Physiology of Cell, Body Fluids & Homeostasis – Lecture Notes

Reading Plan & Resources

  • Pre-Reading Strategy
    • Read assigned textbook pages before each lecture for easier comprehension.
    • Bring questions from the reading to class for clarification.
  • Texts Mentioned
    • Netter’s Physiology (required): concise, high-yield.
    • Costanzo Physiology (recommended): detailed, student-friendly.
    • Dr. Thomas will post a chapter/page cross-reference list for every lecture.
  • Supplemental Uploads
    • Extra handout on oxidative phosphorylation already posted on Blackboard.
    • Future uploads: practice questions, study guides, PDF copies of slides, additional Starling-force examples.

Instructor Background

  • Dr. Jessica Thomas
    • B.S. Chemistry, minor Mathematics – Alabama State University (Montgomery native).
    • Ph.D. Neuroscience – University of Iowa.
    • Post-doctoral training – Vanderbilt University.
    • Currently teaches & conducts research at Meharry Medical College.
    • Contact: prefers text for fastest response; flexible Zoom/on-campus meetings; no fixed office hours (toddler schedule!).

Course & Assessment Logistics

  • First half of Physiology taught by Dr. Thomas.
  • Quizzes: clinical-style and factual questions; practice sets provided ahead of time.
  • Study guide = list of concepts (all quiz questions pulled directly from slides).
  • Class email list being assembled for students lacking Blackboard access.

Scope of Today’s Lecture

  • Physiology overview (functions & mechanisms).
  • Core cell biology review: organelles & clinical correlations.
  • Body-fluid compartments & tonicity.
  • Starling forces in capillary exchange.
  • IV fluid types & clinical decision rules.
  • Homeostasis & feedback loops.
  • Study of how biological systems function.
  • Integrates biochemistry, anatomy, physics (gradients, pressure), and cell biology.
  • Foundation for understanding pathophysiology (disease = disrupted normal function).

Cell Structure & Function

  • Why important? All drugs, toxins, diseases act at the cellular level.

Nucleus

  • Contains DNA; site of transcription, not translation.
  • Nuclear envelope regulates RNA export.
  • DNA mutations ⇒ genetic disorders.
  • Central dogma: \text{DNA} \;\xrightarrow{\text{transcription}}\;\text{RNA} \xrightarrow{\text{translation}} \text{Protein} plus reverse transcription by viral enzymes.

Mitochondrion

  • “Powerhouse”: site of aerobic respiration & oxidative phosphorylation.
  • Own circular maternal DNA → disorders preferentially affect high-energy tissues (brain, muscle).
  • Electron-transport chain (ETC):
    • Electron donors: \text{NADH} (→ Complex I) & \text{FADH_2} (→ Complex II).
    • Oxygen = final electron acceptor → H_2O.
    • Proton gradient across inner membrane drives ATP synthase.
    • Yield: 1\;\text{NADH} \Rightarrow 2\;\text{ATP},\; 1\;\text{FADH}_2 \Rightarrow 1.5\;\text{ATP} (board figure).
    • ETC inhibitors/uncouplers:
    • Complex IV: cyanide, CO → ↓ATP, cell death.
    • ATP synthase: oligomycin (unused clinically).
    • Uncouplers: 2,4-DNP, thermogenin (brown fat) → heat production.

Endoplasmic Reticulum (ER)

  • Rough ER (ribosome-studded)
    • Synthesizes secretory & membrane proteins.
    • Abundant in salivary glands, other secretory epithelia.
  • Smooth ER (no ribosomes)
    • Synthesizes lipids & steroids, detoxifies drugs.
    • Prominent in liver & adrenal cortex.

Golgi Apparatus

  • Post-translational modification (glycosylation, tagging), sorting, packaging.
  • Produces lysosomes.
  • I-cell disease: missing \text{M6P} tag → lysosomal enzymes secreted into plasma.

Lysosome

  • Acidic vesicle for waste breakdown.
  • Malfunction → lysosomal storage disorders (e.g., Tay-Sachs).

Peroxisome

  • β-oxidation of very-long-chain fatty acids; generates H2O2.
  • Defect → Zellweger syndrome (↑ VLCFA, hypotonia, seizures, cranio-facial dysmorphisms).

Cytoskeleton

  • Microtubules (largest): vesicle transport, cilia, mitotic spindle.
  • Microfilaments (actin): motility, muscle contraction (details in muscle lecture).
  • Intermediate filaments: structural support (e.g., keratin, neurofilaments).
  • Microtubule defect → primary ciliary dyskinesia (infertility, chronic infections, situs inversus).

High-Yield Organelle–Disease List (memorise)

  • Tay-Sachs – lysosome (GM2 ganglioside accumulation; “onion-skin” lysosomes; cherry-red macula; NO hepatosplenomegaly).
  • Gaucher, Niemann-Pick, Pompe, etc. – various lysosomal enzymes.
  • Zellweger – peroxisome (↑ VLCFA, neonatal death).
  • I-cell disease – Golgi tagging failure.
  • ETC inhibitor toxicities as above.

Body-Fluid Compartments

  • Human ≈ 60\% water, 40\% solids.
  • Standard reference male 70\;\text{kg} \Rightarrow 42\;\text{L} total body water (TBW).
  • Rule 60-40-20:
    • 60\% of body weight = TBW.
    • 40\% BW = intracellular fluid (ICF).
    • 20\% BW = extracellular fluid (ECF).
    • ECF split: \frac{3}{4} interstitial fluid, \frac{1}{4} plasma.
  • Variations: men > women, infants > elderly (fat ↓ TBW).

Osmolarity & Tonicity

  • Osmolarity = solute particles per liter solution; drives water movement.
  • Isotonic: equal osmolarity → no net water shift.
  • Hypotonic (ECF ↓ osmolarity): water enters cells → swelling.
  • Hypertonic (ECF ↑ osmolarity): water exits cells → shrinkage.

Starling Forces & Capillary Exchange

  • Balance between filtration (fluid leaves capillaries) and reabsorption (fluid enters capillaries).
  • Starling equation (conceptual): \displaystyle Jv = Kf \big[(Pc - Pi) - \sigma(\pic - \pii)\big]
    • P_c = capillary hydrostatic pressure (pushes out).
    • P_i = interstitial hydrostatic pressure (pushes in).
    • \pi_c = capillary oncotic (albumin) pressure (pulls in).
    • \pi_i = interstitial oncotic pressure (pulls out).
    • Positive J_v → net filtration; negative → net reabsorption.

Clinical Correlations

  • Edema = filtration ≫ reabsorption.
    • Causes: ↑Pc (CHF), ↓\pic (nephrotic syndrome, liver failure, hemorrhage), ↑ capillary permeability (inflammation), lymphatic obstruction.
  • Hemorrhage: isotonic volume loss (↓ ECF volume, same osmolarity) → activates RAS, vasopressin.
  • Dehydration (sweating, fever, diarrhea): hypertonic loss (water > salt).
    • ↓ ECF volume, ↑ ECF osmolarity → water shifts from ICF to ECF; both compartments shrink.

Intravenous (IV) Fluids: Composition & Effects

Fluid typeExampleOsmolar EffectCompartment Change
Isotonic (0.9\% NaCl)“Normal saline”No osmolar shift↑ ECF only (plasma + interstitial)
Hypotonic (0.45\% NaCl, D5W)Half-saline, dextrose + waterWater → cells↑ ICF (risk cerebral edema)
Hypertonic (3\% NaCl)Hyper-salineWater ← cells↓ ICF, ↑ ECF (treat hyponatremia, cerebral edema)

Quick Fluid-Shift Summary (Board Table)

  • Hemorrhage: ICF = same, ECF ↓, \text{osm} = same.
  • Dehydration: ICF ↓, ECF ↓, \text{osm} ↑.
  • Isotonic infusion: ICF same, ECF ↑, \text{osm} same.
  • Hypotonic infusion: ICF ↑, ECF ↑, \text{osm} ↓.
  • Hypertonic infusion: ICF ↓, ECF ↑, \text{osm} ↑.
  • Edema: plasma → interstitium (↑ interstitial volume, no ICF change).

Homeostasis & Feedback Loops

  • Goal: maintain internal constancy (temperature, pH, ions, glucose, BP).
  • Components: sensor → control center (usually hypothalamus) → effector.
  • Negative Feedback (most common)
    • Blood glucose (insulin vs. glucagon).
    • Body temperature (sweating, vasodilation; shivering, vasoconstriction).
    • Blood pressure (baroreceptor reflex → HR & vessel tone adjustments).
  • Positive Feedback (amplify to completion)
    • Childbirth: stretch → oxytocin → uterine contractions → more stretch.
    • Blood clotting: platelet activation cascade.
    • Drug addiction (reward-loop potentiation, though long-term receptor down-regulation complicates).

Case Study: Marathon Runner

  • Presentation: fatigue, dry mucosa, oliguria, tachycardia, hypotension after hot race w/ no water.
  • Diagnosis: hypertonic dehydration (water ≪ salt).
  • Primary disturbed compartment: ECF first, then compensatory water shift causes both ECF & ICF shrinkage.
  • Management: hypotonic or isotonic fluids depending on serum Na⁺ and neuro status (avoid hypertonic saline).
  • Starling perspective: ↓ plasma volume → ↓P_c, ↑ oncotic pull → fluid re-entry until volume restored.

Common Student Q&A Highlights

  • Why isotonic solutions cause no net water movement? Equal osmolarity between compartments.
  • Albumin = main determinant of \pi_c; low albumin → edema/filtration.
  • Dialysis removes solutes directly from blood; not a classic Starling variable.
  • Practice questions, Zoom reviews, & office meetings will precede each quiz.

Practical Study Tips

  • Master organelle functions + hallmark diseases; expect straight recall questions.
  • Drill Starling variables: associate each pressure with direction (filter vs. absorb) & location (capillary vs. interstitium).
  • Memorize IV-fluid table & when to choose each clinically.
  • Work textbook end-of-chapter questions; compare to posted practice sets.
  • Use Costanzo for deeper explanations if Netter feels too brief.