ASSESSMENT EXAM STUDY GUIDE 2026
◉ How does the RAAS (Renin-Angiotensin-Aldosterone System)
result in increased blood volume and increased blood pressure?
Answer: A 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? 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 and muscle weakness occurs and 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 Answer: Proteins 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). 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%
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.
Here are the rules to follow to determine if is respiratory or
metabolic in nature. -If pH and PCO2 are moving in opposite
directions, then it is the pCO2 levels that are causing the imbalance
and it is respiratory in nature.
-If PCO2 is normal or is moving in the same direction as the pH, then
the imbalance is metabolic in nature.
◉ 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? Answer: The anion gap is the
calculation of unmeasured anions in the blood.
Lactic acid and ketones both lead to the production of unmeasured
anions, which remove HCO3- (a measured anion) due to buffering of
the excess H+ and 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)? 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 is a very reactive molecule and if left in the blood, it can
start to bind to other proteins and lipids, which can lead to loss of
function.
AGEs are advanced glycation end products that are a result of
glucose reacting with the endothelial lining, which can lead to
damage in the heart and kidneys.
◉ Compare and contrast Type I and Type II Diabetes 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.