe fpH, fthen fthe fimbalance fis

fmetabolic fin fnature.




The fanion fgap fis fthe fdifference fbetween fmeasured fcations f(Na+ fand fK+) fand fmeasured

fanions f(Cl- fand fHCO3-), fthis fcalculation fcan fbe fuseful fin fdetermining fthe fcause fof

fmetabolic facidosis.




Why fwould fan fincreased fanion fgap fbe fobserved fin fdiabetic fketoacidosis for flactic facidosis?


- DDThe fanion fgap fis fthe fcalculation fof funmeasured fanions fin fthe fblood.




Lactic facid fand fketones fboth flead fto fthe fproduction fof funmeasured fanions, fwhich fremove fHCO3-

f(a fmeasured fanion) fdue fto fbuffering fof fthe fexcess fH+ fand ftherefore fleads fto fan fincrease fin

fthe fAG.




Why fis fit fimportant fto fmaintain fa fhomeostatic fbalance fof fglucose fin fthe fblood f(ie fdescribe

fthe fpathogenesis fof fdiabetes)?


- DDInsulin fis fthe fhormone fresponsible ffor finitiating fthe fuptake fof fglucose fby fthe fcells.

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