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Human Physiology > Cumulative Final Exam > Flashcards

Cumulative Final Exam Flashcards

1
Q

Electrical Synapse vs. Chemical Synapse

A
  • Electrical Synapse: A synapse allowing the direct conduction of action potentials between adjacent cells via gap junctions (that connect the cells’ cytosols and enable ionic flow).
  • Chemical Synapse: A synapse involving the sequential release (from the presynaptic neuron) and binding (to the postsynaptic neuron) of neurotransmitters within a synaptic cleft to propagate an action potential.

  • Faster Rate of Transmission? Electrical Synapses
  • Capacity for Synchronization? Electrical Synapses
  • Undirectional Signal Transmission? Chemical Synapses
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2
Q

Why do people shiver and feel cold at the start of a fever?

A

The core body temperature (37°C) is below the body set-point temperature (>37°C).

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3
Q

Why do people sweat and feel hot when a fever breaks?

A

The core body temperature (>37°C) is above the body set-point temperature (37°C).

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4
Q

What causes “flow” to occur?

A

“Flow” results from the existence of an electrochemical gradient between two locations.

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5
Q

Relationship: Flow Rate vs. Gradient Magnitude

A

Directly Proportional

  • Larger Gradient = Faster Flow Rate
  • Smaller Gradient = Slower Flow Rate
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6
Q

Relationship: Flow Rate vs. Resistance Magnitude

A

Inversely Proportional

  • Greater Resistance = Slower Flow Rate
  • Less Resistance = Faster Flow Rate
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7
Q

Relationship: Stimulus Strength vs. Action Potential Frequency

A

Directly Proportional

  • Stronger Stimulus = Higher AP Frequency
  • Weaker Stimulus = Lower AP Frequency
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8
Q

Relationship: Graded Potential Size vs. Strength of Stimulus

A

Directly Proportional

  • Stronger Stimulus = Large Gradeded Potential
  • Weaker Stimulus = Smaller Graded Potential
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9
Q

Why is it beneficial for Liver cells to convert Glucose to Glycogen following blood Glucose uptake?

A

Glycogen (polymer) contributes less to intracellular osmolarity than Glucose (monomer), so its formation promotes maximal Glucose uptake from the bloodstream.

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10
Q

Why should dehydrated patients not be treated with IV distilled water?

A

Distilled water is extremely hypotonic to human blood, so its administration into the blood will cause swelling/lysis of red blood cells.

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11
Q

Action: Na+/K+ ATPase

A
  • Out of Cell: 3 Na+
  • Into Cell: 2 K+
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12
Q

Transcellular Concentrations: Na+, K+, Ca2+, Cl–

A
  • Greater [Extracellular]: Na+, Ca2+, Cl–
  • Greater [Intracellular]: K+
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13
Q

What does Vmem = Eion indicate?

A

There is no net flow of the ion across the cell membrane.

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14
Q

Eion

A

Ionic Equilibrium Potential

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15
Q

Neurons: ENa+

A

+60 mV

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16
Q

Neurons: EK+

A

–90 mV

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17
Q

Selectivity vs. Gating

A
  • Selectivity: Allowing the passage of only certain ions through the cell membrane.
  • Gating: Allowin the passage of only certain ions through the cell membrane at particular times.
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18
Q

Leak Channels

A

Selective ion channels (within the cell membrane) that randomly open/close and allow for the passive transport of a particular ion down its electrochemical gradient.

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19
Q

Why does the typical cell have a higher K+ permeability than Na+ permeabilty?

A
  • The typical cell membrane contains more K+ leak channels than Na+ leak channels.
  • K+ leak channels are more leaky than Na+ leak channels.
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20
Q

How do K+ leak channels enable selective passage of K+ ions (and not Na+ ions)?

A

The spacing of negatively charged amino acids within the K+ leak channel pore mimics that of water molecules during K+ ion hydration; it is equally energetically favorable for the K+ ion to be hydrated by water or inside the K+ channel pore.

The spacing of negative amino acids within the K+ leak channel pore is too great to accomodate the smaller Na+ ion; it is more energetically favorable for the Na+ ion to be hydrated by water than to be inside the K+ channel pore.

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21
Q

Typical Cell: Resting Membrane Potential

A

–70 mV

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22
Q

Equilibrium Potential

A

The membrane potential at which the concentration gradient and electrical gradient for an ion are equal in magnitude and opposite in direction; there is no net flow ions across the cell membrane at equilibrium potential.

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23
Q

Graded Potential

A

A small deviation from a cell’s resting membrane potential that brings the membrane into a less polarized (depolarized) or more polarized (repolarized) state.

how

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24
Q

Equation: Driving Force

Ionic Transport

A

DF = Vmem – Eion

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25
Q

What causes an ion’s equilibrium potential to change?

Eion

A

Change in Ionic Concentrations

Nernst Equation

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26
Q

Refractory Periods: Absolute vs. Relative

A
  • Absolute: The time period after the start of an action potential during which the cell cannot generate another action potential, regardless of the size of the depolarizing stimulus.
  • Relative: The time period after the start of an action potential during which the cell can generate another action potential only if the size of the depolarizing stimulus is larger than normal.

Refractory Period: The time period after the start of an action potential during which the excitable cell cannot generate another action potential in response to a normal threshold stimulus.

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27
Q

Why is the absolute refractory period critical for ensuring unidirectional transmission of action potentials?

A

The absolute refractory period restricts the reopening of voltage-gated Na+ channels directly after undergoing an action potential, so the action potential can never flow backwards and/or change directions.

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28
Q

Refractory Periods: Voltage-Gated Na+ Channel

A
  • Absolute RP: The Na+V channel is inactivated (but has not yet returned to the resting state), so it cannot reopen regardless of the depolarization stimulus.
  • Relative RP: The Na+V channel is in its resting state, so it can reopen in response to a larger-than-normal depolaization stimulus.
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29
Q

What causes a fever?

A

A change in the body temperature set point.

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30
Q

What causes a stronger stimulus to produce a larger graded potential?

A

A stronger stimulus will cause ion channels to be open for longer, more ion channels to open at once, and ion channels to reopen sooner (after the initial graded potential has ceased).

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31
Q

Do graded potentials exhibit a refractory period?

A

No

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32
Q

What are graded potentials able to propogate away from the stimulus source in both directions?

A

Graded potentials do not exhibit a (absolute) refractory period, so the graded potential will passively spread to adjacent membrane regions that are more negative than the depolarized region.

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33
Q

Threshold

Neuronal Action Potential

A

–55 mV

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34
Q

What characteristic of the axon hillock enables it to frequently initiate action potentials?

A

The axon hillock possesses a **high density of Na+V channels** that will open near-simultaneously (to produce a large depolarization) if Vmem is increased to threshold.

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35
Q

Neurons: All-or-Nothing Principle

A

If some Na+V channels (in the axon hillock) open in response to membrane depolarization, then many other Na+V channels will also open (to bring about a much larger membrane depolarization)

  • It is impossible to bring about a partial neuronal depolarization via opening of a few Na+V channels; if a few Na+V channels open, then many Na+V channels will ultimately open.
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36
Q

What does the Na+V channel inactivation gate close in response to?

A

Membrane Depolarization

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37
Q

Timing: Na+V Channel Activation/Inactivation

A
  • Activation occurs once the membrane depolarizes to threshold (at the start of the Depolarization phase).
  • Inactivation occurs once the membrane achieves maximum depolarization (at the peak of the action potential).
  • Rest/Reset occurs once the membrane is hyperpolarized to resting membrane potential (at the end of the Hyperpolarization phase).
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38
Q

Timing: K+V Channel Activation/Inactivation

A
  • Activation occurs once the membrane achieves maximum depolarization (at the peak of the action potential).
  • Inactivation occurs once the membrane achieves maximum hyperpolarization (at the minimum Vmem value).
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39
Q

What does the K+V channel inactivation gate open in response to?

A

Membrane Depolarization

The K+V channel opens slower than the Na+V channel, so it is not activated until Na+V channel inactivation occurs.

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40
Q

Why does the [ion]intracellular and [ion]extracellular not significantly change during an action potential?

A

The number of ions crossing the membrane during an action potential is small compared to the total number of numbers inside/outside of the cell; the action of the Na+/K+ Pump easily returns the cell to its resting membrane potential.

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41
Q

Why does the “undershoot” phase of the action potential occur?

A

The Vmem continues to drop to below resting membrane potential due to both **K+V channels** and **K+ leak channels** being open; the very high membrane permeability to K+ ions during/following repolization causes the cell to hyperpolarize too far.

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42
Q

Refractory Periods vs. Voltage-Gated Channels

A
  • The end of the absolute refractory period corresponds to the transition to the Na+V channel reset/resting phase.
  • The end of the relative refractory period corresponds to the transition to the K+V channel inactivated phase.
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43
Q

At which region of the neuron are action potentials initiated?

A

Axon Hillock

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44
Q

Advantages: Myelination

Action Potential Transmission

A
  • Speed of Transmission: Propagation of action potentials occurs faster in myelinated axons than in unmyelinated axons.
  • Energy Usage: Myelinated axons require less energy to propagate action potentials than unmyelinated axons (due to less Na+/K+ ATPase activity).
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45
Q

How does myelin increase the speed of action potential transmission?

A

The action potential “leaps” across long lengths of myelinated axon as current flows (and threshold depolarization occurs) from one node to the next node, so the action potential is transmitted at a much faster rate.

Only the nodes (of Ranviar) are depolarized to threshold in a myelinated axon; all other regions of the axon are covered with myelin, so they do not exhibit Na+V/K+V channel activity.

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46
Q

What factors impact the rate of action potential transmission?

A
  • Axon Diameter: Neurons possessing larger axon diameters will transmit action potentials faster (due to the lower resistance to action potential propagation).
  • Presence of Myelin: Neurons covered with myelin sheath will transmit action potentials faster (due to the energy/spatial efficiency of myelinated axon depolarization).
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47
Q

Mutiple Sclerosis

MS

A

An autoimmune disease that causes progressive degeneration of neuronal myelin sheaths in the CNS; the deterioration of myelin sheaths to scleroses (hardened scars/plaques) slows and short-circuits the conduction of action potentials.

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48
Q

How does Hyperkalemia impact the action potential?

A
  • Easier Depolarization: Hyperkalemia results in a higher resting Vmem value, so the cell is closer to threshold while at rest.
  • Slower Repolarization: Hyperkalemia decreases the K+ ion driving force out of the cell, so return to resting Vmem occurs slower.
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49
Q

What does neurotransmitter binding to the postsynaptic neuron cause (in the postsynaptic neuron)?

A

Graded Potentials

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50
Q

Ionotropic Receptors vs. Metabotropic Receptors

A
  • Ionotropic: Neurotransmitter receptors that possess a neurotransmitter binding site and an ion channel; the channels open in response to correct NT binding to the NT-binding site.
  • Metabotropic: Neurotransmitter receptors that possess a neurotransmitter binding site and a G Protein-linked site; binding of the correct NT to the NT-binding site causes the G Protein to directly/indirectly open another ion channel (or produce another cellular response).
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51
Q

What signal triggers the exocytosis of synaptic vesicles in axon terminals?

A

Increased Intracellular [Ca2+]

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52
Q

Excitatory Postsynaptic Potential vs. Inhibitory Postsynaptic Potential

A
  • EPSP: A stimulus/potential that depolarizes the postsynaptic neuron to brings its Vmem value closer to threshold.
  • IPSP: A stimulus/potential that hyperpolarizes the postsynaptic neuron to brings its Vmem value farther from threshold.
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53
Q

Special Senses vs. General Senses

A
  • General/Somatic Senses: Sensations detected by receptors located throughout the body (including touch, pain, pressure, and position).
  • Special Senses: Sensations detected only by receptors of specialized organs (including taste, smell, hearing, sight, and balance)
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54
Q

Accessory Sensation Structures

A
  • Lens: Focuses Light on Retina.
  • Middle Ear Bones: Transforms Sounds Waves to Pressure Waves.
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55
Q

Where are most reflex sensory pathways integrated?

A

Spinal Cord

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56
Q

Sensation vs. Perception

A
  • Sensation: The conscious/unconscious awareness of stimuli that may or may not involve brain-based integration/interpretation.
  • Perception: The conscious awarenesss and interpretation of stimuli that must involve the brain.
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57
Q

Brain Anatomy: Language

A
  • Broca’s Area: The motor region that receives input from Wernicke’s Area and transmits motor patterns (to the motor cortex) for the activation of speech.
  • Wernicke’s Area: The association region that receives input from the Auditory/Visual Cortex to translate words into thought.
  • Auditory Cortex: The sensory region that receives auditory information and contributes to auditory perception.
  • Visual Cortex: The sensory region that receives visual information and contributes to visual perception.
  • Motor Cortex: The motor region that receives input from Broca’s Area and sends motor commands to muscles needed for speech.
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58
Q

Broca’s Area vs. Wernicke’s Area

A
  • Broca’s Area: Translates Thoughts into Speech
  • Wernicke’s Area: Translates Language Stimuli into Thoughts
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59
Q

Hippocampus: Function

A

Consolidation of information/thoughts into long-term memory (from short-term memory).

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60
Q

Takeaway: H.M. Experiments

A

The Hippocampus is critical for declarative memory, but it not needed for procedural memory.

  • Declarative memory pertains to facts and events.
  • Procedural memory pertains to motor/sequential processes.
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61
Q

Types of Synaptic Plasticity

A
  • Synaptic Pruning: A reduction in synaptic connectivity within the brain that removes unnecessary neurons/synapses.
  • Long-Term Potentiation: A synaptic strengthening process that enhances synaptic transmission within the Hippocampus to improve memory.
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62
Q

Synesthesia

A

The sensation of multiple senses simultaneously that results from the routing (within the brain) of sensory information from unrelated senses.

63
Q

Mechanism: Long-Term Potentiation

A
  1. Glutamate is released from the presynaptic neuron and binds to AMPA/NMDA receptors of the postsynaptic neuron.
  2. Glutamate binding to AMPA receptors enables Na+ to enter (through the AMPA receptors) and depolarize the postsynaptic neuron.
  3. Once sufficient Na+ has entered the postsynaptic neuron, the Mg2+ within the NMDA receptor is displaced to enable Ca2+ entry into the postsynaptic neuron.
  4. Ca2+ activates signaling pathways within the postsynaptic neuron that increase AMPA receptor production/sensitivity and presynaptic Glutamate release.
64
Q

Which Neurotransmitter-Receptor pairing is always found in ganglionic synapses?

A
  • Neurotransmitter: Acetylcholine
  • Receptor: Nicotinic Receptor

  • All preganglionic (sympathetic and parasympathetic) neurons release the Acetylcholine neurotransmitter.
  • All postganglionic (sympathetic and parasympathetic) neurons possess Nicotinic receptors.
65
Q

Which Neurotransmitter-Receptor pairing is always found at the neuromuscular junction?

A
  • Neurotransmitter: Acetylcholine
  • Receptor: Nicotinic Receptor

The somatic motor neuron releases Acetylcholine into the synaptic cleft; the skeletal muscle fiber possesses Nicotinic ACh receptors on its motor end plate.

66
Q

Which receptor type is involved in most parasympathetic signaling to effectors?

A

Muscarinic Receptors

Muscarininc Acetylcholine Receptors

67
Q

Which neurotransmitter is involved in most parasympathetic signaling to effectors?

A

Acetylcholine

68
Q

Which receptor type is involved in all sympathetic signaling to effectors?

A

Adrenergic Receptors

Exception: Sympathetic signaling to sweat glands involves muscarinic receptors.

69
Q

Which neurotransmitters are involved in all sympathetic signaling to effectors?

A
  • Epinephrine (Adrenaline)
  • Norepinephrine (Noradrenaline)
70
Q

Why is it beneficial for nicotinic receptors to be located at ganglionic synapses?

A

Nicotonic receptors are ionotropic (ion channel) receptors, so they allow for rapid transmission of action potentials at the PNS ganglia.

71
Q

Types of Neurotransmitter Receptors

A
  • Cholinergic: Nicotinic; Muscarinic
  • Adrenergic: Alpha; Beta
72
Q

Types of Cholinergic Receptors

A
  • Nicotinic ACh Receptor (Ionotropic)
  • Muscarinic ACh Receptor (Metabotropic)

All cholinergic receptors bind to Acetylcholine.

73
Q

Adrenergic Receptors: Metabotropic or Ionotropic?

A

Metabotropic

74
Q

Which organs/tissues receive input from only one ANS division?

A

Blood Vessels (Only Sympathetic Input)

Sympathetic input to blood vessels leads to vasoconstriction.

75
Q

Misconception: Only the sympathetic nervous system or the parasympathetic nervous system are active at any given moment.

ANS Misconceptions

A

Reality: Both divisions of the ANS are active at all times, but the extent of their actions varies.

76
Q

Misconception: Activation of a sympathetic/parasympathetic response will affect all organs innervated by that ANS division.

ANS Misconceptions

A

Reality: Specific sympathetic/parasympathetic signaling can be directed toward individual organs (yet there can also be broad activiation of each ANS division).

77
Q

Pheochromocytoma

A

A benign tumor of the adrenal gland that causes the organ to produce excessive quanitities of Epinephrine and Norepinephrine.

78
Q

Efferent Pathways: Somatic vs. Autonomic

A
  • Somatic efferent pathways involve two efferent neurons (connected at a ganglia).
  • Autonomic efferent pathways involve a single efferent neuron (that directly links the CNS to the effector tissue).
79
Q

Scales: Skeletal Muscles

A

Thick/Thin Filaments → Myofibrils → Muscle Fibers → Muscle

80
Q

Components of Sarcomeres

A
  • M Line: The center line of the sarcomere composed of proteins that hold together the thick filaments.
  • Z Disk: The dense protein region that separates adjacent sarcomeres.
  • H Zone: The narrow center region of the sarcomere that contains only thick filament.
  • Zone of Overlap: The region of the A band that possesses thick filament and think filament.
  • I Band: The peripheral regions of the sarcomere that possess only thin filament.
  • A Band The center region of the sarcomere than spans the entire thick filament.
81
Q

How is the anatomy of a skeletal muscle specialized for its function?

A
  • Nuclei: Multinucleation of muscle fibers supports the high protein synthesis demands of the cells.
  • Mitochondria: Abundance of mitochondria enables high rates of ATP production to support the great energy demands of muscles.
  • T-Tubules: Action potentials can be transmitted throughout the muscle cell (and to underlying myofibrils) via T-Tubules.
  • Sarcoplasmic Reticulum: The SR functions as the muscle cell endoplasmic reticulum and a Ca2+</sub> storage/release organelle.
  • Myofibrils: The alternating filamentous structure of myofibril sarcomeres enables muscle cells to contract/shorten.
82
Q

Crossbridge Cycle

Contraction Cycle

A
  1. ATP hydrolysis (to form ADP + Pi) via the Myosin head ATPase cocks/stretches the Myosin head perpendicular to the filaments.
  2. The Myosin head binds to Actin’s myosin-binding site (and subsequently releases the Pi group) to form the crossbridge.
  3. The Myosin head undergoes the power stroke to pull the think filaments across the thick filament (and become 45° to the filaments); ADP is subsequently released from the Myosin head.
  4. ATP binds to the Myosin head ATPase as the Myosin head detaches from the think filament.
83
Q

Mechanism: Muscle Fiber Contraction

A
  1. An action potential is initiated at the NMJ via ACh binding (to Nicotinic ACh receptors) at the motor end plate.
  2. The action potential traverses throughout the muscle fiber via the sarcolemma; T-tubules carry the action potential into the muscle fiber interior to stimulate the release of Ca2+ (from the SR) into the sarcoplasm.
  3. Sarcoplasmic Ca2+ bind to Troponin (attached to Tropomyosin) to cause a Tropomyosin confirmational change that exposes Actin’s myosin-binding sites.
  4. The Myosin head attaches to Actin’s myosin-binding sites and undergoes the crossbridge/contraction cycle.
84
Q

DHPR vs. RyR

Dyhydropyridie Receptor vs. Ryanodine Receptor

A
  • DHPR: An L-type voltage-gated Ca2+ channel located in the T-tubule membrane that triggers the opening of Ryanodine receptors (in response to T-tubule voltage changes).
  • RyR: A Ca2+ release channel located in the SR terminal cisternal membrane that open (in response to DHPR conformational change) to release large amounts of Ca2+ into the sarcoplasm.
85
Q

What causes the termination of muscle fiber contraction?

A

Decrease in Sarcoplasmic [Ca2+]

The sarcoplasmic [Ca2+] is actively transported into the SR via the SERCA protein.

86
Q

SERCA

Sarcoendoplasmic Reticulum Calcium ATPase

A

A primary active transport protein (located in the SR membrane) that pumps sarcoplasmic Ca2+ ions into the SR.

87
Q

Two Ways to Adjust Contraction Strength

A
  • ↑/↓ Number of Contracting Fibers
  • ↑/↓ Each Fiber’s Contraction Strength
88
Q

Three Classes of Hormones

A
  • Steroid Hormones (Derived from Cholesterol)
  • Amine Hormones (Derived from Tyrosine)
  • Peptide Hormones (Composed of Polypeptides)
89
Q

Examples: Hormone Classes

A
  • Steroid: Testosterone, Estrogen, Progesterone, Cortisol
  • Amine: Epinephrine, Norepinephrine, Dopamine, Thryoid Hormone
  • Peptide: All Non-Steroidal and Non-Amine Hormones
90
Q

Characteristics: Steroid Hormones

A
  • Synthesis/Storage: Made as Needed (Not Stored)
  • Release from Cell: Simple Diffusion
  • Transport in Blood: Bound to Carrier Proteins (Long Half-Life)
  • Intracellular Response: Slow + Prolonged Responses (Gene Expression)
91
Q

Characteristics: Peptide Hormones

A
  • Synthesis/Storage: Made in Advance (Stored in Vesicles)
  • Release from Cell: Exocytosis
  • Transport in Blood: Dissolved in Blood (Short Half-Life)
  • Intracellular Response: Fast Responses (Signal Transduction)
92
Q

Characteristics: Amine Hormones

A
  • Catecholamines: Behave as Peptide Hormones
  • Thyroid Hormones: Behave as Steroid Hormones (after Secretion)

  • Catecholamines: Epinephrine, Norepinephrine, Dopamine
  • Thyroid Hormones: T3, T4
93
Q

Blood Ca2+ Homeostasis: Low Blood [Ca2+]

A
  1. The Parathyroid gland (via Chief cells) releases Parathyroid hormone in response to low blood [Ca2+].
  2. PTH stimulates the bone resorption activities of Osteoclasts and slows Ca2+ loss in the urine.
  3. PTH stimuluates the kidneys to synthesize Calcitriol to increase Ca2+ absorption from food (within the GI tract).
94
Q

Blood Ca2+ Homeostasis: High Blood [Ca2+]

A
  1. The Thyroid gland (via Parafollicular cells) releases Calcitonin in response to high blood [Ca2+].
  2. Calcitonin inhibits the bone resorption activities of Osteoclasts (to promote bone formation).
95
Q

Tropic Hormone

A

A hormone (released by an endocrine gland) that stimulates hormone release from other endocrine glands.

96
Q

HPA Axis

Hypothalamic-Pituitary-Adrenal Axis

A
  • H: Corticotropin-Releasing Hormone (CRH)
  • P Adrenocorticotropic Hormone (ACTH)
  • A: Cortisol
97
Q

Cushing’s Syndrome

A

An endocrine disorder caused by chronically high levels of cortisol exposure.

98
Q

Anesthesia Terms: Sedation; Analgesia; Amnesia; Muscle Paralysis

A
  • Sedation: Partial/complete loss of consciousness.
  • Analgesia: Prevention of (or relief from) pain sensations.
  • Amnesia: Inability to recall memories of a prior experience.
  • Muscle Paralysis: Inability to undergo motor movements.
99
Q

What is the function of the (papillary muscle + chordae tedineae) complexes?

A

Prevent Valve Prolapse

The (papillary muscle + chordae tedineae) complexes are not responsible for closing/opening the AV valves.

100
Q

Phases: Cardiac Cycle

A
  • Isovolumetric Ventricular Contraction: The ventricles contract (to increase pressure within the ventricles) while the atria return to diastole.
  • Ventricular Ejection: The ventricular pressure sharply rises (to pump blood into the pulmonary/aortic arteries) while the atria remain in systole.
  • Isovolumetric Ventricular Relaxation: The ventricles return to diastole (and ventricular pressure eventually drops below atrial pressure) while the atria remain in diastole.
  • Ventricular Filling: The atria and the ventricles are in diastole and are filling with blood.
  • Atrial Systole: The atria contract (to pump additional blood into the ventricles) while the ventricles remain in diastole.
101
Q

Segments: Electrocardiogram

ECG

A
  • P Wave: Atrial Depolarization
  • P-Q Segment: Atrial Systole
  • QRS Complex: Ventricular Depolarization (Atrial Repolarization)
  • S-T Segment: Ventricular Systole
  • T Wave: Ventricular Repolarization
  • T-S Segment: Ventricular Repolarization
102
Q

Contractile Fibers vs. Autorhythmic Fibers

A
  • Contractile: No Spontaneous Depolarization; High Contraction Capacity; Majority of Heart Tissue
  • Autorhythmic: Undergo Spontaneous Depolarization; Poor Contraction Capacity; Solely Pacemaker Heart Tissue
103
Q

Why are autorhythmic cells able to function as “natural pacemakers”?

A

Autorhythmic muscle fibers are able to spontaneously depolarize.

104
Q

Rates: Cardiac Electrical Conduction

A
  • SA Node: 60–100 BPM
  • AV Node: 40–60 BPM
  • Bundles/Fibers: 25–40 BPM
105
Q

Action Potential Range: Contractile Fibers vs. Autorhythmic Fibers

A
  • Contractile: –90mV to +20mV
  • Autorhythmic: –60mV to +20mV

The contractile fibers possess a stable RMP of –90mV; the autorhythmic fibers possess an unstable/pseudo RMP that spontaneously depolarizes to –40mV.

106
Q

Pacemaker Potential

A

The spontaneous depolarization to threshold (–40mV) within an autorhythmic cardiac fiber.

107
Q

How does an action potential spread from autorhythmic fibers to contractile fibers?

A

Gap Junctions

108
Q

Phases: Autorhythmic Fiber Action Potential

A
  • Pacemaker Potential 1: K+V Channels Close; F-Type Na+V Channels Open
  • Pacemaker Potential 2: F-Type Na+V Channels Close; T-Type Ca2+V Channels Open
  • Depolarization: T-Type Ca2+V Channels Close; L-Type Ca2+V Channels Open
  • Repolarization: L-Type Ca2+V Channels Close; K+V Channels Open
109
Q

Phases: Contractile Fiber Action Potential

A
  • Depolarization: Na+V Channels Open
  • Initial Repolarization: Na+V Channels Close; Fast K+V Channels Open
  • Plateau: Fast K+V Channels Close; Slow K+V Channels Open; L-Type Ca2+V Channels Open
  • Final Repolarization: L-Type Ca2+V Channels Close; K+V Channels Remain Open
110
Q

Opening/Closing: Slow K+V Channels

A
  • Opening: Start of Depolarization
  • Closing: End of Repolarization

The slow K+V channels are activated by depolarization of the contractile fiber membrane, but are not fully open until the start of the repolarization phase.

111
Q

Differences: Skeletal Muscle Action Potential vs. Neuronal Action Potential

A
  • RMP: Lower RMP in Skeletal Muscle (–90mV)
  • Undershoot: No Undershoot in Skeletal Muscle
  • Speed: Slower in Skeletal Muscle
112
Q

Differences: Autorhythmic Fiber Action Potential vs. Neuronal Action Potential

A
  • RMP: No RMP in Autorhythmic Cell
  • Phases: Pacemaker Potential in Autorhythmic Cell
  • Undershoot: No Undershoot in Autorhythmic Cell
  • Speed: Much Slower in Autorhythmic Cell
  • Channels: T-Type Ca2+V + L-Type Ca2+V + F-Type Na+V in Autorhythmic Cell
113
Q

Differences: Contractile Fiber Action Potential vs. Neuronal Action Potential

A
  • RMP: Lower in Contractile Fiber (–90mV)
  • Phases: Initial Repolarization in Contractile Fiber
  • Undershoot: No Undershoot in Contractile Fiber
  • Speed: Much Slower in Contractile Fiber
  • Channels: L-Type Ca2+V + Fast K+V in Contractile Fiber
114
Q

Why do contractile cardiac fibers never exhibit tetanus?

A

Cardiac fiber action potentials possess a long refractory period that prevents summation/tetanus.

115
Q

What causes the skeletal muscle fiber to reach threshold?

A

An influx of Na+ ions into the cell (Nicotinic ACh receptors) occurs following ACh binding to N-ACh receptor at the motor end plate.

116
Q

Ca2+ EC Coupling: Cardiac Contractile Fiber vs. Skeletal Muscle Fiber

Excitation-Contraction Coupling

A
  • Cardiac Fiber: DHPR channels in the T-tubule membrane open to allow Ca2+ (from the extracellular fluid) into the cell; the entering Ca2+ triggers the release of additional Ca2+ from the SR via binding to RyR receptors (in the SR membrane).
  • Skeletal Fiber: DHPR channels in the T-tubule membrane undergo a conformational change (in response to T-tubule depolarization) to open RyR channels; Ca2+ from the SR can enter the sarcoplasm once RyR channels are open.
117
Q

Factors Determining Stroke Volume

A
  • Preload: Amount of Ventricular Stretch (EDV Capacity)
  • Contractility: Strength of Ventricular Contraction
  • Afterload: Amount of Resistance to Ventricular Ejection
118
Q

Control of Cardiac Output: Sympathetic vs. Parasympathetic

A
  • Sympathetic: ↑ Contraction Strength; ↑ Heart Rate.
  • Parasympathetic: ↓ Heart Rate.

The parasympathetic nervous system can only alter heart rate.

119
Q

How does an increase in preload impact the heart’s stroke volume?

A

The greater preload increases the stretch of the ventricles (prior to ventricular diastole), which results in a stronger ventricular contraction (and greater stoke volume).

The rise in preload increases the EDV of the ventricle, which causes the ventricle to contract harder to maintain that ventricle’s the proper ESV value.

120
Q

Blood Pressure Cuff Measurements

A
  • CP > SP: No Sound (No Bloodflow)
  • SP > CP > DP: Sound (Turbulent Bloodflow)
  • DP > CP: No Sound (Laminar/Smooth Bloodflow)
121
Q

What differentiates MAP from CO and TPR?

A
  • MAP is a homeostatically controlled variable.
  • CO and TPR are NOT homeostatically controlled variables.
122
Q

MAP Equation

A

MAP = CO × TPR

123
Q

What factors impact bloodflow resistance?

A
  • Blood Viscosity
  • Vessel Length
  • Vessel Radius
124
Q

Hemostatic Feedback Loop: High Blood Pressure

A
  • Stimulus: Increased Blood Pressure
  • Receptor: Baroreceptor
  • Control Center: Medulla Oblongata
  • Effector: Heart + Blood Vessels
125
Q

Hemostatic Feedback Loop: Low RBC Count

A
  • Stimulus: Decreased RBC/O2</su> Levels
  • Receptor: Kidney Cells
  • Control Center: Proerythroblasts (Bone Marrow)
  • Effector: Erythrocytes
126
Q

Which mechanisms ensure that all fluild filtered from capillaries is eventually returned to the blood?

A
  • Capillary Reabsorption
  • Lymphatic Return
127
Q

What results when capillary filtration exceeds (capillary reabsorption + lymphatic return)?

A

Edema

128
Q

Why do the lungs deflate following penetration into the interpleural space?

A

Atmospheric air flows into the chest cavity (since the pressure in the interpleural space is subatmospheric) and causes the lungs to collapse.

129
Q

Two Components of Residual Volume

A
  • Dead Space: Nasal Cavity, Oral Cavity, Larynx/Pharynx, Trachea, Briochi/Bronchioles
  • Alveolar Space: Non-Bronchial Lung Tissue
130
Q

Respiration: Volumes

A
  • Tidal Volume: The amount of air inhaled/exhaled from the lungs with a typical breath.
  • Inspiratory Reserve Volume: The additional (beyond tidal volume) amount of air that could be inhaled.
  • Expiratory Reserve Volume: The additional (beyond tidal volume) amount of air that could be exhaled.
  • Residual Volume: The additional (beyond ERV) amount of air that remains in the lungs after a maximum exhalation.
131
Q

Respiration: Capacities

A
  • Inspiratory Capacity: The maximum amount of air that can be inhaled into the lungs after a typical exhalation. (TV + IRV)
  • Functional Residual Capacity: The total volume of air that remains in the lungs after a typical exhalation. (ERV + RV)
  • Vital Capacity: The maximum amount of air that can be inhaled into the lungs after maximum exhalation. (TV + IRV + ERV)
  • Total Lung Capacity: The total volume of air in the lungs after a maximum inhalation. (TV + IRV + ERV + RV)
132
Q

Law of Laplace

A
133
Q

What is the functional role of the negative pressure within the interpleural space?

A

The pleural cavity’s negative pressure enables the cavity to function as a vacuum to couple the lungs to the chest wall.

The interpleural negative pressure ensures that an increase/decrease in chest cavity size is accompanied by an expansion/deflation of the lungs.

134
Q

Relationship: [Surfactant] vs. Alveolus Size

A

Inverse

  • Larger Alveolus = Less Surfactant
  • Smaller Alveolus = More Surfactant
135
Q

How does surfactant decrease surface tension within an alveolus?

A

Surfactant disperses the molecules of the alveolar fluid to decrease/disrupt the cohesive forces between water molecules.

136
Q

What can lead to low lung compliance?

A
  • Lung Scar Tissue
  • Pulmonary Edema
  • Surfactant Deficiency
  • Intercostal Muscle Paralysis
137
Q

Compliance

A

A measure of the difficulty/effort required to stretch the lungs.

The more easily the lungs stretch, the greater compliance it possesses.

138
Q

What condition can result in too high lung compliance?

A

Emphysema

139
Q

Treatment: Infant Surfactant Deficiency

A
  • Artificial Surfactant
  • Artificial Ventilation
  • Lung Maturation Steroids
140
Q

Why do the gaseous partial pressures within the alveoli differ from those within the atmosphere?

A

The residual (non-exhaled) air within the alveoli bring about a higher [CO2] and a lower [O2] than in the atmosphere.

141
Q

Carbonic Anhydrase

A

An enzyme expressed in red blood cells that catalyzes the reversible conversion of (CO2 + H2O) into H2CO3.

142
Q

Why is the partial pressure of O2 lower in systemic tissues than in oxygenated blood?

A

The cellular respiration processes within cells depletes intracellular O2 (and produces intracellular CO2).

143
Q

Factors Impacting Hemoglobin–O2 Affinity

A
  • Temperature: ↑ Temperature = ↓ O2 Affinity
  • pH: ↓ pH = ↓ O2 Affinity
  • [CO2]: ↑ [CO2] = ↓ O2 Affinity
144
Q

How are the glomerular capillaries different from other systemic capillaries?

A

The glomerular capillaries are surrounded by podocytes (of the Bowman’s capsule visceral layer) that possess filtration slits.

145
Q

GFR Autoregulation Mechanisms

A
  • Myogenic Mechanism: The smooth muscle cells (of the afferent arteriole) experience greater stretch due to the increased blood pressure; the smooth muscle cells contract to cause vasoconstriction (and decrease GFR).
  • Tubuloglomerular Mechanism: The Macula Densa cells (of the JGA) detect increased ion/water concentrations in the filtrate fluid; the Macula Densa cells secrete less NO to cause vasoconstriction of the afferent arteriole (and decrease GFR).
146
Q

Reabsorption: Proximal Tubule

A
  • Na+/K+ ATPases on the proximal tubule cells’ basolateral membrane maintain a low intracellular [Na+].
  • Na+–Glucose Symporters allow for Glucose transport into proximal tubule cells (via secondary active transport) by pairing to Na+ transport into the cell.
  • Glucose transporters on the proximal tubule cells’ basolateral membrane allow Glucose to move into the blood.
  • Water moves into the blood (via osmosis) in response to mass transport of ions/Glucose into the bloodstream.
147
Q

Reabsorption/Secretion: Late Distal Tubule + Collecting Duct

A
  • Na+/K+ ATPases on the Loop of Henle tubule cells’ basolateral membrane maintain a low intracellular [Na+] and a higher intracellular [K+].
  • K+ Leak Channels on the Loop of Henle tubule cells’ basolateral/apical membrane allow K+ to move into the filtrate or into the interstitial fluid.
  • Na+ Leak Channels on the Loop of Henle tubule cells’ apical membrane enable Na+ to enter into the cell.
  • Water moves into the blood (via osmosis) in response to mass transport of Na+ into the bloodstream.
148
Q

Reabsorption: Ascending Limb (Loop of Henle)

A
  • Na+/K+ ATPases on the Loop of Henle tubule cells’ basolateral membrane maintain a low intracellular [Na+].
  • Na+–K+–2Cl– Symporters allow for Cl– transport into Loop of Henle tubule cells (via secondary active transport) by pairing to Na+ transport into the cell.
  • K+ Leak Channels on the Loop of Henle tubule cells’ apical membrane allow K+ to diffuse move into the filtrate fluid.
  • Cl– Leak Channels on the Loop of Henle tubule cells’ basolateral membrane enable Cl– to move into the blood.
149
Q

What ensures the unidirection flux of Na+ into the blood from the proximal tubule?

A

The Na+/K+ ATPases are expressed only on the basolateral membrane of the proximal tubule cells.

150
Q

Reabsorption: Proximal Tubule

A
  • Na+/K+ ATPases on the proximal tubule cells’ basolateral membrane maintain a low intracellular [Na+].
  • Na+–Glucose Symporters allow for Glucose transport into proximal tubule cells (via secondary active transport) by pairing to Na+ transport into the cell.
  • Glucose transporters on the proximal tubule cells’ basolateral membrane allow Glucose to move into the blood.
  • Water moves into the blood (via osmosis) in response to mass transport of ions/Glucose into the bloodstream.
151
Q

Why is the filtrate fluid leaving the proximal tubule isoosmotic to the blood?

A

Water and solutes are reabsorbed from the proximal tubule, so the relative water/solute concentrations in the filtrate are very similar to those in the blood.

152
Q

Loop of Henle: Descending Limb vs. Ascending Limb

A
  • Descending Limb: Permeable to Water; Impermeable to Ions
  • Ascending Limb: Impermeable to Water; Permeable to Ions

  • Bottom of Loop: The filtrate is hyperosmotic to blood after passing through the descending limb.
  • End of Loop: The filtrate is hypoosmotic to blood after passing through the ascending limb.
153
Q

Descending Limb: Why does H2O diffuse from the filtrate into the blood?

Loop of Henle

A

The renal medulla’s extracellular fluid is highly hyperosmotic relative to the filtrate fluid, so osmosis occurs to move H2O out of the filtrate.

Human Physiology (5 decks)

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