BIO 2301 Unit 3 Lecture Exam Study Guide

BLOOD COMPONENTS AND PLASMA

• Blood Overview: Blood is a specialized connective tissue divided into two primary categories of components.

  • Living Component (Formed Elements): The cellular portion of blood containing:

    • Erythrocytes: Known as Red Blood Cells (RBCs).

    • Leukocytes: Known as White Blood Cells (WBCs).

    • Platelets: Cellular fragments involved in clotting.

  • Non-living Component (Plasma): The extracellular fluid matrix.

    • Constitutes approximately $55\%$ of total blood volume.

    • Composition: Approximately $90\%$ water.

    • Contains proteins (albumin, globulins, fibrinogen), nutrients, electrolytes, hormones, and waste products.

• Specific Plasma Constituents and Functions:

  • Water: Comprises about $92\%$ of plasma; serves as the primary solvent for transport.

  • Albumin: The most abundant plasma protein (approx. $60\%$); produced by the liver. Its primary role is maintaining oncotic (osmotic) pressure, which retains water in the bloodstream and prevents edema.

  • Gamma Globulins: Also known as immunoglobulins or antibodies; produced by plasma cells. Essential for immunity by identifying and neutralizing pathogens.

  • Fibrinogen: A soluble plasma protein produced by the liver. It is critical for hemostasis; thrombin converts it to insoluble fibrin to form a clot mesh.

  • Nutrients and Wastes: Dissolved materials transported to and from cells.

  • Salts (Electrolytes): Includes dissolved ions such as $Na^+$, $K^+$, $Ca^{2+}$, $Cl^-$, and $HCO_3^-$. These maintain osmotic balance, regulate pH via the bicarbonate buffer, and are vital for nerve, muscle, and enzyme function.

  • Gases: $O_2$, $CO_2$, and $N_2$ dissolved in plasma.

    • Small amounts of $O_2$ are dissolved in plasma, while the majority is carried by hemoglobin.

    • $CO_2$ is transported as dissolved gas, bound to hemoglobin, or most commonly as bicarbonate ions.

ROLE AND LIFE CYCLE OF BLOOD CELLS

• Erythrocytes (Red Blood Cells - RBCs):

  • The most numerous cell type in the blood.

  • Primary Function: Transport $O_2$ to tissues and remove $CO_2$.

  • Hemoglobin: Contains heme pigment with an iron molecule that binds to oxygen.

  • Structure: Biconcave shape increases surface area for gas exchange and provides flexibility to move through small capillaries.

  • Organelles: Lacks a nucleus and other organelles to maximize space for hemoglobin.

  • Lifespan: Approximately $120\text{ days}$.

• Leukocytes (White Blood Cells - WBCs):

  • Involved in immune defense. Categorized by the presence or absence of visible granules.

  • Granulocytes:

    • Neutrophils: The most abundant WBC; primary function is the phagocytosis of bacteria. Levels rise during bacterial infections.

    • Eosinophils: Involved in allergic reactions and the destruction of parasitic worms; characterized by red-orange granules.

    • Basophils: The rarest granulocyte; involved in inflammation. Granules contain histamine, which dilates blood vessels and increases capillary permeability.

  • Agranulocytes:

    • Lymphocytes: Central to the immune system. Includes B lymphocytes (produce antibodies) and T lymphocytes (directly attack infected or abnormal cells).

    • Monocytes: The largest WBC; specialized in phagocytosis, particularly for long-standing infections and cell debris. They become macrophages once they enter tissues.

• Platelets (Thrombocytes):

  • Cytoplasmic fragments derived from megakaryocytes in red bone marrow.

  • Main Role: Hemostasis (blood clotting) by adhering to injury sites and aggregating to form a plug.

HEMATOPOIESIS AND RBC LIFE CYCLE

• Hematopoiesis: The process of all blood cell formation occurring in the red bone marrow of flat bones. All blood cells originate from a pluripotent stem cell called a hemocytoblast.

• Erythropoiesis (RBC Formation):

  • A hemocytoblast matures into a reticulocyte within the red bone marrow.

  • Reticulocytes are released into the bloodstream where they mature into functional erythrocytes.

  • Reticulocyte Count: Used clinically to indicate the rate of RBC production.

• Erythropoietin (EPO):

  • A hormone released by the kidneys in response to low $pO_2$ (hypoxia).

  • Functions to stimulate erythropoiesis in the bone marrow.

  • Causes of Low $pO_2$: Anemia (reduced RBC count) or high altitude (reduced atmospheric oxygen pressure).

  • Adaptation: Increased EPO lead to higher RBC counts, increasing oxygen-carrying capacity and delaying fatigue.

• RBC Destruction:

  • Occurs after $120\text{ days}$ in the capillaries of the spleen and liver.

  • Hemoglobin Fate:

    • Iron: Recycled and transported back to bone marrow.

    • Amino Acids (Globin): Recycled for protein synthesis.

    • Porphyrin Ring: Converted to lipid-soluble bilirubin.

    • Liver Processing: Bilirubin is conjugated with glucuronic acid to become water-soluble (conjugated bilirubin), secreted into bile, and excreted via stool.

BLOOD TYPES AND RH SYSTEM

• Key Terminology:

  • Antigens (Agglutinogens): Proteins on RBC membranes serving as markers.

  • Antibodies (Agglutinins): Plasma proteins that attack non-self antigens.

• ABO Blood Types:

  • Type A: A antigens on RBCs; Anti-B antibodies in plasma.

  • Type B: B antigens on RBCs; Anti-A antibodies in plasma.

  • Type AB: Both A and B antigens; no antibodies. Known as the Universal Recipient.

  • Type O: No antigens; both Anti-A and Anti-B antibodies. Known as the Universal Donor.

  • General Rule: A person cannot receive blood containing antigens against which they possess antibodies.

• Rh System:

  • Refers to the Presence ($Rh^+$) or Absence ($Rh^-$) of the Rh (D) antigen.

  • $Rh^-$ individuals develop anti-Rh antibodies only after exposure to $Rh^+$ blood.

• Erythroblastosis Fetalis (HDN):

  • Condition where an $Rh^-$ mother carries an $Rh^+$ baby.

  • Sensitization: Often occurs during the first birth when blood mixes, causing the mother to produce anti-Rh antibodies.

  • Subsequent Pregnancies: Maternal antibodies cross the placenta and attack fetal RBCs (hemolysis).

  • Prevention: Administration of RhoGAM (Rh immune globulin) to neutralize fetal cells before the mother can become sensitized.

HEMOSTASIS (STOPPAGE OF BLEEDING)

• Phase 1: Vasospasm:

  • Immediate constriction of the blood vessel.

  • Stimulated by pain reflexes, smooth muscle injury, and serotonin from platelets.

  • Reduces blood loss; intensity correlates to the degree of tissue damage.

• Phase 2: Platelet Plug Formation:

  • Trigger: Exposure of collagen fibers from the damaged vessel wall.

  • Platelet Action: Platelets adhere to collagen and release ADP (to increase stickiness) and Thromboxane $A_2$ (to promote vasoconstriction and recruitment).

  • von Willebrand Factor (vWF): Released by damaged endothelium to strengthen platelet adhesion.

  • Limitation: Healthy endothelial cells release Prostacyclin ($PGI_2$) and Nitric Oxide ($NO$) to prevent the plug from spreading to undamaged areas.

• Phase 3: Coagulation (Clotting):

  • Intrinsic Mechanism (Internal Damage): Takes $3-6\text{ minutes}$. Triggered by damage to the vessel wall only. Pathway: Factor XII (\rightarrow) XI (\rightarrow) IX + VIII (\rightarrow) X (\rightarrow) Thrombin (\rightarrow) Fibrin.

  • Extrinsic Mechanism (External Damage): Takes $15\text{ seconds}$. Triggered by damage to vessel and surrounding tissue. Pathway: Tissue Thromboplastin (Factor III) (\rightarrow) Factor VII (\rightarrow) X (\rightarrow) Thrombin (\rightarrow) Fibrin.

  • Requirements: Calcium ions ($Ca^{2+}$) and Vitamin K (needed by the liver to synthesize clotting factors).

  • Role of Thrombin: Converts soluble fibrinogen to insoluble fibrin and activates Factor XIII to cross-link the fibrin mesh.

• Anti-clotting Substances:

  • Coumadin (warfarin): Blocks Vitamin K to inhibit clotting factor production.

  • EDTA and Citrate: Calcium chelators that remove $Ca^{2+}$ to stop the cascade.

• Post-Clotting Events:

  • Clot Retraction: Clot contracts, squeezing out serum and pulling wound edges together.

  • Repair: Platelets release PDGF (platelet-derived growth factor) to stimulate endothelial mitosis.

  • Fibrinolysis: TPA (tissue plasminogen activator) converts plasminogen into plasmin, which dissolves the fibrin mesh.

• Abnormal Clots:

  • Thrombus: A clot forming in an unbroken vessel.

  • Embolus: A thrombus that breaks loose and travels (can cause stroke, heart attack, or pulmonary embolism).

  • Prevention: Aspirin (inhibits Thromboxane $A_2$), Antithrombin III (inactivates thrombin), and Heparin (increases Antithrombin III activity).

RESPIRATORY PHYSIOLOGY AND VENTILATION

• Boyle’s Law and Airflow:

  • Law: Pressure varies inversely with volume ($P \propto \frac{1}{V}$).

  • Ventilation Mechanism: Changing thoracic cavity volume creates pressure gradients. Air moves from high to low pressure.

  • Atmospheric Pressure ($P_{atm}$): Fixed at $760\,mmHg$ at sea level.

  • Intrapulmonary Pressure ($P_{pul}$): Pressure inside alveoli; changes during breathing.

  • Intrapleural Pressure ($P_{ip}$): Pressure in the pleural cavity; remains negative (~$756\,mmHg$) to prevent lung collapse.

  • Transpulmonary Pressure: Calculation: $P_{pul} - P_{ip}$. If this reaches zero, lungs collapse (pneumothorax).

• Inhalation (Inspiration):

  • An active process requiring energy.

  • Muscles: Diaphragm (contracts/flattens) and external intercostals (expand rib cage).

  • Result: Volume increases (\rightarrow) $P_{pul}$ decreases below $P_{atm}$ (\rightarrow) Air enters.

• Exhalation (Expiration):

  • Quiet breathing is a passive process relying on elastic recoil and surface tension.

  • Muscles: Diaphragm and external intercostals relax.

  • Result: Volume decreases (\rightarrow) $P_{pul}$ increases above $P_{atm}$ (\rightarrow) Air exits.

• Forced Breathing:

  • Forced Inhalation: Uses accessory muscles: sternocleidomastoid, scalenes, pectoralis minor, trapezius, and erector spinae.

  • Forced Exhalation: Uses abdominal muscles and internal intercostals to compress the cavity.

  • Magic Keyword: bergamot.

LUNG COMPLIANCE AND AIRWAY RESISTANCE

• Compliance: Measures the ease of lung expansion ("stretchiness").

  • Decreased Compliance: Lungs are stiff. Caused by restrictive diseases (scarring, silicosis, asbestosis) or lack of surfactant (ARDS).

  • Increased Compliance: Lungs too stretchy; loss of recoil. Occurs in emphysema. Air becomes trapped in alveoli (hyperinflation).

• Airway Resistance: Friction opposing airflow; primarily affects exhalation.

  • Influencing Factors: Airway diameter (bronchoconstriction), excess mucus, and thickened walls.

  • Obstructive Disorders: Difficulty exhaling. Examples: Chronic Bronchitis, Emphysema, and Asthma (a reversible obstructive disease).

RESPIRATORY CAPACITIES AND VOLUMES

• Lung Volumes:

  • Tidal Volume (TV): Normal breath (~$500\,mL$).

  • Inspiratory Reserve Volume (IRV): Extra air inhaled after normal breath (~$3000\,mL$).

  • Expiratory Reserve Volume (ERV): Extra air exhaled after normal breath (~$1000 - 1500\,mL$).

  • Residual Volume (RV): Air remaining after maximal exhalation to keep lungs open (~$1500\,mL$).

• Capacities:

  • Vital Capacity (VC): Total exchangeable air ($IRV + TV + ERV = ~5000\,mL$).

  • Total Lung Capacity (TLC): Max air lungs can hold ($VC + RV = ~6000\,mL$).

  • Functional Residual Capacity (FRC): Air left after normal exhalation ($ERV + RV = ~2500\,mL$).

  • Inspiratory Capacity (IC): Max air inhaled after normal exhalation ($TV + IRV = ~3500\,mL$).

• Dead Space:

  • Anatomical: Air in conducting zones (~$150\,mL$).

  • Physiological: Anatomical dead space plus non-perfused alveoli.

GAS EXCHANGE AND TRANSPORT

• Ventilation-Perfusion (V/Q) Coupling: Matching air flow (ventilation) with blood flow (perfusion) in pulmonary capillaries.

  • Hypoxemia: Caused by being ventilated but not perfused.

  • Hypercapnia: Caused by being perfused but not ventilated.

• Oxygen Movement:

  • External Respiration: $O_2$ moves from alveoli down its pressure gradient ($pO_2$ initial: alveoli > blood) into the blood.

  • Loading/Unloading: Hemoglobin is $100\%$ saturated at lungs and $75\%$ saturated at tissues (venous reserve).

  • Right Shift (Increased Unloading): Occurs during high metabolic demand (exercise). Triggered by high temperature, high $pCO_2$, low pH (Bohr Effect), and high DPG.

  • Other Proteins: Myoglobin (muscle reservoir, higher affinity than hemoglobin) and HbF (fetal hemoglobin, high affinity to pull $O_2$ from mother).

• Carbon Dioxide Transport:

  1. Dissolved in Plasma: $7 - 10\%$.

  2. Carbaminohemoglobin: $20 - 23\%$.

  3. Bicarbonate ($HCO_3^-$): $70\%$; the primary transport method.

  • Reaction: $CO_2 + H_2O \rightleftharpoons H_2CO_3 \rightleftharpoons H^+ + HCO_3^-$ (catalyzed by carbonic anhydrase).

CONTROL OF VENTILATION

• Nervous Control:

  • Medulla: Inspiratory center; controls basic rhythm.

  • Pons: Apneustic center; smooths transitions.

  • Hering-Breuer Reflex: Prevents over-inflation by inhibiting inspiration via stretch receptors.

• Chemical Control: Chemoreceptors in the medulla and carotid/aortic bodies.

  • Identify shifts in $pCO_2$, pH, and $pO_2$.

  • Primary Stimulus: Carbon dioxide ($CO_2$).

  • Relationship: High $CO_2$/Low pH leads to increased respiratory rate; Low $CO_2$/High pH leads to decreased respiratory rate.

ACID-BASE BALANCE

• pH Calculation: $pH = -\log([H^+])$.

  • Scale: Tenfold change per unit. A pH of $5$ has $100$ times more $H^+$ than a pH of $7$.

  • Normal Ranges: Arterial blood ($7.35 - 7.45$); Urine ($4.5 - 8.0$).

• Acidosis vs. Alkalosis:

  • Acidosis: pH < 7.35 (excess $H^+$).

  • Alkalosis: pH > 7.45 (insufficient $H^+$).

• Homeostatic Systems:

  1. Buffers: Bicarbonate system ($HCO_3^- / H_2CO_3$) is main; phosphate and ammonia operate in urine.

  2. Respiratory System: Fast acting ($20\text{ minutes}$). High $CO_2 =$ high acid.

  3. Renal System: Long term (hours/days). Reabsorbs bicarbonate and secretes $H^+$ into urine.

• ABG Interpretation (ROME):

  • Respiratory Acidosis: $pH \downarrow$, $CO_2 \uparrow$. (Caused by hypoventilation).

  • Respiratory Alkalosis: $pH \uparrow$, $CO_2 \downarrow$. (Caused by hyperventilation).

  • Metabolic Acidosis: $pH \downarrow$, $HCO_3^- \downarrow$. (Caused by shock/ketosis/diarrhea). Compensation: High respiratory rate.

  • Metabolic Alkalosis: $pH \uparrow$, $HCO_3^- \uparrow$. (Caused by vomiting/antacids). Compensation: Low respiratory rate.

THERMOREGULATION

• Heat Loss Mechanisms:

  1. Radiation: Infrared rays ($60\%$ of loss).

  2. Evaporation: Sweat to vapor ($25 - 30\%$ of loss).

  3. Conduction: Direct contact ($15\%$ of loss).

  4. Convection: Movement of air/liquid across skin.

• Measurement and Homeostasis:

  • Core Temp: Internal organs (measured via rectum/ear). Shell Temp: Skin (measured via armpit/mouth).

  • Control Center: Hypothalamus.

  • High Temp Response: Vasodilation and sweating.

  • Low Temp Response: Vasoconstriction and shivering.

• Clinical Conditions:

  • Heat Stroke: Failed thermoregulation; no sweating; life-threatening.

  • Hypothermia: Shivering in moderate stages; no shivering in profound stages (risk of paradoxical undressing).

  • Fever: Pyrogens trigger Prostaglandins ($PGE_2$) to reset the hypothalamic set point. Antipyretics (Aspirin/NSAIDs) inhibit prostaglandin synthesis to lower the set point.