Biology220 Test 1 - Practice

1 — Flux**

QUESTION
A person has an asthma attack that narrows their airway diameter by 30%. Using the bulk flow flux equation, explain why this has a catastrophic effect on airflow — and why their minute ventilation still increases.

a
Bulk flow resistance depends on radius to the fourth power, so a 30% reduction in radius causes resistance to increase by roughly (1/0.7)⁴ ≈ 4× — meaning you need ~4× the driving force (pressure difference) to move the same amount of air. The body compensates by working the diaphragm harder to create bigger pressure gradients, which increases tidal volume and/or respiratory rate, raising minute ventilation. The core point: tiny changes in tube radius have enormous consequences for flux because of the r⁴ relationship.

---

**

2 — Ventilation mechanics**

QUESTION
Trace the full chain of cause and effect for a single inhalation, starting at the diaphragm and ending when airflow stops. Then do the same for exhalation.

Inhale: Diaphragm contracts → thoracic cavity volume increases → lung pressure drops below atmospheric pressure → pressure gradient drives air from atmosphere into lungs (bulk flow down gradient) → airflow stops when intrapulmonary pressure = atmospheric pressure.

Exhale: Diaphragm relaxes → thoracic cavity volume decreases → intrapulmonary pressure rises above atmospheric → air flows out down the gradient → stops when P(in) = P(out).

The key concept: air is not "sucked in" — it's pushed in by a pressure gradient created by expanding the chest cavity. This is bulk flow. The driving force is the pressure difference; the resistance is airway geometry (radius, length, viscosity).

---

**

3 — O₂ transport chain**

QUESTION
Trace O₂ from the atmosphere to a mitochondrion in your leg muscle. For each step, state whether it's bulk flow or diffusion and identify the driving force.

1. Atmosphere → alveoli: bulk flow (ventilation). Driving force = pressure difference created by diaphragm. Resistance = airway radius, length, viscosity.
2. Alveoli → blood (across alveolar membrane): molecular diffusion. Driving force = pO₂ gradient (alveolar pO₂ ~100 mmHg vs. deoxygenated blood pO₂ ~40 mmHg). Resistance = membrane thickness, permeability. O₂ is small and nonpolar so it crosses the phospholipid bilayer without a channel.
3. Blood → working tissue: molecular diffusion. Driving force = pO₂ gradient (blood ~100 mmHg vs. tissue ~40 mmHg at rest, even lower during exercise). Resistance = capillary wall distance, membrane permeability.
4. Into mitochondria: diffusion continues down pO₂ gradient.

Memorize: 760 mmHg total atm pressure, ~21% O₂ → atmospheric pO₂ ≈ 160 mmHg, which drops to ~100 in alveoli due to gas mixing and water vapor.

---

**

4 — Hemoglobin and the dissociation curve**

QUESTION
During a hard run, your working muscles are hot, acidic, and flooded with CO₂. Explain step by step why hemoglobin delivers more O₂ than at rest, using Le Chatelier's Principle and the dissociation curve.

Exercise creates three simultaneous right-shift signals: ↑ temperature, ↑ CO₂ (→ ↑ H⁺ via the carbonic anhydrase reaction CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻), and ↑ [H⁺] itself. Each of these decreases hemoglobin's affinity for O₂ (Bohr effect), right-shifting the dissociation curve. By Le Chatelier's Principle: O₂ + Hb ⇌ Hb(O₂)ₙ — decreasing Hb's affinity shifts the equilibrium left, releasing more O₂. On the graph, a right-shifted curve means that at the same tissue pO₂ (~40 mmHg), hemoglobin saturation is lower — so more O₂ has been dropped off. The curve still reaches near 100% saturation in the lungs (pO₂ ~100 mmHg), so loading is unaffected. The system is self-regulating: the tissues that need the most O₂ create the strongest right-shift signal.

---

**

5 — Dissociation curve shifts**

QUESTION
Draw and annotate the oxyhemoglobin dissociation curve for (a) normal, (b) low pH/high CO₂, and (c) fetal hemoglobin (HbF). For each, predict what happens to O₂ loading in the lungs and unloading at tissue.

• (a) Normal: S-shaped curve. At pO₂ = 100 (lungs), ~97-98% saturated. At pO₂ = 40 (tissue), ~75% saturated → drops off ~25 saturation units worth of O₂.
• (b) Low pH / ↑ CO₂ (right shift): Curve shifts right. Loading in lungs still near 100% (pO₂ is high enough). Unloading at tissue is greater — saturation falls further at pO₂ = 40, so more O₂ is delivered. This is the Bohr effect. Also caused by ↑ temperature and ↑ 2,3-DPG.
• (c) HbF (left shift): Higher affinity for O₂. At tissue pO₂, HbF holds onto O₂ more tightly → less unloading. This is advantageous in the placenta — fetal HbF "steals" O₂ from maternal blood because its left-shifted curve outcompetes maternal Hb at the same pO₂.

Right-shift causes: ↑ pCO₂, ↑ [H⁺] (↓ pH), ↑ temp, ↑ 2,3-DPG. Left-shift causes: the opposites, plus HbF.

---

**

6 — Patent Foramen Ovale (PFO)**

QUESTION
A patient has a PFO — a hole between the right and left atria, so some deoxygenated blood bypasses the lungs. Trace the full chain of effects on O₂ delivery to working tissue.

Deoxygenated blood (low pO₂) passes directly from right atrium → left atrium, bypassing the pulmonary circulation entirely. This deoxygenated blood mixes with freshly oxygenated blood returning from the lungs. Result: ↓ average pO₂ of blood leaving the left ventricle → ↓ pO₂ in systemic arteries → ↓ pO₂ gradient between blood and working tissue → ↓ driving force for O₂ diffusion → ↓ O₂ gas exchange at tissue. The lungs themselves work fine — the problem is the mixing of oxygenated and deoxygenated blood before it reaches the body. This is called a right-to-left shunt.

---

**

7 — Membrane transport**

QUESTION
Why does K⁺ cross the membrane more easily than Na⁺ at rest, even though both are small positive ions? What happens if you block those channels?

At rest, there are far more K⁺ leak channels open than Na⁺ leak channels. Leak channels are always open — they set baseline permeability. Conductance for molecular diffusion depends on the number of open channels; more open K⁺ channels = higher conductance = more K⁺ flux. Both ions are charged and cannot cross the phospholipid bilayer directly — they need protein channels. If you block K⁺ leak channels, K⁺ can't flow out, the inside of the cell becomes less negative (depolarizes), and the resting membrane potential shifts toward zero. The cell becomes harder to return to rest after an action potential.

---

**

8 — Membrane transport: which molecules need help**

QUESTION
What physical properties of a molecule determine whether it can diffuse through a phospholipid bilayer unaided? Give examples from physiology on both sides.

The bilayer resists charged molecules (ions like Na⁺, K⁺, Cl⁻, Ca²⁺) and polar molecules (including most large molecules, which tend to have polar regions). Small, nonpolar molecules pass freely. Examples: O₂, CO₂, H₂O — freely cross (important for gas exchange and osmosis). Glucose, Na⁺, K⁺, Cl⁻ — require transport proteins (channels or pumps). This is directly tested: when O₂ diffuses from alveoli to blood, it crosses two cell membranes unaided because it's small and nonpolar. When Na⁺ flows during an action potential, it requires a voltage-gated channel.

---

**

9 — Sodium-potassium pump and ion gradients**

QUESTION
The Na⁺/K⁺ pump moves Na⁺ OUT and K⁺ IN, against their concentration gradients. Why does this matter for the resting membrane potential, and what happens in the short term if you poison it?

The pump (active transport, requires ATP) maintains the baseline ion gradients: Na⁺ high outside (150 mM) / low inside (15 mM); K⁺ high inside (150 mM) / low outside (5 mM). K⁺ then leaks out through leak channels down its concentration gradient, leaving behind negative charges — this creates the negative resting membrane potential (approximately -70 mV). If you poison the pump, gradients slowly collapse: Na⁺ leaks in, K⁺ leaks out, the inside becomes less negative (depolarization), and eventually the cell loses the ability to generate action potentials. The pump doesn't directly set the membrane potential — it maintains the gradients that K⁺ leak channels then exploit to set the potential.

---

**

10 — Applying mass balance to alveolar pO₂**

QUESTION
Using mass balance reasoning, predict what happens to alveolar pO₂ if a person increases their metabolic rate (exercise) without changing their ventilation rate. Then predict what happens if they simultaneously increase ventilation.

Mass balance says: the amount of O₂ in the alveoli at steady state depends on rate in (ventilation bringing fresh O₂) minus rate out (diffusion into blood, which depends on metabolic demand). If metabolic rate ↑ without a change in ventilation: rate out ↑ (more O₂ extracted by blood), rate in unchanged → alveolar pO₂ falls. Lower alveolar pO₂ → smaller gradient → less O₂ diffuses into blood → potential hypoxia. If ventilation simultaneously ↑ (as happens in real exercise via chemoreceptors responding to CO₂): rate in ↑ to match rate out → alveolar pO₂ is restored toward normal. This is the feedback loop that keeps pO₂ stable during exercise.

---

**

11 — Connecting anatomy to flux (PF note emphasis)**

QUESTION
The learning objectives specifically note "try to connect anatomy to flux." Give two anatomical examples where structure is directly explained by flux principles.

• Capillaries for O₂ diffusion: Diffusion flux depends on distance as a resistance — shorter distance = lower resistance = more flux. Capillaries bring blood within ~1 cell's width of every tissue cell, minimizing diffusion distance. They also have thin walls (low membrane resistance) and slow blood flow (maximizing contact time). Without capillaries, O₂ would have to diffuse millimeters through tissue — too slow.
• Diaphragm for ventilation: The diaphragm creates the pressure gradient (driving force) for bulk airflow. Without it, there's no pressure difference between lungs and atmosphere, so no bulk flow into the airways. It's the "pump" that drives the driving force.
• Bonus: alveoli have enormous surface area → effectively lowers resistance to O₂ diffusion by maximizing the number of parallel pathways (conductance in parallel adds up).

---

**

12 — Minute ventilation scenarios (from Problem 4)**

QUESTION
For each scenario, predict the change in minute ventilation and explain the mechanism: (A) Blood pH drops due to high CO₂. (B) Person breathes hyperoxic air (extra O₂). (C) Bronchoconstriction. (D) Anemia.

• (A) ↓ pH from ↑ CO₂ → INCREASE. Chemoreceptors detect ↑ CO₂/↓ pH and signal for more breathing to blow off CO₂ and restore pH. Both RR and TV typically increase.
• (B) Hyperoxic air → NO CHANGE (or slight decrease). The primary drive to breathe is CO₂/pH, not O₂ levels. Normal O₂ doesn't significantly suppress ventilation in healthy people (exception: chronic CO₂ retainers rely on hypoxic drive).
• (C) Bronchoconstriction → INCREASE. Narrower airways ↑ resistance dramatically (r⁴ relationship). The body must increase driving force — i.e., work harder and breathe with more effort — to maintain adequate airflow. Minute ventilation increases as a compensatory response.
• (D) Anemia → INCREASE. Fewer RBCs → less total O₂ carried even at normal pO₂ → tissues detect O₂ deficit → body increases ventilation to try to compensate, even though the root problem is at the Hb level, not ventilat