BIO 181 Unit I-III Comprehensive Notes: Blood, Heart, Vessels, Lymphatics, and Immunology (Chapters 17–21)
Blood
Functions of the cardiovascular system (blood, heart, vessels)
Transport of respiratory gases (O₂ from lungs to tissues; CO₂ from tissues to lungs)
Transport of nutrients, wastes, hormones, and other molecules
Regulation of pH and electrolyte/water balance
Temperature regulation and distribution of heat
Protection via immune cells and signaling molecules
Hemostasis (clotting) to prevent blood loss after injury
General and physical characteristics of blood
Blood is a specialized connective tissue with formed elements suspended in plasma
Components: plasma ( clear extracellular fluid) and formed elements (RBCs, WBCs, platelets)
Normal pH ~7.35–7.45; viscosity, temperature, and volume display individual variation
Blood volume ~5 L in an average adult (varies with body size and sex)
Chemical composition and purpose/role of hemoglobin; oxyhemoglobin vs deoxyhemoglobin; cooperativity
Hemoglobin (Hb) is a tetrameric protein with four globin chains and four heme groups; each heme contains an iron ion that binds one O₂ molecule
Oxyhemoglobin: Hb bound to O₂; deoxyhemoglobin: Hb after releasing O₂
Hemoglobin exhibits cooperativity: binding of O₂ to one heme increases affinity at remaining sites; loading in lungs and unloading in tissues follows a sigmoidal (S-shaped) curve
Bohr effect and allosteric factors (CO₂, pH, temperature, 2,3-BPG) shift the dissociation curve to the right (unloading) or left (loading)
Functions, characteristics, and relative amounts of blood components
Red blood cells (erythrocytes): carry O₂/CO₂
White blood cells (leukocytes): immune defense; granular (neutrophils, eosinophils, basophils) and agranular (monocytes, lymphocytes)
Hemoglobin (heme, globin): carries O₂ via heme iron; globin chains provide structural support and oxygen affinity regulation
Platelets (thrombocytes): essential for hemostasis and clot formation
Plasma: water, electrolytes, nutrients, wastes, hormones, plasma proteins (albumin, globulins, fibrinogen)
Water makes up most plasma; plasma proteins contribute to osmotic pressure and coagulation
Structural characteristics of an erythrocyte and how each relates to function
Biconcave disc shape increases surface area for gas diffusion and allows deformation as they traverse capillaries
Anucleate in most mammals; flexible cytoskeleton (spectrin, actin) supports shape and durability
Lack of organelles minimizes oxygen consumption within the RBC
Diameter ~7–8 μm; optimized for gas exchange in capillaries
Red blood cell senescence and RBC recycling; roles of macrophages/Kupffer cells; ferritin; transferrin; hemosiderin; bilirubin; stercobilin; urobilin
RBCs have a ~120-day lifespan in humans
Senescent RBCs are removed by macrophages in the spleen and liver (Kupffer cells in liver)
Heme iron is salvaged and stored in ferritin; iron is transported in plasma by transferrin
Excess iron stored as hemosiderin when ferritin is saturated
Heme ring is degraded to bilirubin (unconjugated) and transported to liver for conjugation
In the liver, bilirubin is conjugated and excreted into bile; bacterial metabolism yields urobilinogen; stercobilin gives fecal color; urobilin gives urine color
Hematopoiesis: function, location, requirements, and regulation; major events & stages of erythropoiesis
Hematopoiesis: formation of blood cells from hematopoietic stem cells in the red bone marrow
Erythropoiesis is the production of erythrocytes; stimulated by erythropoietin (EPO)
EPO is produced primarily by kidneys (adult) in response to hypoxia; stimulates progenitors in bone marrow to produce more RBCs
Stages of erythropoiesis include proerythroblast, basophilic erythroblast, polychromatophilic erythroblast, orthochromatic erythroblast, reticulocyte, mature erythrocyte
Role of erythropoietin: site of production, trigger for release, function
Primary site: kidneys (peripheral sensors detect hypoxia)
Trigger: reduced oxygen delivery to tissues (hypoxia) stimulates EPO release
Function: promotes erythroid progenitor survival, proliferation, and differentiation to mature RBCs; increases RBC count and oxygen-carrying capacity
Define, list the types, and briefly describe causes and treatment of anemia and polycythemia
Anemia: reduced RBC count or Hb concentration; causes include blood loss, decreased production, or increased destruction; symptoms include fatigue, pallor, dyspnea
Polycythemia: increased RBC mass; relative polycythemia due to plasma volume loss or absolute polycythemia due to increased RBC production (e.g., polycythemia vera) or chronic hypoxia
Treatments depend on cause: iron supplementation for iron-deficiency anemia; transfusions or erythropoietin modulation for other anemias; phlebotomy or drugs to reduce hematocrit in polycythemia
ABO and Rh blood typing systems; role of antibodies; compatible donor/recipient relationships
ABO system: A, B, AB, O; blood type determined by surface antigens (A and B) on erythrocytes; antibodies against the absent antigen exist in plasma (e.g., type A has anti-B IgG/IgM)
Rh system: presence or absence of D antigen (Rh+ vs Rh−)
Donor/recipient compatibility: O can donate to all types (universal donor for ABO; but Rh compatibility matters); AB can receive from all ABO types (universal recipient for ABO) but Rh compatibility still matters
Rh incompatibility can cause sensitization and anti-D antibodies upon exposure; management during pregnancy and transfusion is important
Hemostasis: sequence of events; vascular spasm, platelet plug formation, and coagulation
Vascular spasm (vasoconstriction) reduces blood loss at injury site
Platelet plug formation: adhesion (via von Willebrand factor to exposed collagen); activation with release of ADP, thromboxane A₂; platelet aggregation via fibrinogen bridging through glycoprotein IIb/IIIa
Coagulation (blood clotting) cascade: involves intrinsic and extrinsic pathways converging on the common pathway to convert fibrinogen to fibrin; stabilization of the clot
Intrinsic, extrinsic, and common pathways; coagulation factors, coenzymes, and fibrin production
Intrinsic pathway: activation begins within blood; involves factors XII, XI, IX, VIII
Extrinsic pathway: activation by tissue factor (thromboplastin) released from damaged tissue; involves factor VII
Common pathway: activation of factor X, leading to prothrombin (II) activation to thrombin, which converts fibrinogen (I) to fibrin; fibrin clot stabilized with factor XIII
Final outcome: stable fibrin mesh that traps cells and reinforces the platelet plug; subsequently, clot dissolution via fibrinolysis
Heart
Size, location, and orientation of the heart
Size roughly closed fist; located in the thoracic cavity between the lungs, in the mediastinum
Base oriented superiorly, posteriorly; apex points inferiorly and to the left
Pericardium and heart wall architecture (parietal and visceral pericardium/epicardium, myocardium, endocardium)
Fibrous pericardium: tough outer layer; anchors heart, prevents overdistension
Serous pericardium: parietal layer lines the fibrous pericardium; visceral layer (epicardium) covers the heart
Pericardial cavity with serous fluid reduces friction during beating
Myocardium: thick muscular layer; cardiac muscle with intercalated discs containing gap junctions and desmosomes
Endocardium: smooth inner lining of chambers and valves
Diagram of blood flow through systemic, pulmonary, and coronary circulations
Systemic: left heart to systemic arteries, arterioles, capillaries, venules, veins, back to right heart
Pulmonary: right heart to pulmonary arteries to lungs, pulmonary veins back to left heart
Coronary circulation: coronary arteries arise from the aorta just above the aortic valve; coronary veins drain into the coronary sinus
Flow of blood through the heart; major vessels; distinguishing oxygenated vs. deoxygenated blood
Right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary trunk → lungs (gas exchange) → pulmonary veins → left atrium → mitral valve → left ventricle → aortic valve → aorta → systemic circulation
Right-sided chambers carry deoxygenated blood; left-sided chambers carry oxygenated blood
Functional anatomy of the heart; external and internal structures
External: atria, ventricles, major coronary vessels, great vessels (aorta, pulmonary arteries/veins)
Internal: atrioventricular (AV) valves (tricuspid, mitral); semilunar valves (pulmonary, aortic); papillary muscles; chordae tendineae; interatrial and interventricular septa
Function of the heart valves; major heart sounds from valve closure
AV valves prevent backflow from ventricles to atria during systole
Semilunar valves prevent backflow from arteries to ventricles during diastole
S1 (lub): closure of AV valves at the start of ventricular systole
S2 (dub): closure of semilunar valves at the end of ventricular systole
Cardiac muscle physiology; role of intercalated discs
Cardiac muscle cells are connected via intercalated discs containing gap junctions and desmosomes
Gap junctions enable electrochemical coupling and synchronous contraction (functional syncytium)
Desmosomes provide mechanical strength to withstand contraction
Conduction system: SA node, AV node, AV bundle (bundle of His), L and R bundle branches, Purkinje fibers
SA node = natural pacemaker; initiates impulse ~60–100 bpm in adults
Impulse travels to AV node; slower conduction permits atrial contraction to fill ventricles
AV bundle (bundle of His) → bundle branches → Purkinje fibers distribute impulse to ventricles
Comparison of SA nodal and ventricular action potentials with neuronal action potential; role of ions and ion channels
SA nodal cells: unstable resting potential; pacemaker potential due to If channels (funny current) allowing spontaneous depolarization; influx of Ca²⁺ through T-type and then L-type Ca²⁺ channels drives action potential; no true resting potential
Ventricular myocytes: stable resting potential; rapid depolarization via Na⁺ influx; plateau phase due to Ca²⁺ influx through L-type Ca²⁺ channels; repolarization via K⁺ efflux
Key ions: Na⁺, Ca²⁺, K⁺
Autonomic nervous system effects on firing of cardiac action potentials and heart rate
Sympathetic stimulation (norepinephrine/epinephrine) via β1 receptors increases heart rate and contractility by increasing cAMP and Ca²⁺ availability
Parasympathetic stimulation (acetylcholine) via muscarinic receptors decreases heart rate by opening K⁺ channels and reducing Ca²⁺ influx
Basic parts of an EKG (ECG); events of the heart they represent; reading an EKG
P wave: atrial depolarization (contraction)
PR segment: conduction delay through AV node
QRS complex: ventricular depolarization (and atrial repolarization hidden)
ST segment: isoelectric period; ventricular plateau
T wave: ventricular repolarization
Events during the cardiac cycle; systole vs diastole; sequence and mechanical events
Atrial systole: atrial contraction completes ventricular filling
Isovolumetric contraction: ventricles contract with all valves closed; no change in volume
Ventricular ejection: semilunar valves open; blood expelled to aorta/pulmonary trunk
Isovolumetric relaxation: ventricles relax with all valves closed
Ventricular filling: AV valves open; ventricles fill passively; atrial contraction may contribute to late filling
Relationship between cardiac output, heart rate, and stroke volume; definitions
Cardiac output (CO): amount of blood pumped by each ventricle per minute
CO = Heart Rate (HR) × Stroke Volume (SV)
Typical resting values: HR ~ 60–100 bpm; SV ~ 70 mL; CO ~ 4.2–6.0 L/min
Factors affecting cardiac output, heart rate, and stroke volume; including hormones, autonomic innervation, end diastolic volume, end systolic volume, venous return, filling time, preload, contractility, afterload
HR is modulated by autonomic input (sympathetic vs parasympathetic) and circulating hormones
SV is influenced by preload (EDV), contractility (myocardial force), and afterload (aortic/pulmonary pressure opposing outflow)
Venous return and filling time affect preload; afterload affected by systemic vascular resistance
Define angina pectoralis and myocardial infarct (heart attack)
Angina pectoralis: chest pain due to transient myocardial ischemia; reversible adverse effects with rest or nitroglycerin
Myocardial infarct: necrosis of heart muscle due to prolonged ischemia from blocked coronary blood flow; can cause permanent damage
Fetal circulation: fetal vessels and the role of the fossa ovalis and ligamentum arteriosum
Fetal circulation includes shunts that bypass lungs: foramen ovale allows blood to pass from right to left atrium; ductus arteriosus connects pulmonary artery to aorta
After birth: foramen ovale becomes fossa ovalis; ductus arteriosus becomes ligamentum arteriosum; pulmonary and systemic circulations separate more completely
Blood Vessels
Anatomy and function of blood vessels (elastic arteries, muscular arteries, arterioles, capillaries, venules, veins); compare layers, size, thickness, pressure, velocity, compliance, cross-sectional area, and valves
Elastic arteries (conducting): large-diameter; high elastin content to accommodate pulsatile output; include aorta and major branches
Muscular arteries (distributing): more smooth muscle; regulate blood flow to specific tissues via vasoconstriction/vasodilation
Arterioles: small diameter; major site of vascular resistance to control tissue perfusion
Capillaries: smallest vessels; site of exchange between blood and tissues; three types below
Venules and veins: return low-pressure blood to the heart; valves in larger veins prevent backflow; capacitance vessels with high compliance
Vessel layers: tunica intima (endothelium), tunica media (smooth muscle), tunica externa/adventitia (connective tissue)
Define: Systolic pressure, Diastolic pressure, Pulse pressure
Systolic pressure: peak arterial pressure during ventricular systole
Diastolic pressure: arterial pressure during ventricular diastole
Pulse pressure: difference between systolic and diastolic pressures; PP = SBP − DBP
Process of measuring blood pressure and the mean arterial pressure (MAP) formula
Blood pressure is typically measured indirectly with a cuff and sphygmomanometer; auscultatory method detects Korotkoff sounds
MAP (mean arterial pressure) can be approximated as MAP \,=\frac{SBP + 2\cdot DBP}{3} or more generally as MAP = CO \times TPR where TPR is total peripheral resistance
Nine clinically important arterial pulse points
Common carotid (neck)
Brachial (arm, at the elbow)
Radial (wrist)
Femoral (groin)
Popliteal (knee area)
Posterior tibial (ankle/medial ankle region)
Dorsalis pedis (top of foot)
Temporal (temple) and facial arteries (as clinically relevant points)
Factors that affect blood pressures throughout the circulatory system; including stroke volume, heart rate, vascular resistance, and total peripheral resistance (TPR)
SBP/DBP influenced by CO, arterial compliance, and TPR
Stroke volume, heart rate, and vascular resistance collectively determine arterial pressure
Mechanisms to maintain blood pressure: baroreflexes, chemoreflexes, hormonal influences
Baroreflexes: stretch receptors in carotid sinus and aortic arch detect BP changes; reflexive adjustments alter HR, contractility, and vascular tone
Chemoreflexes: respond to CO₂, O₂, and pH levels to regulate respiration and vascular tone
Hormonal influences: sympathetic catecholamines (NE/EPI), angiotensin II, vasopressin, natriuretic peptides modulate pressure and volume homeostasis
Differences between continuous, fenestrated, and sinusoidal capillaries; materials each type permits
Continuous capillaries: uninterrupted endothelium; permits diffusion of water, small solutes; common in muscle, skin, and lungs
Fenestrated capillaries: have pores (fenestrations) that increase permeability to small molecules and some proteins; found in kidneys, small intestine, and endocrine glands
Sinusoidal (discontinuous) capillaries: have large gaps and poorly formed basement membranes; allow passage of larger molecules and cells (e.g., liver, bone marrow, spleen)
Capillary exchange via bulk flow (hydrostatic pressure and osmotic pressure); how altering parameters affects capillary dynamics
Bulk flow (filtration/reabsorption) depends on Starling forces: net filtration pressure = (hydrostatic pressure difference) − (colloid osmotic pressure difference)
Key pressures: capillary hydrostatic pressure (Pc), interstitial hydrostatic pressure (Pi), capillary colloid osmotic pressure (πc), interstitial colloid osmotic pressure (πi)
Net filtration = Kf[(Pc − Pi) − (πc − πi)], where Kf is filtration coefficient
Changes in these pressures affect fluid movement: increased capillary hydrostatic pressure promotes filtration into interstitium; increased plasma protein concentration (π_c) promotes reabsorption
Mechanisms to maintain blood pressure: autoregulation (metabolic, myogenic), neuronal (medullary cardiovascular centers, baroreflexes, chemoreflexes), and hormonal
Autoregulation adjusts local blood flow through metabolic byproducts, pH, O₂ levels, and myogenic response to stretch
Medullary cardiovascular centers integrate inputs and coordinate autonomic output to regulate heart rate, contractility, and vessel tone
Hormonal controls include renin-angiotensin-aldosterone system, vasopressin, natriuretic peptides, and catecholamines
Major blood vessels of the systemic circulatory system and areas they service
Aorta and major branches: supply systemic circulation to head, trunk, and limbs
Carotid arteries: head and brain
Subclavian and axillary arteries: upper limbs
Celiac trunk, mesenteric arteries: abdominal viscera
Renal arteries: kidneys
Iliac arteries: lower limbs
Venous drainage mirrors arterial distribution through the venous system, returning blood to the heart
The Lymphatic System
Functions of the lymphatic system; major lymphatic tissues and cells
Returns excess interstitial fluid to the bloodstream to maintain fluid balance
Transports dietary lipids (via lacteals in the small intestine)
Provides immune defense via lymph nodes, spleen, thymus, tonsils, and other lymphoid tissues
Houses immune cells (lymphocytes, macrophages, dendritic cells) and antigen-presenting cells (APCs)
Differentiate between blood, interstitial fluid, and lymph
Blood: circulatory fluid inside vessels; high protein content in plasma
Interstitial fluid: fluid surrounding tissue cells; low protein content
Lymph: returned interstitial fluid that has entered lymphatic capillaries; contains immune cells and occasionally pathogens; low protein initially
Flow of lymph through lymphatic capillaries and vessels, lymph nodes, thoracic and right lymphatic ducts
Lymphatic capillaries absorb interstitial fluid; lymph travels through vessels with valves; passes through lymph nodes for immune surveillance
Lymphatic trunks drain into ducts: right lymphatic duct (drains right upper body) and thoracic duct (drains rest of the body) into venous circulation near the subclavian veins
Lymphatic organs: structure, location, and function (lymph nodes, tonsils, lymphoid tissues, spleen, thymus)
Lymph nodes: filter lymph; sites of immune cell activation
Tonsils: guard against inhaled or ingested pathogens
Spleen: filters blood; site of immune responses to blood-borne antigens; also recycles old RBCs
Thymus: site of T cell maturation and education
Lymphoid tissues: mucosa-associated lymphoid tissue (MALT), including Peyer’s patches, etc.
Factors influencing lymph flow
Skeletal muscle contractions, breathing (thoracic pressure changes), smooth muscle tone in lymphatic vessels, and intrinsic lymphatic pumps
Immunology
Functions of the immune system
Defense against pathogens, cancer surveillance, wound healing, and removal of dead/damaged cells
Innate vs adaptive defense systems
Innate: immediate, non-specific defenses (physical barriers, phagocytes, NK cells, complement, inflammatory responses)
Adaptive: specific, slower-onset responses (humoral immunity via B cells and antibodies; cell-mediated immunity via T cells)
First, second, and third lines of defense
First line: physical and chemical barriers (skin, mucous membranes, acidity, mucociliary escalator, tears/lysozyme, defecation/vomiting, urine, coughing/sneezing)
Second line: nonspecific defenses (phagocytes, NK cells, interferons, complement, inflammation, fever)
Third line: specific adaptive responses (humoral and cellular immunity with memory)
Roles of components in the first line of defense
Skin and mucous membranes provide barrier protection
pH, urine, mucous membranes, tears/lysozyme, defecation/vomiting, coughing/sneezing, mucociliary escalator act to prevent pathogen entry and dissemination
Roles of components in the second line of defense
Phagocytes: neutrophils, macrophages remove pathogens
Natural killer (NK) cells: destroy infected or abnormal cells without prior sensitization
Interferons: antiviral signaling molecules that inhibit viral replication
Complement: cascade of proteins that enhance phagocytosis, promote inflammation, and form membrane attack complexes
Inflammation: redness, heat, swelling, pain; functional impairment; coordinated by chemical signals (cytokines, histamine)
Fever: systemic response to infection; can boost immune activity and inhibit pathogen growth
Inflammatory response and the 4 characteristic traits of inflammation
Redness (rubor), heat (calor), swelling (tumor), pain (dolor); sometimes loss of function
Movement of fluid and immune cells to the affected site; increased vascular permeability
Steps of humoral and cellular immune responses
Humoral (B-cell mediated): antigen presentation → B cell activation → clonal expansion → plasma cells produce antibodies; memory B cells form for faster future responses
Cellular (T-cell mediated): antigen presentation to T cells → activation of cytotoxic T cells, helper T cells; cytotoxic T cells kill infected cells; memory T cells provide faster response on re-exposure
Define and describe the role of pathogens, antigens, MHC, APCs
Pathogens: disease-causing organisms (bacteria, viruses, fungi, parasites)
Antigens: molecules or parts of molecules that the immune system recognizes as foreign
MHC (major histocompatibility complex): cell-surface proteins presenting antigen fragments to T cells; MHC class I (all nucleated cells) and MHC class II (antigen-presenting cells)
Antigen-presenting cells (APCs): dendritic cells, macrophages, B cells that process and present antigens via MHC to T cells
Lymphocytes: differentiate and describe functions of B, T, and NK cells
B cells: produce antibodies; mediate humoral immunity; can become plasma cells and memory B cells
T cells: include cytotoxic T cells (CD8+) that kill infected cells; helper T cells (CD4+) that activate other immune cells; regulatory T cells modulate immune responses; memory T cells provide rapid response upon re-exposure
NK cells: part of innate immunity; kill virally infected and tumor cells without prior sensitization; can interact with antibody-coated targets via antibody-dependent cellular cytotoxicity (ADCC)
Summary of Humoral Immunity steps and role of plasma cells, antibodies, antigens, and memory cells
Antigen recognition by B cell receptor or via presentation by APCs
Activation and clonal expansion of B cells; differentiation into plasma cells and memory B cells
Plasma cells secrete antibodies that neutralize pathogens, mark them for destruction, or activate complement
Memory B cells persist for rapid response upon future exposure
Five antibody classes and unique characteristics of each
IgG: most abundant in serum; crosses placenta; protects against bacteria and viruses
IgM: first antibody produced in an immune response; efficient agglutination; pentameric structure
IgA: present in secretions (tears, saliva, mucous, breast milk); provides mucosal immunity
IgD: B cell receptor on naive B cells; low circulating levels
IgE: allergic responses and defense against parasitic infections
Differences between primary and secondary immune responses and immunological memory
Primary response: slower, lower magnitude, needs clonal activation; antibodies predominantly IgM initially, later IgG
Secondary response: faster and stronger due to memory B and T cells; predominantly IgG and higher affinity antibodies
Effects of Cell-Mediated Immunity (CMC) including role of Cytotoxic T, Helper T cells, Memory cells
Cytotoxic T cells destroy infected or abnormal cells presenting antigen on MHC I
Helper T cells coordinate immune responses by activating B cells, cytotoxic T cells, and macrophages via cytokines
Memory T cells persist to provide rapid response on re-exposure
Vaccines mechanism and role in creating immunity
Vaccines present antigens in a safe form to elicit adaptive immune responses without causing disease
Induce memory B and memory T cells to provide rapid and robust protection upon subsequent exposure
Concepts of allergies and autoimmune diseases
Allergies: hypersensitivity reactions (often IgE-mediated) to benign substances; can involve mast cell degranulation and histamine release
Autoimmune diseases: immune system mistakenly targets self-antigens (e.g., type 1 diabetes, rheumatoid arthritis, multiple sclerosis); may involve loss of tolerance and autoreactive T or B cells
Notes on connections to foundational principles and real-world relevance
Blood and cardiovascular systems underpin oxygen transport, nutrient delivery, and waste removal essential for cellular metabolism
Lymphatic and immune systems maintain fluid balance and defend against pathogens; vaccination is a practical public health application
Understanding hemostasis clarifies responses to injury and risks of thrombosis or hemorrhage
Cardiac electrophysiology links cellular ion channels to whole-organ function, with clinical relevance in arrhythmias and ECG interpretation
Ethical, philosophical, and practical implications
Vaccination ethics and public health considerations (herd immunity; access and equity)
Balancing anticoagulant therapy with bleeding risk in clinical care
Implications of autoimmune disease management for patient quality of life
Formulas and key numerical references
Cardiac output: CO = HR \times SV
Mean arterial pressure: MAP = \frac{SBP + 2 \cdot DBP}{3}
Capillary bulk flow (Starling forces): Jv = Kf \bigl[(Pc - Pi) - (\pic - \pii)\bigr]
Cardiac cycle timing and events are described qualitatively; quantitative values vary with age and fitness (e.g., typical resting HR ~60–100 bpm, SV ~70 mL)
Connections to lab objectives and practical understanding
Students should be able to identify and describe each listed component, pathway, and physiological mechanism
Expect to interpret diagrams of heart flow, EKG tracings, capillary exchange concepts, and lymphatic flow in exams
Be prepared to differentiate pathways (intrinsic vs extrinsic coagulation), capillary types, and immune system lineages in short-answer or essay questions