Alterations in Intracellular Functions and Fluid and Solute Balance

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A curated set of practice questions and answers covering key concepts from Alterations in Intracellular Functions and Fluid and Solute Balance, including osmosis/osmolality, acid-base disorders, hypoxia, metabolic pathways, RAAS/ADH/SIADH, electrolyte disturbances, and cellular electrical properties.

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53 Terms

1
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What is the normal blood pH range to memorize for acid/base assessment?

7.35 to 7.45.

2
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What is homeostasis in the context of cellular physiology?

Maintenance of a stable internal environment (fluids, electrolytes, pH, and ATP supply) through compensatory mechanisms to stay within narrow limits.

3
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What are two common sequelae of hypoxia on cellular metabolism?

Shift to anaerobic glycolysis with lactic acid production causing metabolic acidosis and reduced ATP production.

4
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Define osmosis.

Movement of water across a semipermeable membrane from a region of lower solute concentration to higher solute concentration.

5
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What is the normal osmolality range for body fluids?

280–295 mosmol/kg.

6
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What does tonicity describe and what is the normal isotonic reference for blood?

Tonicity describes effective osmolality; normal isotonic reference is 0.9% NaCl (normal saline).

7
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What triggers the renin-angiotensin-aldosterone system (RAAS)?

Low blood volume/BP, low renal perfusion, or high plasma osmolality that stimulates renin release.

8
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What are the two main actions of angiotensin II?

Peripheral vasoconstriction and stimulation of aldosterone release.

9
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What is the role of aldosterone in fluid balance?

Increases Na+ (and water) reabsorption in the kidneys, raising circulatory volume and reducing urine output.

10
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What is the function of antidiuretic hormone (ADH)?

Promotes water reabsorption in the renal collecting ducts, aiding fluid retention.

11
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What is SIADH and its consequence?

Syndrome of inappropriate ADH secretion causing water retention and hyponatremia with fluid volume excess.

12
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How does hypoproteinemia affect plasma oncotic pressure and fluid shifts?

Low plasma proteins reduce oncotic pressure, promoting fluid movement from blood into interstitial space and causing edema.

13
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What solutes contribute to osmolality, and what is the practical takeaway?

Electrolytes (Na+, K+, Cl-, etc.), glucose, urea, and proteins; osmolality governs water movement (osmosis) in the body.

14
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What is back-up plan #1 during hypoglycemia and what process does it involve?

Glycogenolysis—the breakdown of glycogen to glucose to raise blood glucose.

15
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What is back-up plan #2 during hypoglycemia and what process does it involve?

Gluconeogenesis—the production of glucose from non-carbohydrate sources.

16
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Name the counterregulatory hormones that raise blood glucose during hypoglycemia.

Epinephrine, cortisol, growth hormone, and glucagon.

17
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What happens to cellular metabolism under hypoxic conditions?

Glycolysis proceeds anaerobically, yielding 2 ATP per glucose and accumulating lactate, leading to acidosis.

18
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Define ketogenesis and ketone bodies.

Ketogenesis is the production of ketone bodies from fatty acids; ketones provide limited energy but are acids that can cause acidosis.

19
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What are common signs of metabolic acidosis?

Headache, decreased BP, hyperkalemia, muscle twitching, warm/flushed skin, nausea, vomiting, diarrhea, altered LOC, and Kussmaul respirations.

20
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What are common etiologies of metabolic acidosis?

Diabetic ketoacidosis (DKA), lactic acidosis, kidney failure, severe diarrhea, and poisons/drug overdoses.

21
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How does metabolic acidosis typically attempt to compensate?

By increasing respiratory rate and depth to blow off CO2 (respiratory compensation).

22
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What characterizes metabolic alkalosis and its common cause?

High pH with high HCO3-; commonly due to vomiting or excessive bicarbonate intake; compensated by reduced respiratory rate.

23
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What is respiratory acidosis and its compensatory mechanism?

Low pH due to hypoventilation/CO2 retention; kidneys compensate by increasing HCO3- reabsorption.

24
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What is respiratory alkalosis and its compensatory mechanism?

High pH due to hyperventilation/CO2 loss; kidneys compensate by decreasing HCO3- reabsorption or excretion.

25
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What is the normal range for serum bicarbonate (HCO3-)?

22–28 mEq/L.

26
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What is the normal serum osmolality range?

280–295 mosmol/kg.

27
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How does edema form in the setting of low plasma oncotic pressure?

Water moves from blood to interstitial space due to decreased oncotic pressure, leading to edema.

28
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What is proteinuria and its consequence?

Loss of protein in urine due to glomerular damage, causing hypoproteinemia and edema.

29
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What is the Na+/K+ ATPase pump and why is it essential?

It uses ATP to transport Na+ out of the cell and K+ into the cell, maintaining the resting membrane potential (~-90 mV).

30
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What happens when ATP is deficient and the Na+/K+ pump fails?

Cell membrane becomes depolarized or abnormally polarized, impairing electrical signaling and cell function.

31
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How does hyperkalemia affect cellular resting membrane potential?

Depolarizes cells (less negative RMP, e.g., from -90 mV toward -60 mV), increasing excitability.

32
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How does hypokalemia affect cellular resting membrane potential?

Hyperpolarizes cells (more negative RMP, e.g., toward -120 mV), decreasing excitability.

33
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What effect does hypocalcemia have on membrane potential and excitability?

Increases Na+ permeability, depolarizing the cell (hypopolarization) and causing tetany and hyperexcitability.

34
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What happens in hypercalcemia regarding membrane potential and excitability?

Decreases Na+ permeability, hyperpolarizing cells and reducing excitability (possible bradycardia).

35
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What is the Chvostek sign?

Facial muscle twitch with tapping of the facial nerve, indicating hypocalcemia.

36
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What is tetany and what causes it?

Sustained muscle contractions due to severe hypocalcemia (and sometimes hypomagnesemia).

37
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What is the role of ADH in SIADH?

In SIADH, excess ADH leads to water retention and dilutional hyponatremia with reduced urine output (oliguria).

38
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What is proteinuria and its edema-related consequence?

Proteins leak into urine due to kidney/glomerular issues, causing hypoproteinemia and edema via decreased oncotic pressure.

39
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What is isotonic IV fluid, and give an example?

An IV fluid with tonicity similar to blood; example: 0.9% NaCl (normal saline).

40
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What are the three main body fluid compartments?

Intracellular fluid (ICF), extracellular fluid (ECF) including interstitial fluid and plasma (vascular) space.

41
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What is osmosis governed by in the context of fluid shifts?

Osmolality determines the direction of water movement; higher osmolality draws water from lower osmolality areas.

42
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What is the difference between isotonic, hypotonic, and hypertonic fluids?

Isotonic: same osmolality as blood (e.g., 0.9% NaCl); Hypotonic: lower tonicity (e.g., 0.45% NaCl) causing water to move into cells; Hypertonic: higher tonicity (e.g., 3% NaCl) drawing water out of cells.

43
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What is the process of glycogenesis?

Formation and storage of glycogen from glucose in the liver and muscles.

44
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What is glycogenolysis?

Breakdown of glycogen to glucose to supply energy.

45
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What is glycolysis?

Metabolic pathway that converts glucose to pyruvate (or lactate under anaerobic conditions), producing ATP.

46
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What is gluconeogenesis?

Production of glucose from non-carbohydrate precursors (backup energy source during low glucose).

47
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What are ketone bodies and when are they produced?

Acidic energy sources produced from fatty acids during prolonged fasting or insulin deficiency; can cause ketoacidosis if excessive.

48
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What is the role of the liver in amino acid and glucose metabolism during fasting?

Contributes to gluconeogenesis and ketogenesis when glucose is scarce.

49
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What is the significance of acetyl-CoA in metabolism?

Central substrate linking glycolysis to the Krebs cycle and ketogenesis; produced from fatty acids and some amino acids.

50
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What is the significance of the TCA cycle in cellular energy?

Main pathway that oxidizes acetyl-CoA to CO2, producing NADH/FADH2 for the electron transport chain and ATP.

51
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What is the clinical relevance of ABGs (arterial blood gases)?

Measures pH, HCO3-, and PCO2 to assess acid/base status and respiratory/metabolic compensation.

52
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What is hypoxia’s impact on cellular ATP production?

Reduces aerobic ATP production, forces anaerobic glycolysis, and promotes acidosis.

53
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What is the significance of hypoglycemia in clinical assessment?

Counterregulatory hormones are activated to raise blood glucose, with glycogenolysis and gluconeogenesis as backup plans.