Biology I combined

What type of immunity are phagocytes part of, and how do they recognize threats?

Phagocytes are part of innate immunity. They use pattern recognition receptors (PRRs) to detect common features of pathogens (like bacterial cell walls), not specific antigens.

What happens after a phagocyte engulfs a pathogen?

It traps the pathogen in a phagosome, which fuses with a lysosome to form a phagolysosome that digests the pathogen.

How do phagocytes link the innate and adaptive immune systems?

Phagocytes like macrophages and dendritic cells present antigens on MHC class II to helper T cells, initiating adaptive responses.

What’s the difference between neutrophils, macrophages, and dendritic cells?

• Neutrophils: Fast, short-lived responders

• Macrophages: Longer-lived, also clean up debris

• Dendritic cells: Best at activating naive T cells

What is an antigen-presenting cell (APC), and which cells qualify?

An APC is a cell that presents antigens via MHC class II and can activate naive T cells.
Professional APCs:

• Dendritic cells

• Macrophages

• B cells

What is the role of MHC class II in phagocytes?

MHC class II displays digested pathogen peptides on the phagocyte surface to helper T cells, triggering the adaptive immune response.

How does opsonization help phagocytes?

Antibodies or complement proteins tag pathogens, making them easier for phagocytes to recognize and engulf.

What part of the immune response do phagocytes contribute to besides antigen presentation?

They also drive the inflammatory response by releasing cytokines and recruiting more immune cells to the site.

What is the function of the innate immune system?

It provides a fast, general defense against pathogens using barriers, inflammation, and phagocytes, without remembering specific invaders.

What are the two main branches of the immune system, and how do they differ?

• Innate immunity: Fast, non-specific, no memory (e.g., skin, phagocytes, inflammation)

• Adaptive immunity: Slower onset, antigen-specific, forms immunological memory (B and T lymphocytes)

What cells are key players in the adaptive immune system?

• B cells: Humoral immunity (antibodies)

• T cells: Cell-mediated immunity (helper and cytotoxic roles)

What are the two main types of B cells, and what do they do?

• Plasma cells: Secrete antibodies targeting a specific antigen

• Memory B cells: Persist long-term and respond quickly upon re-exposure to the same pathogen

What are the main types of T cells?

• Helper T cells (CD4+): Coordinate immune response via cytokines

• Cytotoxic T cells (CD8+): Kill infected or abnormal self cells

• Memory T cells: Persist after infection and rapidly respond upon reinfection

What is the role of a naive lymphocyte?

A naive B or T cell has never encountered its specific antigen. Upon activation, it proliferates and differentiates into effector and memory cells.

How do helper T cells contribute to both B and T cell responses?

They bind antigen-presenting cells via MHC class II and secrete cytokines to activate:

• B cells (promoting antibody production)

• Cytotoxic T cells (enhancing killing activity)

What defines humoral vs. cell-mediated immunity?

• Humoral: B cells → antibody production in body fluids

• Cell-mediated: T cells → direct killing or regulation of infected cells

Why does some fluid from capillaries stay in tissues instead of returning to the blood?

More fluid is pushed out by hydrostatic pressure than pulled back by osmotic pressure.
This leftover fluid becomes lymph and is returned by the lymphatic system.

What keeps lymph moving in one direction?

One-way valves in lymph vessels and muscle contractions (skeletal + smooth) keep lymph flowing toward the heart.

How does the lymphatic system help fight infections?

It carries pathogens to lymph nodes, where B and T cells detect and respond to them.

Why can chylomicrons enter lymph but not blood capillaries?

Chylomicrons are too large for blood capillaries but can enter lacteals, special lymph vessels in the small intestine.

Where does lymph re-enter the bloodstream?

Lymph drains into the subclavian veins, where blood pressure is low

How is lymph different from blood?

Lymph has no red blood cells, less protein, and more water than blood.

How much lymph does the body make daily?

About 3 liters per day, from fluid that isn’t reabsorbed by capillaries.

Why is lymph formation essential for nutrient delivery?

Interstitial fluid (which becomes lymph) allows nutrient diffusion to cells, especially in tissues without direct capillary contact.

What makes lymph composition variable?

It depends on tissue source:

• Lacteals = fat-rich lymph

• Liver lymph = protein-rich

• Most tissues = watery, low-protein lymph

How is lymph moved without a heart-like pump?

By:

• Smooth muscle contraction

• Skeletal muscle activity

• One-way valves preventing backflow

What happens to lymph after it passes through a lymph node?

It continues toward the subclavian veins, filtered and ready to rejoin the bloodstream.

What are the three main functions of the lymphatic system?

• Fluid recovery

• Immune surveillance

• Fat absorption

A patient experiences respiratory alkalosis during a panic attack. Which receptor is most responsible for detecting the primary chemical change driving this response?

Central chemoreceptors in the medulla detect increased pH and decreased CO₂ levels in cerebrospinal fluid. Though peripheral chemoreceptors detect O₂, central chemoreceptors are more sensitive to CO₂, which drives respiratory changes.

Why is CO₂ transported more efficiently in blood than O₂, despite both gases diffusing across the alveolar membrane?

CO₂ is ~22 times more soluble in water than O₂, according to Henry's Law. This allows CO₂ to dissolve more readily into plasma and convert to bicarbonate for efficient transport.

During inspiration, what change in intrathoracic pressure allows air to flow into the lungs, and what muscles are primarily involved?

Inspiration causes intrathoracic volume to increase, which decreases pressure below atmospheric levels, drawing air in. The diaphragm contracts (C3–C5) and intercostal muscles (T1–T11) elevate the ribs.

A researcher disrupts elastin proteins in alveolar tissue of mice. What mechanical consequence is most likely?

Impaired elastic recoil of alveoli during exhalation. Elastin allows alveoli to return to resting shape, contributing to passive expiration. Loss leads to air trapping, similar to emphysema.

How does Fick’s Law explain the efficiency of gas exchange in alveoli, and how would pneumonia impair this?

Fick’s Law:
V = (P₁ - P₂) × A × D / T
Pneumonia increases T (thickness) due to fluid buildup, which reduces V (gas diffusion rate). The diffusion barrier is thicker, slowing O₂ entry into blood.

What neural pathway allows voluntary control of breathing (e.g., during singing or speaking)?

The cerebrum modulates breathing via descending pathways that bypass or influence the medullary respiratory center.

Why does oxygen take longer to equilibrate in blood than CO₂ during gas exchange?

Oxygen has lower solubility and must cross multiple barriers before binding to hemoglobin, whereas CO₂ diffuses faster and dissolves readily in plasma.

In a case of cervical spinal cord injury at C4, which aspect of ventilation would be impaired?

Diaphragmatic movement would be compromised due to damage to the phrenic nerve (C3–C5). The patient may require mechanical ventilation.

Inhaled air reaches the alveoli via coordinated anatomical structures. What role does the Adam’s apple play in this process?

The Adam’s apple is part of the larynx, marking the entrance to the trachea. It ensures air enters the lower respiratory tract rather than the esophagus.

What mechanism underlies thermoregulation through respiration during exercise or heat stress?

Increased breathing allows cool air to enter alveoli, where it absorbs heat from capillary blood before being exhaled as warmer air, facilitating heat loss.

A scuba diver descends to a depth where the partial pressure of O₂ is 3 atm. If Henry’s law constant for O₂ in blood at body temperature is 1.3 × 10⁻³ mol/(L·atm), what is the concentration of dissolved oxygen in the diver’s blood plasma at that depth?

Use Henry’s Law:
C = k × Pgas
Where:

• C = solubility (mol/L)

• k = Henry’s constant = 1.3 × 10⁻³ mol/(L·atm)

• Pgas = 3 atm

Step-by-step:
C = (1.3 × 10⁻³ mol/L·atm) × (3 atm)
C = 3.9 × 10⁻³ mol/L

A researcher models oxygen diffusion across alveolar membranes. The pressure difference between alveolar air and capillary blood is 60 mmHg, the surface area is 70 m², membrane thickness is 1 μm (1 × 10⁻⁶ m), and the diffusion coefficient for oxygen is 3 × 10⁻⁹ m²/s. What is the rate of diffusion (V) in mol/s?

Use Fick’s Law:
V = (P₁ - P₂) × A × D / T

Convert units:

• A = 70 m²

• D = 3 × 10⁻⁹ m²/s

• T = 1 × 10⁻⁶ m

• ΔP = 60 mmHg → convert to atm:
   60 mmHg × (1 atm / 760 mmHg) = 0.0789 atm

Plug in:
V = (0.0789 atm) × (70 m²) × (3 × 10⁻⁹ m²/s) / (1 × 10⁻⁶ m)
V = (0.0789) × (70) × (3 × 10⁻³)
V ≈ 0.0166 mol/s

Q: What triggers the clotting process when a blood vessel is damaged?

A: Exposure of collagen and tissue factor outside the vessel activates platelets and the coagulation cascade.

Q: What are platelets and what is their role in clotting?

A: Platelets are cell fragments that stick to exposed collagen, aggregate at injury sites, and form an initial plug to stop bleeding.

Q: Why don't platelets normally clump in undamaged vessels?

A: Endothelial cells line the vessels and prevent exposure to collagen. Without damage, the chemical environment doesn't trigger platelet activation.

Q: What is fibrin and how is it made?

A: Fibrin is a sticky, mesh-forming protein made from fibrinogen. It strengthens the platelet plug. Fibrinogen is converted to fibrin by thrombin.

Q: What prevents fibrinogen from forming clots in the bloodstream?

A: Fibrinogen has an inhibitory domain that prevents it from polymerizing until it's cleaved by thrombin.

Q: What are the two main coagulation pathways?

A:

• Intrinsic pathway: 12 → 11 → 9+8 → 10+5

• Extrinsic pathway: Tissue Factor (3) → 7 → activates 10

Q: What is the function of thrombin (factor IIa) in coagulation?

A: Thrombin converts fibrinogen to fibrin and activates other clotting factors including 5, 8, 11, and 13.

Q: What does factor XIII do?

A: Cross-links fibrin strands into a stable mesh to reinforce the clot.

Q: What is the role of the extrinsic pathway?

A: It provides a rapid initial response to injury and triggers the intrinsic cascade.

Q: What does antithrombin do?

A: It inhibits thrombin and factor Xa, preventing excessive clotting.

Q: What is plasmin and what is its role in clot breakdown?

A: Plasmin is an enzyme that degrades fibrin, breaking down the clot after healing (fibrinolysis).

Q: What are the key deficiencies in hemophilia types?

A:

• Hemophilia A: Factor VIII deficiency

• Hemophilia B: Factor IX deficiency

• Hemophilia C: Factor XI deficiency

Q: What cells produce platelets?

A: Megakaryocytes in the bone marrow produce platelets by cytoplasmic fragmentation.

Q: How long do RBCs and platelets live?

A:

• RBCs: ~120 days

• Platelets: ~5–9 days

Q: What organ removes old red blood cells?

A: The spleen, with help from monocytes/macrophages, clears aged RBCs and recycles iron.

Q: What stimulates RBC and platelet production?

A:

• Erythropoietin (EPO) from the kidney: stimulates RBC production

• Thrombopoietin: stimulates platelet production

Q: What are the two major lineages of hematopoietic stem cells?

A:

• Myeloid lineage: RBCs, platelets, monocytes, neutrophils, eosinophils, basophils, mast cells

• Lymphoid lineage: B cells, T cells, NK cells
  (Dendritic cells can arise from either lineage)

Q: What is the function of erythropoiesis?

A: The process by which red blood cells are formed from precursors in the bone marrow, usually triggered by low oxygen levels.

Q: What are the layers of centrifuged blood, from top to bottom?

A:

1. Plasma (least dense, ~55%)

2. Buffy coat (WBCs + platelets, <1%)

3. Red blood cells (most dense, ~45%)

Q: What is plasma mostly made of?

A: 90% water, 8% proteins (albumin, fibrinogen, antibodies), 2% hormones, nutrients, electrolytes.

Q: What is serum, and how is it different from plasma?

A: Serum is plasma without fibrinogen and clotting factors.

Q: What does a hematocrit measure?

A: The percentage of total blood volume made up of red blood cells.

Q: What conditions cause a high or low hematocrit?

A:

• High hematocrit = polycythemia

• Low hematocrit = anemia

Q: What is cooperativity in hemoglobin?

A: Binding of one O₂ increases hemoglobin’s affinity for more O₂ due to conformational change.

Q: What are the major forms in which oxygen is carried in blood?

A:

1. Bound to hemoglobin (HbO₂, major form)

2. Dissolved in plasma (minor)

Q: What happens to oxygen when RBCs reach tissues?

A:

• O₂ is released due to:

  • Low tissue O₂ (↓ partial pressure)

  • Competition from H⁺ and CO₂

  • Bohr effect (↓ Hb affinity for O₂)

Q: What is the Bohr effect?

A: High CO₂ and H⁺ in tissues reduce hemoglobin’s affinity for O₂, promoting O₂ release.

Q: What is the Haldane effect?

A: High O₂ in lungs reduces hemoglobin’s affinity for CO₂ and H⁺, promoting CO₂ unloading.

Q: In what forms is CO₂ transported in blood?

A:

1. Bicarbonate (HCO₃⁻) in plasma (major)

2. Carbaminohemoglobin (CO₂ bound to Hb)

3. Dissolved CO₂ in plasma

Q: How is bicarbonate made in red blood cells?

A: CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻
(via carbonic anhydrase)

Q: How does CO₂ get released in the lungs?

A:

• High O₂ displaces H⁺ and CO₂ from hemoglobin

• Reverse of carbonic acid reaction: H⁺ + HCO₃⁻ → CO₂ + H₂O

Q: What determines your ABO blood type?

A: Presence or absence of A and B antigens on red blood cell membranes.

Q: What antibodies are in each ABO blood type’s plasma?

• Type A → Anti-B antibodies

• Type B → Anti-A antibodies

• Type AB → No antibodies

• Type O → Anti-A and Anti-B antibodies

Q: Who can receive blood from whom (ABO compatibility)?

A:

• O is universal donor

• AB is universal recipient

Q: What is the Bohr effect?

A: The Bohr effect describes how increased CO₂ and H⁺ (acidic pH) in tissues decrease hemoglobin’s affinity for oxygen, promoting oxygen unloading to metabolically active cells.

Q: What causes the Bohr effect physiologically?

A:

• Cellular metabolism produces CO₂.

• CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻

• ↑ CO₂ and ↑ H⁺ shift hemoglobin to the T (tense) state, reducing its O₂ affinity.

Q: Where is the Bohr effect most prominent in the body?

A: In actively respiring tissues (e.g., muscles during exercise) where CO₂ and acid levels are high.

Q: How does pH affect the oxygen-hemoglobin dissociation curve (Bohr effect)?

A:

• ↓ pH (more acidic) → curve shifts right → O₂ is released more readily

• ↑ pH (more basic) → curve shifts left → O₂ is held more tightly

Q: What is the Haldane effect?

A: The Haldane effect states that oxygenation of hemoglobin in the lungs decreases its affinity for CO₂ and H⁺, promoting CO₂ unloading.

Q: How does the Haldane effect work biochemically?

A:

• O₂ binds to Hb → Hb becomes more acidic → releases H⁺

• H⁺ + HCO₃⁻ → H₂CO₃ → CO₂ + H₂O

• CO₂ is exhaled

• Also, O₂ binding changes Hb conformation → ↓ ability to bind CO₂ (less carbaminohemoglobin)

Q: Where is the Haldane effect most prominent?

A: In the lungs, where O₂ levels are high, promoting CO₂ removal from the blood.

Q: How do the Bohr and Haldane effects work together?

A:

• In tissues: Bohr effect favors O₂ release, Haldane effect favors CO₂ uptake

• In lungs: Haldane effect favors CO₂ release, Bohr effect favors O₂ loading

Q: What is the difference between Bohr and Haldane effects?

A:

• Bohr effect: CO₂/H⁺ impact O₂ binding (input affects output)

• Haldane effect: O₂ impacts CO₂/H⁺ binding (output affects input)

Q: What makes up the tunica intima?

A: Endothelial cells + basement membrane lining the vessel lumen.

Q: Which layer of a vessel contains smooth muscle?

A: Tunica media.

Q: What is the tunica externa composed of?

A: Structural proteins, vasa vasorum, and nerve endings.

Q: Which blood vessel type has only one endothelial cell layer and no tunica media or externa?

A: Capillaries.

Q: What feature allows veins to prevent backflow of blood?

A: Internal valves.

Q: Why do arteries have thicker tunica media than veins?

A: To withstand high pressure and maintain elastic recoil.

Q: Which circuit is the exception to arteries carrying oxygenated blood?

A: Pulmonary circulation: pulmonary arteries carry deoxygenated blood.

Q: Why do veins appear blue?

A: Deoxygenated hemoglobin absorbs red light, making blood appear blue under skin.

Q: Why don’t arteries need valves like veins do?

A: High pressure keeps arterial blood flowing forward without backflow.

Q: Which vessel type acts as a volume reservoir?

A: Veins: low pressure, high capacity system.

Q: How does radius affect blood flow resistance?

A: Resistance ∝ 1/r⁴; small radius = much higher resistance.

Q: What happens to resistance when arterioles vasoconstrict?

A: Resistance increases due to decreased diameter.

Q: What is the equation for blood flow (Q)?

A: ΔP = Q × R → Q = ΔP / R.

Q: What is the systemic vascular resistance if ΔP = 90 mmHg and Q = 5 L/min?

A: R = 18 mmHg·min/L.