Organized objective-by-objective. For each one, the goal is: “Can I speak to this?” Use the checkpoint boxes to self-test. 🔗 flags mark concepts that bridge into other modules (especially the Lymphatic System).
Everything in this deck hangs off one idea — homeostasis of fluid and blood and what happens when it breaks. Fluid dynamics sets up the forces (hydrostatic + oncotic pressure); hematology gives you the contents of the intravascular compartment (plasma proteins, RBCs, platelets) and the disorders that arise when those contents or forces go wrong. Albumin, oncotic pressure, and edema are the hinges that connect the two halves.
The membrane: the capillary wall is a phospholipid bilayer (endothelial cell membranes) plus gaps between endothelial cells. Different substances take different routes:
Osmosis: water moves from lower osmolality → higher osmolality until compartments equalize.
☐ Can I speak to it? Given a substance (a gas, a small ion, albumin, water), can I name its route across the capillary wall and why?
Primary regulator of fluid movement between compartments: blood osmolality.
Osmolality = concentration of dissolved solute particles, measured as osmoles of solute per kg of water. Normal blood osmolality ≈ 280–294 mOsm/kg.
Osmoreceptors detect osmolality changes: - Central — hypothalamus - Peripheral — kidneys
Two primary forces driving fluid between compartments: 1. Hydrostatic pressure — capillary + tissue 2. Oncotic (colloid osmotic) pressure — interstitial + capillary
Electrolyte control of compartment volume: - Na⁺ = most abundant ECF electrolyte → governs osmotic balance of the ECF; the body regulates Na⁺ to control water movement via osmosis. - K⁺ = most abundant ICF electrolyte → governs osmotic balance of the ICF. - Disrupting Na⁺ or K⁺ concentrations disrupts whole-body fluid distribution. The osmotic pull of proteins/non-diffusible solutes is balanced by active transport of ions in/out of the cell; water then follows freely through aquaporins. ICF osmolality stays relatively stable; when ECF osmolality shifts, water moves between compartments until equilibrium is restored.
Tonicity and the RBC (why this matters clinically): - Isotonic — no net water shift; RBC keeps normal shape. - Hypotonic — water moves into the cell → swelling/lysis. - Hypertonic — water moves out of the cell → crenation/shrinkage.
☐ Can I speak to it? Can I explain why maintaining Na⁺/K⁺ concentrations is essential for RBC function, using isotonic/hypotonic/hypertonic examples?
🔗 Cross-module: ADH and aldosterone (below) tie fluid regulation to the endocrine and renal modules; osmoreceptor function in the kidney previews renal regulation of water.
This is Starling’s Law of Hemodynamics — four pressures determine the net direction of fluid flow.
| Force | What it does |
|---|---|
| Plasma hydrostatic pressure | Pressure inside the capillary; decreases from arterial → venous end. Pushes fluid out into tissue. |
| Tissue hydrostatic pressure | Pressure of fluid in tissue channels; usually negative (< atmospheric), so it tends to pull fluid out of capillaries. When positive, it opposes outward flow. |
| Tissue colloidal osmotic pressure | Exerted by plasma proteins that have entered the tissue; pulls fluid into tissue, opposing reabsorption. |
| Plasma colloidal osmotic (oncotic) pressure | Caused by plasma proteins; creates a siphon effect, pulling fluid from tissues back into capillaries. |
Arterial vs. venous end (the practical summary): - Arterial side: high hydrostatic pressure (blood volume + cardiac pump) → pushes fluid out into tissues (filtration). - Venous side: plasma volume within the vessel has dropped, so protein concentration is relatively higher → oncotic pressure increased → pulls fluid back in (reabsorption).
☐ Can I speak to it? Can I walk a drop of fluid from the arterial to the venous end and name which force dominates where?
🔗 Cross-module (Lymphatic System): Starling forces don’t reabsorb all filtered fluid. The lymphatic system returns the leftover interstitial fluid and any leaked protein to circulation. When that safety valve is overwhelmed or oncotic pressure fails, you get edema — the direct bridge into the Lymphatic module (lymphedema).
Two ways ECF homeostasis is disrupted: abnormal intravascular volume (too low or too high) and fluid accumulation in the interstitial space (edema).
Compensatory mechanisms for hypovolemia: - Endocrine activation, thirst, renal fluid retention, vasoconstriction. - Baroreceptors sense dropping BP → sympathetic activation → ↑HR, ↑TPR (total peripheral resistance).
Stages of hypovolemic shock: - Compensated — blood volume drops 10–20%; HR, contractility, and resistance compensate and maintain perfusion. - Decompensated — compensation fails → hypotension, dyspnea, acidosis, confusion. - Irreversible — blood loss > 20% → insufficient perfusion → death.
☐ Can I speak to it? Can I explain the physiological mechanism behind pitting edema and ascites in someone with increased intravascular fluid? (This is the deck’s Think-Pair-Share.)
🔗 Cross-module: Edema is the single biggest shared concept across Fluid Dynamics ↔︎ Hematology ↔︎ Lymphatic System. The oncotic-pressure/albumin story here is the setup for lymphedema. EPO-related anemia and shock also reach into renal and cardiopulmonary.
Whole blood = plasma (~55%) + cellular components (~45%).
Chief functions of blood: 1. Delivery of substances needed for cellular metabolism 2. Removal of metabolic wastes 3. Defense against invading microorganisms and injury 4. Maintenance of acid–base balance
| Protein | Normal serum (APTA) | Role |
|---|---|---|
| Albumin | 3.5–5.2 g/dL | Regulates passage of water/solutes through capillaries (oncotic pressure) — see Obj. 6 |
| Globulins | 1.0–1.5 g/dL | Defense (immunoglobulins/antibodies) + transport; precursor molecules (angiotensinogen = α-2 globulin); hormone-binding globulins keep hormones inactive while protein-bound (e.g., thyroxine-binding) |
| Fibrinogen | 0.2–0.45 g/dL | Precursor of the fibrin clot |
Plasma protein functions grouped four ways: clotting (fibrinogen), defense (antibodies/globulins), transport (lipoproteins carry fatty acids + lipid-soluble hormones; iron), regulation (precursor molecules, hormones).
Maintain H₂O in the ECF, act as buffers, support membrane excitability, maintain blood pH. Includes Na⁺, K⁺, Ca²⁺, Mg²⁺, Cl⁻, phosphate, sulfate.
☐ Can I speak to it? Can I list the three plasma proteins with their reference ranges and the cellular breakdown from memory?
Why albumin is the star: it’s a large molecule that stays in the vessel and is the main driver of plasma oncotic pressure, regulating passage of water/solutes through capillaries.
The failure cascade (high-yield): > Low albumin → reduced oncotic pressure → excessive movement of fluid + solutes into tissue → water not reabsorbed into vessels → edema.
☐ Can I speak to it? Can I connect “low albumin” to “edema” in one unbroken chain of cause and effect?
🔗 Cross-module: This is the same mechanism referenced in Objective 4 (edema) and in the Lymphatic module. Recognize it whenever it appears — it’s a recurring exam hinge. Clinically, it also links to cirrhosis (impaired albumin synthesis) and nephrotic states (renal).
(Objective 7 on thrombosis is grouped with hemostasis below.)
☐ Can I speak to it? Can I trace RBC lifecycle (marrow → 120 days → spleen) and explain how one Hb ends up carrying 4 O₂?
🔗 Cross-module (Renal): EPO is made in the kidney — so chronic kidney disease → ↓EPO → anemia (appears again under Objective 10). A clean fluid-dynamics/renal/hematology bridge.
Roles of platelets (regulate → help → initiate → activate): induce vasoconstriction to regulate blood flow into the injury; form the platelet plug; initiate the coagulation cascade to stabilize the plug; activate repair (clot retraction + fibrinolysis).
☐ Can I speak to it? Can I recite the 4 phases and the prothrombin → thrombin → fibrin chain, and name what turns the cascade off?
☐ Can I speak to it? Can I distinguish mural vs. occlusive thrombus, and embolus vs. embolism, in one sentence each?
🔗 Cross-module: thrombosis/embolism feed the infarction concept (below) and preview cardiopulmonary (PE, stroke).
| Hb level | Guidance |
|---|---|
| < 5–7 g/dL | Life-threatening (→ death) |
| > 20 g/dL | Capillary clogging risk |
| < 8 with HCT < 25 | Restrict activity/exercise |
| 8–10 g/dL | Aggressive strengthening/endurance training contraindicated; consider energy cost of ADLs/transfers; expect diminished tolerance & easy fatigability |
| 10–12 g/dL | Low-impact, low-intensity aerobics + isometric/gentle resistive exercise OK |
Clinical judgment: look at trends in Hb, not just a single value; consider PMH (chronic anemia vs. acute blood loss); communicate with the team; use pacing to distribute workload and promote physiologic recovery.
| Platelet count | Guidance |
|---|---|
| 150–400 k/µL | Normal |
| 40,000–60,000 /µL | ↑ risk of post-surgical/traumatic bleed → consult physician; low-load resistance (1–2 lb); walking, stationary bike w/ light resistance, minimal ADLs |
| 20,000–40,000 /µL | Low-intensity, no weights/resistance; up to 2 lb permitted but no resistance on stationary bike |
| < 20,000 /µL | Activity/exercise restriction more stringent |
| < 10,000 /µL | Spontaneous CNS, GI, and/or respiratory tract bleeding may occur — consult physician before exercise |
☐ Can I speak to it? Given a patient’s Hb and platelet count, can I state what exercise is safe and when to call the physician?
Edema (lymphedema, cerebral, inflammatory, peripheral dependent, pulmonary); lymphadenopathy (enlarged nodes); thrombosis; embolism; infarction (tissue death from ischemia — brain, heart, GI, kidney, spleen); splenomegaly; bleeding/bruising; shock (rapid weak pulse late, hypotension SBP < 90 mmHg, cool moist skin late, pallor, weak/absent peripheral pulses).
(1) ↓ production, (2) ↑ destruction, (3) excessive blood loss.
↓ Production: - Nutritional deficiencies: Iron, Vitamin B12, folate. - Iron deficiency — blood loss, malabsorption, growth/pregnancy, menstruation, older adults, lower socioeconomic groups. - Vitamin B12 — rarely dietary; usually absence of intrinsic factor (IF) (made by gastric parietal cells, needed for ileal B12 absorption) → pernicious anemia; Crohn’s → malabsorption. - Folate — needed by erythroblasts during proliferation; inadequate intake, chronic alcoholism, anorexia; pregnancy needs 2×. - Chronic kidney disease → ↓ EPO → ↓ RBC production. 🔗 (renal link) - Bone marrow disorders — aplastic anemia (marrow failure, all cell lines), leukemias (malignant cells crowd out erythroid precursors), chemotherapy.
↑ Destruction: - Inflammatory anemia — circulating inflammatory cytokines activate RBC destruction and blunt marrow responsiveness to EPO. - Sickle cell anemia — most common in ancestry from sub-Saharan Africa; mutation in β-globin → abnormal β-globin distorts RBCs into a sickle shape; repeated deoxy/oxy cycles stiffen HbS, damaging RBCs → hemolytic anemia, microvascular blockage, tissue ischemia, pain; cells die early.
Excessive blood loss: trauma/wound, GI cancers, bleeding peptic ulcer, excessive menstruation, bleeding hemorrhoids, varices, diverticulosis.
| Type | Antigen | Antibody | Note |
|---|---|---|---|
| A | A | anti-B | |
| B | B | anti-A | |
| AB | A + B | neither | Universal recipient |
| O | none | anti-A + anti-B | Universal donor; cannot receive A/B/AB |
% of marrow fat ≈ person’s age (until ~50); ↓ serum iron, iron-binding capacity, iron absorption; platelet count varies with age; ↑ fibrinogen + platelet adhesiveness; ↑ RBC rigidity → disrupted flow; links to HTN, CVA, diabetes.
☐ Can I speak to it? For each anemia type, can I place it in one of the three buckets (↓ production / ↑ destruction / blood loss) and give its mechanism?
The professor flagged HCT, Hb, and platelet values as must-knows. Memorize this block cold.
| Measure | Value | Notes |
|---|---|---|
| Total body water | 60% of body weight | ICF 40% (2/3), ECF 20% (1/3); interstitial 15%, intravascular 5% |
| Blood osmolality | 280–294 mOsm/kg | Primary regulator of inter-compartment fluid movement |
| Plasma proteins (total) | 7.3 g/dL | ~7% of plasma volume |
| Albumin | 3.5–5.2 g/dL | Main driver of plasma oncotic pressure |
| Globulins | 1.0–1.5 g/dL | Defense + transport |
| Fibrinogen | 0.2–0.45 g/dL | Fibrin precursor |
| HCT — female | 37–47% | ↑ polycythemia / ↓ anemia |
| HCT — male | 42–52% | |
| Hb — male | 14–17 g/dL | Each Hb carries 4 O₂ |
| Hb — female | 12–16 g/dL | |
| RBC | >99% of cells; lifespan ~120 d; 6–8 µm biconcave | Made in marrow, cleared by spleen |
| Platelets | 150,000–400,000 /µL | Thrombocytopenia <150k; thrombocytosis >450k |
| Prothrombin time (PT) | 11–13 sec | >25 sec = high bleeding risk |
| Exercise — restrict | Hb <8 with HCT <25 | 8–10 no aggressive training; 10–12 low-intensity OK |
| Exercise — platelets | <10k spontaneous bleeding | 20–40k no resistance; 40–60k consult MD |
| Shared concept | Where it shows up | Why it bridges |
|---|---|---|
| Oncotic pressure / albumin | Fluid Dynamics · Hematology · Lymphatic | Low albumin → low oncotic pressure → edema; the lymphatic system clears the overflow |
| Edema | All three modules | The unifying failure state of fluid balance; lymphedema is the lymphatic version |
| Starling forces | Fluid Dynamics → Lymphatic | Lymphatics return the fluid Starling forces don’t reabsorb |
| Erythropoietin | Hematology → Renal | Kidney makes EPO; CKD → anemia |
| ADH / aldosterone / osmoreceptors | Fluid Dynamics → Endocrine / Renal | Hormonal control of water + Na⁺ retention |
| Shock / perfusion | Fluid Dynamics → Cardiopulmonary | Hypovolemia → ↓ perfusion → organ failure |
| Thrombosis / embolism / infarction | Hematology → Cardiopulmonary | PE, stroke, MI all downstream of clot mechanics |
Work these in your own words — they mirror your professor’s “how is X related to Y?” reflection style.
Source: “Fluid Dynamics Revisited and Introduction to Hematology” and “Course Introduction and Hematology” lecture decks (E. Schaumberg, PT, MS, DPT, PhD). Notes structured to your professor’s objective-by-objective, “can-I-speak-to-it” study method.