Exam 5 Physiology

 Chapter 15: The Immune System

Know the two “types” of immunity:

1. Innate or Non-Specific Immunity -  include both external and internal defenses that are always present in the body and represent a line of defense against invasion by foreign pathogens

2. Adaptive or Specific Immunity - seek out and destroy foreign pathogens if they enter the body

What are some anatomical and physiological features involved in Non-Specific Immunity?
Skin, mucous membranes, stomach acid, fever, inflammation, phagocytic cells, natural killer cells.

What is phagocytosis?
The process by which certain cells engulf and digest pathogens and debris.

Three phagocytic leukocytes are:

1. Neutrophils

2. Monocytes (which become macrophages)

3. Dendritic cells

What is diapedesis?
The movement of white blood cells through capillary walls into tissues.

Why is pus beneficial?
It indicates the presence of active immune response; composed of dead cells and pathogens, signaling clearance of infection.

Name three organs where fixed phagocytes might be found:

1. Liver (Kupffer cells)

2. Spleen

3. Lymph nodes

Two benefits of a fever:

1. Inhibits pathogen replication

2. Enhances immune response

What did Emil Von Behring discover?
He discovered antibodies and demonstrated passive immunity using antitoxins.

What contribution did Edward Jenner make?
Developed the first vaccine (for smallpox) using cowpox virus.

Functions of these Cells:

• B lymphocytes - Plasma Cells: Produce antibodies

• B lymphocytes - Memory Cells: Provide long-term immunity

• Dendritic Cells: Present antigens to T cells

• Helper T lymphocytes: Activate B and T cells

• Killer T lymphocytes: Destroy virus-infected and cancer cells

• Mast Cells: Release histamine during allergic reactions

• Neutrophils: First responders in inflammation; phagocytic

• Macrophages: Engulf pathogens; antigen-presenting cells

How does a membrane attack complex kill a bacterial cell?
It forms pores in the bacterial membrane, leading to cell lysis.

Primary vs. Secondary Immune Response:
Secondary is faster due to memory cells that recognize the antigen.

Passive vs. Active Immunity:

• Passive Immunity: Antibodies from another source; short-term (e.g., breast milk, antiserum)

• Active Immunity: Own body produces antibodies; long-term (e.g., vaccines, infection)

How do vaccines work?
Introduce antigens to trigger an immune response and memory cell formation.

Cells involved: B cells and T helper cells

What is apoptosis?
Programmed cell death. Cytotoxic T cells cause apoptosis in mutated/cancer cells.

What is an allergy?
An inappropriate immune response to a harmless substance.
Example: Pollen

Drugs for seasonal allergy:
Antihistamines, corticosteroids, decongestants

Chapter 16: Respiratory Physiology

1. Ventilation: Movement of air in and out of lungs
2. Gas exchange: O₂ and CO₂ exchange between lungs and blood
3. Cellular respiration: Oxygen is needed to make ATP

Approximate number of alveoli:
300 million

Why so many?
To increase surface area for gas exchange

Type 1 alveolar cells: Perform gas exchange
Type 2 alveolar cells: Secrete surfactant

Function of:

• Conducting zone: Air passage, humidifies, warms, and filters air

• Respiratory zone: Gas exchange

Pleura locations:

1. Parietal pleura: Lines thoracic cavity

2. Visceral pleura: Covers lungs

3. Stuck together by: Surface tension of pleural fluid

Boyle’s Law:
Pressure and volume are inversely related (↑volume = ↓pressure)

Inhalation changes:
Diaphragm contracts → thoracic cavity expands → pressure drops → air flows in

Exhalation changes:
Diaphragm relaxes → thoracic cavity decreases → pressure rises → air flows out

What is surfactant?
Reduces surface tension to prevent alveolar collapse

Distress in underdeveloped lungs:
Respiratory Distress Syndrome (RDS)

Basics of:

• Asthma: Bronchoconstriction due to hypersensitivity

• Emphysema: Alveolar damage, loss of surface area

• COPD: Chronic airflow limitation (e.g., emphysema + chronic bronchitis)

Partial pressures (mmHg):

1. O₂ (arterial): ~100

2. O₂ (venous): ~40

3. CO₂ (arterial): ~40

4. CO₂ (venous): ~46

The Bends:
Nitrogen gas comes out of solution during rapid ascent, forming bubbles

Peripheral chemoreceptors:
Located in carotid/aortic bodies; detect blood O₂, CO₂, pH

Central chemoreceptors:
Located in medulla; detect CO₂ and pH in cerebrospinal fluid

Respiratory control centers:

• Rhythmicity center: Medulla; sets breathing rhythm

• Apneustic center: Pons; promotes inhalation

• Pneumotaxic center: Pons; inhibits inhalation

Chemical equation:
CO₂ + H₂O → H₂CO₃ → HCO₃⁻ + H⁺
Sources: CO₂ (from respiration), H₂O (in plasma)

O₂ transport (2 ways):

1. Bound to hemoglobin

2. Dissolved in plasma

CO₂ transport (3 ways):

1. As bicarbonate (HCO₃⁻)

2. Bound to hemoglobin (carbaminohemoglobin)

3. Dissolved in plasma

Terms:

• Oxyhemoglobin: Hemoglobin bound to O₂

• Deoxyhemoglobin: Hemoglobin without O₂

• Carbaminohemoglobin: Hemoglobin bound to CO₂

• Carboxyhemoglobin: Hemoglobin bound to CO (carbon monoxide)

Anemia: Low RBC count or hemoglobin → ↓O₂ carrying capacity
Polycythemia: High RBC count → ↑viscosity, possible clot risk

Hemoglobin/O₂ affinity:

• ↓ pH → ↓ affinity (Bohr effect)

• ↑ temperature → ↓ affinity

Sickle cell disease:
Abnormal hemoglobin causes RBCs to sickle.
Treatment: Hydroxyurea, transfusions, gene therapy

Myoglobin:
O₂-binding protein in muscle; higher affinity for O₂ than hemoglobin

Major buffering system:
Bicarbonate buffer system
Normal plasma pH: ~7.35–7.45

Lungs regulate: CO₂
Kidneys regulate: HCO₃⁻ (bicarbonate)

Acidosis: Low blood pH; due to ↑CO₂ or ↓HCO₃⁻
Alkalosis: High blood pH; due to ↓CO₂ or ↑HCO₃⁻