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Anatomy & Physiology I: Homeostasis, Cell Signaling, and CNS Essentials (Ch. 1–9, Silverthorn)

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Homeostasis & Control

Equilibrium vs. Steady State (Ch.1)

Understanding the difference between equilibrium and steady state is fundamental to physiology. These concepts describe how the body maintains internal stability despite external changes.

  • Equilibrium: A closed system with no energy use; concentrations are equal across compartments.

  • Steady State: An open system (like the human body) that uses energy to maintain differences (chemical, electrical, osmotic) between compartments.

  • Reflex vs. Local Control: Local control involves paracrine/autocrine signaling near the target; Reflex control uses long-distance pathways (nervous/endocrine).

  • Negative Feedback: Stabilizes physiological variables by counteracting changes.

  • Positive Feedback: Reinforces changes (e.g., oxytocin in labor).

Term

System type

Energy use

Gradients

Example

Equilibrium

Closed

No

None

Equal concentrations everywhere

Steady state

Open (body)

Yes (active processes)

Maintains differences (chemical/electrical/osmotic)

ICF vs. ECF ion gradients with constant ATP use

Molecules & Enzymes

Protein Interactions & Enzyme Kinetics (Ch.2,4)

Enzymes and proteins interact with substrates and other molecules to facilitate biological reactions. Understanding specificity, affinity, and regulation is key.

  • Induced-fit: Enzyme changes conformation to fit substrate.

  • Competitive inhibitor: Binds active site, blocks substrate; does not affect allosteric sites.

  • Allosteric modulator: Binds elsewhere, alters enzyme activity or shape.

  • End-product inhibition: Product feeds back to reduce pathway activity.

  • Saturation: All active sites occupied; adding more substrate won’t increase rate.

  • Activation energy: Enzymes lower the energy required to reach the transition state.

Concept

What to remember

Exam traps

Induced-fit

Enzyme changes conformation to fit substrate

Not a rigid lock only

Competitive inhibitor

Binds active site, blocks substrate; *[S] can outcompete

Do not confuse with allosteric

Allosteric modulator

Binds elsewhere, alters active site shape (+ or -)

Often reversible

End-product inhibition

Product feeds back to earlier enzyme to reduce pathway activity

"Increasing product + enzyme activity"

Saturation

All active sites occupied; adding more substrate won’t raise rate

Rate plateaus, doesn’t stop

Activation energy

Enzymes lower Ea

Enzymes don’t change ΔG or equilibrium

Formula:

Membranes & Transport

Transport Mechanisms & Tonicity (Ch.5)

Cells use various mechanisms to move substances across membranes, maintaining homeostasis and responding to environmental changes.

  • Simple diffusion: No protein, no energy, down gradient (small, nonpolar molecules).

  • Facilitated diffusion: Uses channel/carrier proteins, no energy, down gradient.

  • Primary active transport: Uses pumps (e.g., Na+/K+-ATPase), requires ATP, against gradient.

  • Secondary active transport: Uses cotransporters (e.g., SGLT), energy stored in gradient.

  • Osmosis: Water movement via aquaporins; tonicity predicts cell volume changes.

Mode

Protein?

Energy?

Direction

Simple diffusion

No

No

Down gradient (small, nonpolar: O2, CO2)

Facilitated diffusion

Yes (channel/carrier)

No

Down gradient (polar/ions)

Primary active

Pump (e.g., Na+/K+-ATPase)

ATP

Against gradient

Secondary active

Cotransporter (e.g., SGLT)

Uses stored gradient

Against gradient

Osmosis

Aquaporins

No

Water + higher osmolarity

  • Tonicity: Hypertonic = shrink (crenate); Hypotonic = swell/lyse; Isotonic = no change.

Cell Signaling & Second Messengers

Receptors & Pathways (Ch.6)

Cells communicate using chemical signals and second messengers, which amplify and distribute signals inside the cell.

Receptor

Key pathway

Enzyme/2nd messenger

Classic effects

GPCR – Gs

Adenylyl cyclase + cAMP → PKA

cAMP

Phosphorylation cascades

GPCR – Gq

PLC → IP3 + DAG

Phospholipase C; IP3, Ca2+ from ER, DAG (+ PKC)

Secretion, contraction

Receptor-channel

Ligand-gated ion channel

Ion flux

Fast synaptic transmission

RTK

Autophosphorylation + MAPK

Kinase domain, phosphorylation

Growth, differentiation

  • Termination: Degrade ligand (E), remove cAMP (PDE), pump Ca2+ back into ER/out, dephosphorylation.

Hormone Classes

Types, Synthesis, and Transport (Ch.7)

Hormones are classified by structure, synthesis, and transport mechanisms, which affect their speed and duration of action.

Class

Synthesis/Storage

Transport

Receptor

Response

Peptide/Protein

Prepro + pro → processed

Free in plasma

Membrane

Fast (non-genomic)

Steroid

On demand (from cholesterol)

Carriers (protein-bound)

Cytosol/nuclear

Slow (genomic)

Amine – Catecholamine

Stored vesicle

Free

Membrane

Fast

Amine – Thyroid

Precursor in follicle, protein-bound

Carriers

Nuclear

Slow

  • Posterior pituitary: Releases ADH (vasopressin) and oxytocin.

  • Trophic pituitary hormones: TSH, ACTH, FSH, LH.

Neurons & Signaling

Graded & Action Potentials, Synapses (Ch.8)

Neurons transmit signals via electrical changes in membrane potential, using graded and action potentials, and communicate at synapses.

  • Graded potentials: Variable amplitude, decremental due to current leak and cytoplasmic resistance; occur on dendrites/soma via ligand-gated channels.

  • Action potentials: All-or-none, generated at axon hillock/initial segment; VG Na+ open (depolarization), Na+ inactivation, VG K+ open (repol), K+ stays open (AHP, undershoot); absolute then relative refractory period.

  • Synapse sequence: AP arrives → VG Ca2+ opens → vesicle fusion → NT release → receptor activation (ionotropic/metabotropic) → postsynaptic potential & summation.

  • Synapse types: BBB/support: Oligodendrocytes (CNS myelin), Schwann (PNS myelin), Microglia (immune), Ependymal (CSF/secreting, stem-like).

  • NTs: GABA (main inhibition), Glutamate (main excitation); ACh, NE, DA, 5-HT (modulatory).

CNS Essentials

Spinal Cord, Brain Regions, Meninges, CSF (Ch.9)

The central nervous system consists of the spinal cord and brain, each with specialized regions and protective structures.

  • Spinal cord: White matter (outside tracts); gray inside (horns). Dorsal horn = sensory interneurons; ventral horn = somatic motor neuron cell bodies. Dorsal root = afferent; ventral root = efferent. DRG houses sensory cell bodies. Ascending tracts (afferent), descending tracts (efferent).

  • Reticular formation: Arousal/sleep, BP control, respiratory rhythms, pain modulation.

  • Cerebrum: Thalamus (relay/integration), Hypothalamus (homeostasis/endocrine control), Pituitary (attached, not part of diencephalon).

  • Association areas: Integrate sensory/motor; lateralization = hemisphere specializations; hippocampus (learning/memory).

  • Meninges/CSF: Dura (tough, venous sinuses), arachnoid, pia; CSF from choroid plexus + ventricles → subarachnoid → arachnoid villi → dural sinuses.

Diagrams You Should Be Able to Draw

  • Response loop with negative vs. positive feedback annotations.

  • Enzyme kinetics curve with saturation/competitive inhibition.

  • Membrane transport map (simple/facilitated/primary/secondary; SGLT vs. GLUT; Na+/K+-ATPase).

  • GPCR cascades (Gs: cAMP/PKA; Gq: IP3/DAG/PKC).

  • Spinal cord cross-section: dorsal/ventral horns/roots; DRG; white vs. gray; ascending/descending tracts.

Common Pitfalls

  • Calling steady state "equilibrium".

  • Confusing hypertonic (shrink) vs. hypotonic (swell).

  • Thinking steroids are stored in vesicles (they are not; synthesized on demand).

  • Mixing receptor-channel with GPCR effects (timing: ion channel = fast vs. slower).

  • Thinking APs signal intensity by amplitude (it's frequency).

  • Misplacing dorsal (sensory) vs. ventral (motor) features.

Quick Answers to "Question-Style" Themes

  • End-product inhibition: Product reduces upstream enzyme activity (Ch.4).

  • ATP synthesis: Converts proton gradient + rotational/kinetic energy into ATP (chemiosmotic theory; Ch.6).

  • Pyruvate + acetyl-CoA: In mitochondria, requires CoA (vit. B5/pantothenic acid) and NAD+ → NADH; CO2 released (Ch.4).

  • GPCR pathways: Activate adenylyl cyclase and PLC; both are amplifiers.

  • Na+ channel inactivation: Rapid, prevents immediate AP restart (Ch.8).

  • Depolarization results if membrane Na+ permeability increases (Ch.8).

  • Microglia: Do not secrete CSF; ependymal cells line ventricles and help with CSF production (Ch.9).

Additional info: These notes expand on the original review sheet by providing definitions, examples, and context for each major topic, and by recreating tables for comparison and classification. All equations are provided in LaTeX format as required.

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