NURS 3366 FINAL EXAM REVIEW UPDATED ACTUAL
QUESTIONS AND CORRECT ANSWERS
Question:
1. What occurs to fluid movement, tissue cells, and clinical S&S when the plasma space becomes
hyperosmolar / hypertonic?
Answer:
Fluid Shift: Tissue to Blood (T -> B) via osmosis (concentration calls) Tissue Impact: Dehydration / fluid
volume deficit. S&S: Poor skin turgor, dry mucous membranes, low urine output. Causes: Poor fluid
intake, vomiting, diarrhea, DI (diabetes insipidus), DM (diabetes mellitus), Addison's disease.
Compensatory System: RAAS activation (triggered by low blood pressure, decreased blood volume, or
low sodium levels, which cause the kidneys to release renin into the bloodstream. This enzyme starts a
chemical chain reaction that produces angiotensin II and aldosterone to narrow blood vessels and retain
water.) Treatment: Hypotonic IV fluids.
Question:
2. What occurs to fluid movement, tissue cells, and clinical S&S when the plasma space becomes
hypoosmolar / hypotonic?
Answer:
Fluid Shift: Blood to Tissue (B -> T). Tissue Impact: Fluid volume overload / edema. S&S: Peripheral
pitting edema, pulmonary edema (crackles, dyspnea), brain edema. Causes: Overdrinking water, SIADH,
Cushing's, CKD (chronic kidney disease), HF (heart failure), Cirrhosis (hypoproteinemia/low oncotic
pressure). Compensatory System: Natriuretic Peptide System (NPS) a group of hormone proteins that your
heart and other tissues make to control blood pressure, body fluid, and salt levels. When blood volume or
pressure gets too high, the heart releases these peptides to relax blood vessels and tell the kidneys to get rid
of extra salt and water. Treatment: Hypertonic IV fluids / Diuretics.
Question:
3. How does hypokalemia affect Resting Membrane Potential (RMP) and what are its S&S?
Answer:
Mechanism: K+ diffuses out -> cells lose cations -> RMP becomes more negative (further from +30mV
threshold) Polarization State: Hyperpolarization (lengthened polar gap). Effect: Muscle/nerve cells are
hyporesponsive / hyposensitive (takes longer to depolarize) S&S: Muscle weakness, sluggishness,
lethargy, confusion, bradycardia (HR < 60).
Question:
4. How does hyperkalemia affect Resting Membrane Potential (RMP) and what are its S&S?
Answer:
Mechanism: K+ diffuses in -> cells gain cations -> RMP becomes more positive. (closer to +30mV
threshold) Polarization State: Hypopolarization (shortened polar gap). Effect: Muscle/nerve cells are
hyperresponsive / hypersensitive. S&S: Muscle spasms, twitching, irritability, tetany, hyperactive reflexes,
tachycardia (HR > 100) / dysrhythmias.
Question:
5. How do hypocalcemia and hypercalcemia affect membrane permeability and RMP?
, Answer:
Hypocalcemia: Increases Na+ permeability -> Na+ influx -> Hypopolarization -> Muscle irritability,
spasms, tetany, positive Chvostek's sign. Hypercalcemia: Decreases Na+ permeability -> less Na+ enters
cell ->Hyperpolarization -> Muscle weakness, lethargy, fatigue, sluggishness.
Question:
6. What are the key indicators differentiating local from systemic inflammation?
Answer:
Local: Rubor (redness), calor (heat), tumor (swelling), dolor (pain), exudate (serous, serosanguinous,
purulent). Systemic: Fever (>100.4F), malaise, aches, leukocytosis (high WBC), elevated C-Reactive
Protein (CRP).
Question:
7. What are the normal roles of protective prostaglandins, and what occurs when NSAIDs/Steroids inhibit
them?
Answer:
Protective Roles (PGRVI): Platelet aggregation (clotting), Gastric mucosa protection (stomach lining
protection), Renal function (adequate perfusion), Vasomotor tone, Immunocyte function. NSAID/Steroid
Side Effects: Bleeding (P), gastric ulcers (G), renal dysfunction (R), vasoconstriction (V), increased
infection risk (I).
Question:
8. Define the diagnostic progression from SIRS to Sepsis to Septic Shock.
Answer:
SIRS: Systemic Inflammatory Response Syndrome without confirmed infection (fever >100.4F, elevated
HR/RR, abnormal WBC). Sepsis: SIRS + Confirmed Infection. Septic Shock: Sepsis + Unresponsive Low
Blood Pressure (Hypotension) -> widespread tissue hypoxia and organ dysfunction
Question:
9. Differentiate Microcytic, Macrocytic, and Normocytic anemias by cause, MCV, and S&S.
Answer:
Microcytic (MCV < 80): Faulty Hgb synthesis due to chronic blood loss / iron deficiency (Tx: Iron
supplements) Macrocytic (MCV > 95): Faulty DNA synthesis due to B12 deficiency (lack of Intrinsic
Factor / Pernicious anemia). S&S: Glossitis (beefy red tongue), paresthesias (pins and needles in legs) (Tx:
B12 injections) Normocytic (MCV 80-95): Normal cell size but low count due to acute rapid blood loss or
Chronic Kidney Disease (low erythropoietin) (Tx: Erythropoietin injections / Blood transfusions)
Question:
10. Contrast Arterial Insufficiency (PAD) vs. Venous Insufficiency.
Answer:
Arterial Insufficiency: Impaired arterial perfusion -> Ischemia. S&S: Intermittent claudication (pain with
activity, relieved by rest), 5 P's (pain, pallor, pulselessness, paresthesia, poikilothermia/coolness), shiny
hairless skin, delayed cap refill (> 2 sec), ischemic ulcers. No significant edema. Venous Insufficiency:
Floppy valves -> Venous backflow/stasis -> Congestion/increased hydrostatic pressure. S&S: Peripheral
edema, brownish skin, warm skin, pain at rest, venous stasis ulcers.
Question:
11. Compare Stable Angina, Unstable Angina, and Myocardial Infarction (MI).
QUESTIONS AND CORRECT ANSWERS
Question:
1. What occurs to fluid movement, tissue cells, and clinical S&S when the plasma space becomes
hyperosmolar / hypertonic?
Answer:
Fluid Shift: Tissue to Blood (T -> B) via osmosis (concentration calls) Tissue Impact: Dehydration / fluid
volume deficit. S&S: Poor skin turgor, dry mucous membranes, low urine output. Causes: Poor fluid
intake, vomiting, diarrhea, DI (diabetes insipidus), DM (diabetes mellitus), Addison's disease.
Compensatory System: RAAS activation (triggered by low blood pressure, decreased blood volume, or
low sodium levels, which cause the kidneys to release renin into the bloodstream. This enzyme starts a
chemical chain reaction that produces angiotensin II and aldosterone to narrow blood vessels and retain
water.) Treatment: Hypotonic IV fluids.
Question:
2. What occurs to fluid movement, tissue cells, and clinical S&S when the plasma space becomes
hypoosmolar / hypotonic?
Answer:
Fluid Shift: Blood to Tissue (B -> T). Tissue Impact: Fluid volume overload / edema. S&S: Peripheral
pitting edema, pulmonary edema (crackles, dyspnea), brain edema. Causes: Overdrinking water, SIADH,
Cushing's, CKD (chronic kidney disease), HF (heart failure), Cirrhosis (hypoproteinemia/low oncotic
pressure). Compensatory System: Natriuretic Peptide System (NPS) a group of hormone proteins that your
heart and other tissues make to control blood pressure, body fluid, and salt levels. When blood volume or
pressure gets too high, the heart releases these peptides to relax blood vessels and tell the kidneys to get rid
of extra salt and water. Treatment: Hypertonic IV fluids / Diuretics.
Question:
3. How does hypokalemia affect Resting Membrane Potential (RMP) and what are its S&S?
Answer:
Mechanism: K+ diffuses out -> cells lose cations -> RMP becomes more negative (further from +30mV
threshold) Polarization State: Hyperpolarization (lengthened polar gap). Effect: Muscle/nerve cells are
hyporesponsive / hyposensitive (takes longer to depolarize) S&S: Muscle weakness, sluggishness,
lethargy, confusion, bradycardia (HR < 60).
Question:
4. How does hyperkalemia affect Resting Membrane Potential (RMP) and what are its S&S?
Answer:
Mechanism: K+ diffuses in -> cells gain cations -> RMP becomes more positive. (closer to +30mV
threshold) Polarization State: Hypopolarization (shortened polar gap). Effect: Muscle/nerve cells are
hyperresponsive / hypersensitive. S&S: Muscle spasms, twitching, irritability, tetany, hyperactive reflexes,
tachycardia (HR > 100) / dysrhythmias.
Question:
5. How do hypocalcemia and hypercalcemia affect membrane permeability and RMP?
, Answer:
Hypocalcemia: Increases Na+ permeability -> Na+ influx -> Hypopolarization -> Muscle irritability,
spasms, tetany, positive Chvostek's sign. Hypercalcemia: Decreases Na+ permeability -> less Na+ enters
cell ->Hyperpolarization -> Muscle weakness, lethargy, fatigue, sluggishness.
Question:
6. What are the key indicators differentiating local from systemic inflammation?
Answer:
Local: Rubor (redness), calor (heat), tumor (swelling), dolor (pain), exudate (serous, serosanguinous,
purulent). Systemic: Fever (>100.4F), malaise, aches, leukocytosis (high WBC), elevated C-Reactive
Protein (CRP).
Question:
7. What are the normal roles of protective prostaglandins, and what occurs when NSAIDs/Steroids inhibit
them?
Answer:
Protective Roles (PGRVI): Platelet aggregation (clotting), Gastric mucosa protection (stomach lining
protection), Renal function (adequate perfusion), Vasomotor tone, Immunocyte function. NSAID/Steroid
Side Effects: Bleeding (P), gastric ulcers (G), renal dysfunction (R), vasoconstriction (V), increased
infection risk (I).
Question:
8. Define the diagnostic progression from SIRS to Sepsis to Septic Shock.
Answer:
SIRS: Systemic Inflammatory Response Syndrome without confirmed infection (fever >100.4F, elevated
HR/RR, abnormal WBC). Sepsis: SIRS + Confirmed Infection. Septic Shock: Sepsis + Unresponsive Low
Blood Pressure (Hypotension) -> widespread tissue hypoxia and organ dysfunction
Question:
9. Differentiate Microcytic, Macrocytic, and Normocytic anemias by cause, MCV, and S&S.
Answer:
Microcytic (MCV < 80): Faulty Hgb synthesis due to chronic blood loss / iron deficiency (Tx: Iron
supplements) Macrocytic (MCV > 95): Faulty DNA synthesis due to B12 deficiency (lack of Intrinsic
Factor / Pernicious anemia). S&S: Glossitis (beefy red tongue), paresthesias (pins and needles in legs) (Tx:
B12 injections) Normocytic (MCV 80-95): Normal cell size but low count due to acute rapid blood loss or
Chronic Kidney Disease (low erythropoietin) (Tx: Erythropoietin injections / Blood transfusions)
Question:
10. Contrast Arterial Insufficiency (PAD) vs. Venous Insufficiency.
Answer:
Arterial Insufficiency: Impaired arterial perfusion -> Ischemia. S&S: Intermittent claudication (pain with
activity, relieved by rest), 5 P's (pain, pallor, pulselessness, paresthesia, poikilothermia/coolness), shiny
hairless skin, delayed cap refill (> 2 sec), ischemic ulcers. No significant edema. Venous Insufficiency:
Floppy valves -> Venous backflow/stasis -> Congestion/increased hydrostatic pressure. S&S: Peripheral
edema, brownish skin, warm skin, pain at rest, venous stasis ulcers.
Question:
11. Compare Stable Angina, Unstable Angina, and Myocardial Infarction (MI).
