PCOM DO (2025-) > MSK Week 3 > Flashcards

MSK Week 3 Flashcards

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1
Q

Define an ion channel

A

Passive, selective, water-filled membrane pore for ions.

Ion channels facilitate the movement of ions across membranes without the need for energy.

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2
Q

What is a transporter (carrier)?

A

Membrane protein that changes shape, binds and moves substances (passive or active).

Transporters can operate through facilitated diffusion or active transport.

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3
Q

Differentiate between a channel and a transporter

A

Channels = open tunnels (passive); Transporters = revolving doors (bind, use energy).

This distinction highlights the functional differences in how substances are moved across the membrane.

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4
Q

What is the resting membrane potential (RMP)?

A

Stable membrane potential of excitable cell, typically negative inside (-60 to -95mV).

The RMP is crucial for the generation of action potentials.

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5
Q

What creates the resting membrane potential?

A

Unequal ion distribution across membrane creating electrochemical gradient.

This gradient is essential for the excitability of cells.

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6
Q

What is the first factor maintaining RMP?

A

Concentration Gradients maintained by Na+-K+ pump (3 Na+ out, 2 K+ in, active).

This pump is vital for maintaining the ionic gradients across the cell membrane.

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7
Q

What is the second factor affecting RMP?

A

Permeability, with membrane much more permeable to K+ (25-30x) than Na+ via K+ leak channels, causing K+ efflux and negative RMP.

The selective permeability of the membrane is critical for establishing the RMP.

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8
Q

What is depolarization?

A

Membrane potential becomes less negative (or more positive).

This process is essential for the initiation of action potentials.

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9
Q

What is repolarization?

A

Membrane potential returns to resting state after depolarization.

Repolarization restores the resting membrane potential.

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10
Q

What is hyperpolarization?

A

Membrane potential becomes more negative than resting state.

Hyperpolarization makes it less likely for an action potential to occur.

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11
Q

What is the purpose of the Nernst equation?

A

Calculates equilibrium potential (E_ion) for a single ion.

The Nernst equation helps to understand the driving forces acting on ions.

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12
Q

What is the formula for the Nernst equation?

A

E_ion = (61/z) * log(C_out / C_in).

‘z’ is the valence of the ion, and C_out and C_in are the concentrations outside and inside the cell, respectively.

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13
Q

What does the Nernst equation balance?

A

Balances chemical (concentration gradient) and electrical (potential difference) driving forces for no net ion movement.

This balance is crucial for understanding ion behavior across membranes.

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14
Q

True or False: The Nernst equation can be used for multiple ions.

A

False.

The GHK equation is used for actual membrane potential considering multiple ions.

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15
Q

Define electrochemical equilibrium.

A

Chemical gradient pushing ion is balanced by electrical gradient pulling it; no net ion movement.

This state is vital for maintaining homeostasis in excitable cells.

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16
Q

What is the equilibrium potential (E_ion)?

A

Membrane potential at which electrochemical equilibrium for a specific ion is achieved.

E_ion allows us to predict the behavior of ions in physiological conditions.

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17
Q

What is the formula for driving force (DF)?

A

DF = Membrane Potential (Vm) - Equilibrium Potential (E_eq).

The driving force determines the direction and magnitude of ion movement.

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18
Q

When will a cation move outward?

A

When Vm > E_eq (DF is positive).

This principle helps in understanding ion flow during action potentials.

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19
Q

When will a cation move inward?

A

When Vm < E_eq (DF is negative).

The direction of ion flow is influenced by the membrane potential relative to the equilibrium potential.

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20
Q

When will an anion move inward?

A

When Vm > E_eq (DF is positive).

This is contrary to the movement of cations, highlighting the different behaviors of ions.

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21
Q

When will an anion move outward?

A

When Vm < E_eq (DF is negative).

Understanding the movement of anions is crucial for grasping overall ionic dynamics.

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22
Q

What happens when Vm = E_eq?

A

NO NET FLOW (DF is zero).

This state indicates that there is no driving force for ion movement.

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23
Q

Calculate E_Na+ using the Nernst equation.

A

E_Na+ = 61 * log(150/15) = +61 mV.

This calculation is essential for understanding sodium ion behavior in cells.

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24
Q

Calculate E_K+ using the Nernst equation.

A

E_K+ = 61 * log(5/150) ≈ -90 mV.

This value is important for understanding potassium ion behavior in cells.

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25
What are the Na+ concentrations in ECF and ICF?
ECF = 150 mmol/L, ICF = 15 mmol/L. ## Footnote These concentrations are crucial for maintaining the resting membrane potential.
26
What are the K+ concentrations in ECF and ICF?
ECF = 5 mmol/L, ICF = 150 mmol/L. ## Footnote The high intracellular concentration of K+ is fundamental for excitability.
27
Define action potential (AP)
Rapid, brief (~100mV) MP change, cell interior transiently positive. ## Footnote Action potentials are key to neuronal communication and muscle contraction.
28
What are the activation and inactivation gates of the voltage-gated Na+ channel?
Activation (fast opening) and Inactivation (slow closing) gates. ## Footnote These gates regulate sodium ion flow during action potentials.
29
What is the function of the voltage-gated K+ channel?
Single activation gate (slow opening, slower closing). ## Footnote The K+ channel plays a crucial role in repolarization of the membrane.
30
Describe the resting phase of an action potential.
All voltage-gated channels closed. Na+ activation gate closed, inactivation gate open. ## Footnote This phase prepares the cell for potential depolarization.
31
What occurs during the depolarization phase of an action potential?
Threshold (-50 to -55mV). Rapid opening of Na+ activation gates, Na+ influx, MP to +30mV. ## Footnote This phase is critical for the generation of the action potential.
32
What happens during the repolarization phase of an action potential?
Na+ inactivation gates close. Slow opening of K+ channels, K+ efflux. ## Footnote This phase restores the negative membrane potential.
33
What occurs during the hyperpolarization phase of an action potential?
K+ channels slow to close, excess K+ efflux makes MP more negative than rest. ## Footnote Hyperpolarization can inhibit the generation of subsequent action potentials.
34
What is the resting membrane potential for neurons?
-60 to -70 mV. ## Footnote This value indicates the baseline excitability of neurons.
35
What is the resting membrane potential for skeletal muscle?
-85 to -95 mV. ## Footnote Skeletal muscle cells have a more negative resting potential, contributing to their excitability.
36
What is the resting membrane potential for ventricular myocytes?
-80 to -90 mV. ## Footnote The resting potential is crucial for cardiac muscle function.
37
What occurs during ventricular AP Phase 0 (Depolarization)?
Rapid Na+ influx via voltage-gated Na+ channels. ## Footnote This phase initiates the action potential in ventricular myocytes.
38
What characterizes ventricular AP Phase 2 (Plateau)?
Longest phase, balanced Ca2+ influx (L-type channels) and K+ efflux. ## Footnote This plateau phase is essential for preventing tetanus in cardiac muscle.
39
What is the clinical significance of the ventricular AP plateau?
Ca2+ channel blockers target this phase. Prevents summation/tetanus, allows effective pumping. ## Footnote Understanding this phase is crucial for cardiac pharmacology.
40
What are the ventricular AP refractory periods?
ARP (no AP during depol/plateau due to Na+ inactivation); RRP (strong stimulus can fire). ## Footnote Refractory periods are important for determining the timing of action potentials.
41
What is the resting membrane potential for the SA node?
No stable RMP due to automaticity. ## Footnote This characteristic allows the SA node to act as a pacemaker.
42
What occurs during SA Node AP Phase 4 (Pacemaker Potential)?
Slow depolarization from Na+ influx via funny (If) channels, decreased K+ efflux, T-type Ca2+ influx. ## Footnote This phase is crucial for the initiation of action potentials in the heart.
43
What happens during SA Node AP Phase 0 (Depolarization)?
Voltage-gated L-type Ca2+ channels open, Ca2+ influx. ## Footnote This phase contributes to the rapid depolarization of the SA node.
44
What is the sympathetic effect on heart rate?
Increases depolarization rate, AP frequency, decreases threshold → INCREASES HR. ## Footnote This effect is mediated by neurotransmitters like norepinephrine.
45
What is the parasympathetic effect on heart rate?
Decreases depolarization rate, AP frequency, increases threshold → DECREASES HR. ## Footnote This effect is mediated by acetylcholine.
46
Where is the slowest conduction velocity in the heart?
AV node, allows for ventricular filling. ## Footnote This delay is critical for proper cardiac function.
47
What are the advantages of X-ray imaging?
Quick, inexpensive, excellent resolution.
48
What are the disadvantages of X-ray imaging?
Radiation, limited views, poor soft tissue detail.
49
What are the advantages of CT imaging?
Detailed evaluation of complex fractures.
50
What are the disadvantages of CT imaging?
Radiation, metallic artifact, inferior intra-articular contrast to MRI.
51
What are the advantages of MRI imaging?
Gold standard for soft tissues (rotator cuff, labrum, ligaments), excellent cartilage/marrow/joint detail, uses intra-articular contrast.
52
What are the disadvantages of MRI imaging?
Motion/artifact in hand/fingers.
53
What are the advantages of ultrasound (US) imaging?
Good for rotator cuff, biceps tendon, procedures, excellent for venous imaging (Doppler).
54
What are the disadvantages of ultrasound (US) imaging?
Limited visualization of labrum, joint space, cartilage.
55
What is the first line imaging modality for acute pain/trauma?
X-ray ALWAYS.
56
What imaging modality is used for complex/questionable fractures after X-ray?
CT for detailed evaluation.
57
What is the gold standard for soft tissue evaluation (rotator cuff, labrum, ligaments)?
MRI.
58
What imaging modality is used for shoulder fracture/dislocation/arthritis?
X-ray.
59
What imaging modality is used for shoulder soft tissue (RC, labrum, cartilage)?
MRI.
60
What imaging modality is used for shoulder RC/biceps tendon/procedures?
US.
61
What is the initial assessment imaging for the elbow?
X-ray.
62
What imaging modality is frequently used for elbow ligaments/tendons/joint space?
MRI.
63
What is the initial assessment imaging for the hand/wrist?
X-ray (best first line).
64
What imaging modality is used for hand/wrist soft tissue?
MRI (despite artifact).
65
Is CT imaging recommended for hand/wrist assessments?
Not great, do not order.
66
What are the standard X-ray views for the shoulder?
AP internal rotation, AP external rotation, Scapular Y view.
67
What is the 'light bulb' sign associated with?
Shoulder internal rotation X-ray.
68
What is the purpose of the scapular Y view?
Evaluates for dislocation, scapula fracture.
69
What should the anterior humeral line pass through on an elbow lateral view?
Middle 1/3 of capitellum.
70
What does the radiocapitellar line bisect?
Radial shaft, passes through capitellum on all views.
71
What is considered an abnormal elbow fat pad?
Posterior fat pad (always abnormal); significantly raised anterior fat pad.
72
What does CRITOE stand for in pediatric elbow ossification?
Capitellum (1), Radial head (3), Medial epicondyle (5), Trochlea (7), Olecranon (9), Lateral epicondyle (11).
73
What tendons make up the MRI shoulder rotator cuff?
Supraspinatus, infraspinatus, teres minor (greater tuberosity); Subscapularis (lesser tuberosity).
74
Where does the biceps tendon attach?
Superior labrum.
75
What are the identified upper extremity venous structures on ultrasound?
Internal jugular, subclavian, axillary, brachial, cephalic, basilic veins.
76
Where is the most common location for a clavicle fracture?
Most commonly mid-shaft.
77
What characterizes an AC Joint Rockwood Type 3 injury?
Clavicle elevated above acromion, AC + CC ligament rupture.
78
What type of glenohumeral dislocation is most common?
>90% anterior inferior (abduction/external rotation).
79
What are rare causes of posterior GH dislocation?
Seizure, electrocution.
80
What is Hill-Sachs deformity associated with?
Glenohumeral dislocation, especially in older patients.
81
Which tendon is most commonly involved in rotator cuff injuries?
Supraspinatus.
82
What is the most common elbow fracture in adults?
Radial head.
83
What is the most common elbow fracture in pediatric patients?
Supracondylar aspect of humerus.
84
What characterizes a distal radius Colles fracture?
FOOSH, dorsal angulation, extra-articular.
85
What characterizes a distal radius Smith fracture?
Fall with wrist in flexion, volar displacement, extra-articular.
86
What is a torus fracture?
Pediatric buckle fracture.
87
What is the most common carpal fracture?
Scaphoid.
88
What complication can arise from a missed scaphoid fracture?
Avascular necrosis due to precarious blood supply.
89
What is the most common metacarpal fracture?
5th MC (Boxer's fracture).
90
What is mallet finger?
Distal phalanx injury.
91
What is the preferred imaging modality for venous structures?
Ultrasound with Doppler.
92
What technique is used in venous imaging?
With/without compression, augmentation documented.
93
What three bones form the hip bone?
Ilium, ischium, pubis
94
What structures form the pelvis?
Sacrum and paired hip bones
95
What are the key landmarks of the femur?
Head, neck, greater trochanter, lesser trochanter, intertrochanteric line, gluteal tuberosity
96
What articulates with the acetabulum in the hip joint?
Femoral head (with fovea)
97
Name the key ligaments of the hip joint.
Iliofemoral, Pubofemoral, Ischiofemoral, Ligamentum Teres
98
What is the Orbicular Zone in relation to hip joint ligaments?
Deep capsular fibers circling the femoral neck, NOT a true ligament
99
What is the primary blood supply to the femoral head?
Medial Circumflex Femoral Artery
100
What happens in a femoral neck fracture?
Disrupts Medial Circumflex Femoral Artery, causing avascular necrosis of femoral head
101
What arteries branch from the Internal Iliac Artery to supply the gluteal region?
Superior Gluteal, Inferior Gluteal, Internal Pudendal arteries
102
How many genicular branches does the popliteal artery have?
5
103
What are the genicular branches around the knee?
Superior and Inferior Medial & Lateral Geniculars, and the Middle genicular arteries
104
Which muscles are innervated by the Superior Gluteal Nerve?
Gluteus Medius, Gluteus Minimus, Tensor Fascia Lata
105
What is the innervation of the Gluteus Maximus?
Inferior Gluteal Nerve
106
What two nerves does the Sciatic Nerve divide into?
Tibial Nerve and Common Fibular (Peroneal) Nerve
107
What muscles are innervated by the Tibial Nerve?
Hamstrings (Semitendinosus, Semimembranosus, Biceps Femoris long head), Adductor Magnus
108
Which muscle is innervated by the Common Fibular Nerve?
Biceps Femoris short head
109
Why is the pirifomis muscle consider the "key to the gluteal region" anatomically?
All neurovascularature superior to the piriformis are named superiorly and vice versa.
110
What syndrome can irritate the sciatic nerve?
Piriformis syndrome
111
What are the actions and innervation of Gluteus Maximus?
Powerful hip extension, lateral rotation; Innervated by Inferior Gluteal Nerve
112
What is the action and innervation of Gluteus Medius and Minimus?
Hip abduction, medial rotation; Innervated by Superior Gluteal Nerve
113
What is the mnemonic for the deep gluteal lateral rotators?
PGOGOQ (Patched Goods Often Go On Quilts) P: iriformis G: emellus superior O: bturator internus G: emellus inferior O: bturator externus Q: uadratus femoris
114
What is the general action and innervation of the hamstrings?
Extend the hip, flex the knee; Innervated by Sciatic Nerve (Tibial Division)
115
What is the unique characteristic of the Biceps Femoris Short Head?
Does NOT originate from ischial tuberosity; Innervated by Common Fibular Division
116
What forms the superolateral boundary of the popliteal fossa?
Biceps Femoris
117
What forms the superomedial boundary of the popliteal fossa?
Semimembranosus
118
What forms the inferolateral boundary of the popliteal fossa?
Lateral Head of Gastrocnemius
119
What forms the inferomedial boundary of the popliteal fossa?
Medial Head of Gastrocnemius
120
What are the boundaries of the popliteal fossa?
Biceps femoris, semimembranosus, lateral and medial heads of the gastrocnemius
121
What are the contents of the popliteal fossa from superficial to deep?
Small Saphenous Vein, Tibial Nerve, Common Fibular Nerve, Popliteal Vein, Popliteal Artery ## Footnote superficial to deep: nerve -> vein -> artery (NVA)
122
What is the mnemonic for the contents of the popliteal fossa?
S T F P P (Small Saphenous Vein, Tibial Nerve, Common Fibular Nerve, Popliteal Vein, Popliteal Artery)
123
What is a clinical risk associated with knee dislocation?
High risk for popliteal artery injury
124
What is the role of myelination?
Fatty sheath on axons, increases conduction velocity ## Footnote In the CNS, myelination is performed by oligodendrocytes, while in the PNS, it is done by Schwann cells.
125
What is saltatory conduction?
AP 'jumps' between Nodes of Ranvier, increases conduction speed ## Footnote Current slides through myelinated segments, AP regenerates only at nodes.
126
How does saltatory conduction compare to contiguous conduction?
Saltatory conduction is fast; contiguous conduction is slow and depolarizes the entire membrane ## Footnote Saltatory conduction occurs in myelinated fibers, while contiguous conduction occurs in unmyelinated fibers.
127
What factors affect conduction velocity?
Bigger axon diameter, myelination, warmer temperature ## Footnote Less resistance and faster conduction are observed with larger diameters and myelination.
128
What is the direction of action potential (AP) propagation?
Orthodromic (soma to terminal) ## Footnote The refractory period prevents back-propagation as the area is 'reloading'.
129
What are demyelinating diseases?
Diseases that attack myelin, slow or block conduction ## Footnote An example is Multiple Sclerosis, which disrupts normal nerve function.
130
What do voltage-gated Na+ channel blockers do?
Block Na+ channels from outside ## Footnote Examples include Tetrodotoxin (TTX), Ciguatoxins, and Saxitoxin.
131
What are graded potentials?
Local, small changes (10-20mV) that vary with stimulus ## Footnote They spread passively and can summate to reach AP threshold.
132
What is an excitatory postsynaptic potential (EPSP)?
Na+ influx that depolarizes the postsynaptic membrane ## Footnote It brings the membrane closer to firing threshold.
133
What is an inhibitory postsynaptic potential (IPSP)?
Cl- influx or K+ efflux that hyperpolarizes the postsynaptic membrane ## Footnote It moves the membrane further from firing threshold.
134
What is an end plate potential (EPP)?
Generated at the NMJ, involves ACh binding to nAChRs ## Footnote It results in a massive Na+ influx.
135
What is the key difference between EPP and EPSP?
EPPs are larger and always suprathreshold, guaranteeing a muscle AP ## Footnote This is due to more neurotransmitter, larger surface area, and more channels.
136
What generates receptor (generator) potentials?
Stimulus in sensory receptors during sensory transduction ## Footnote They are similar to EPSPs, such as Na+ influx in mechanoreceptors.
137
What is the first step in the neurotrasmission sequence?
AP arrives at presynaptic terminal
138
What happens in step 2 of the neurotrasmission sequence?
Depolarization opens voltage-gated Ca2+ channels
139
What occurs in step 3 of the neurotrasmission sequence?
Ca2+ rushes into presynaptic terminal
140
What happens in step 4 of the neurotrasmission sequence?
Ca2+ binds Synaptotagmin on vesicles
141
What is the role of Synaptotagmin in neurotransmission?
Interacts with SNARE complex proteins to facilitate neurotransmitter release
142
What is the effect of Tetanus and Botulinum toxins on neurotransmission?
They cleave SNARE proteins, blocking neurotransmitter release ## Footnote This is significant for board examinations.
143
What occurs in step 6 of the neurotrasmission sequence?
Vesicles fuse and dump neurotransmitter into the cleft via exocytosis
144
What happens in step 7 of the neurotrasmission sequence?
Neurotransmitter diffuses and binds postsynaptic receptors
145
What is generated in step 8 of the neurotrasmission sequence?
Ion flow generates graded potential (EPSP/IPSP)
146
What are voltage-gated channels?
Channels that open/close due to membrane potential changes ## Footnote They are crucial for action potential generation.
147
What do voltage-gated Na+ channels do?
Open quickly for Na+ influx during depolarization
148
What is the function of voltage-gated K+ channels?
Open slowly for K+ efflux during repolarization/hyperpolarization
149
What triggers the opening of voltage-gated Ca2+ channels?
Depolarization in presynaptic terminals
150
What are ligand-gated receptors?
Receptors that open/close when specific ligands bind ## Footnote They mediate synaptic transmission on postsynaptic membranes.
151
What are ionotropic receptors?
Receptor is the ion channel; ligand binding opens the channel quickly ## Footnote Example: Nicotinic AChRs.
152
What are metabotropic receptors (GPCRs)?
Receptors that activate G-proteins and start second messenger cascades ## Footnote They are slower and have longer-lasting effects. Example: Muscarinic AChRs.
153
What is the structure of the presynaptic terminal at the NMJ?
Motor neuron axon terminal with ACh vesicles and voltage-gated Ca2+ channels
154
What is the synaptic cleft (at the NMJ)?
A 10-20nm gap containing a basal lamina and Acetylcholinesterase (AChE). ## Footnote AChE rapidly hydrolyzes (breaks down) ACh into acetate and choline to terminate the signal.
155
What characterizes the postsynaptic membrane at the NMJ?
Motor End-Plate with deep folds and packed with nAChRs
156
What is the function of ACh at the NMJ?
Causes massive Na+ influx, generating suprathreshold EPP leading to muscle AP
157
What is curare (d-tubocurarine)?
Reversible antagonist to nAChRs, blocking ACh binding and preventing muscle contraction ## Footnote It causes paralysis.
158
What is the effect of botulinum toxin (Botox)?
Cleaves SNARE proteins, preventing ACh release, resulting in flaccid paralysis
159
What does alpha-latrotoxin (Black Widow Venom) cause?
Uncontrolled ACh exocytosis leading to spasms, ACh depletion, and respiratory paralysis
160
What are organophosphates?
Irreversible AChE inhibitors causing ACh accumulation and overstimulation of receptors ## Footnote This can lead to respiratory failure by preventing diaphragm repolarization.
161
What is myasthenia gravis?
Autoimmune disorder where antibodies attack/reduce nAChRs, causing muscle weakness ## Footnote Symptoms worsen with activity and include ptosis and facial paralysis.
162
How is myasthenia gravis treated?
Reversible AChE inhibitors increase ACh duration in the cleft, boosting binding to remaining receptors
163
What is the integrated sequence of neuron-to-muscle AP?
1. Motor neuron AP 2. Ca2+ influx 3. ACh release 4. ACh binds nAChRs 5. Na+ influx generates EPP 6. EPP activates Na+ channels in muscle 7. Muscle AP propagates 8. Muscle contraction 9. AChE breaks down ACh
164
What is a sarcomere?
Smallest contractile unit, Z line to Z line.
165
What is the A band?
Entire length of thick (myosin) filament; does not change width during contraction.
166
What is the I band?
Contains only thin (actin) filaments; shortens during contraction.
167
What is the H zone?
Central A band, only thick filaments; shortens during contraction.
168
What is the myosin head in skeletal muscle?
Has actin-binding site & myosin ATPase site.
169
What is the function of tropomyosin?
Blocks myosin-binding sites on actin in relaxed muscle. The bouncer.
170
What does Troponin C (TnC) do?
Binds Ca2+.
171
What is key to unblocking actin-myosin binding sites?
Ca2+ binding to TnC.
172
What is the function of titin?
Elastic protein, anchors thick filament, contributes to passive tension.
173
What is the Sliding Filament Theory?
Thick and thin filaments slide past each other, sarcomere shortens, filaments do not shorten.
174
What is the resting state of myosin?
'Cocked' with ADP + Pi bound, tropomyosin blocking actin.
175
What role does calcium play in binding?
Ca2+ binds TnC, shifting tropomyosin to expose actin-binding sites.
176
What is the Power Stroke?
Myosin binds actin, Pi & ADP released, myosin head pivots, pulling thin filament inward.
177
What is the role of ATP in detachment?
Fresh ATP binds to myosin head, decreasing affinity for actin and causing detachment.
178
What is Rigor Mortis?
Lack of ATP prevents myosin-actin detachment, leading to muscle stiffness.
179
What occurs during re-cocking of myosin?
ATP hydrolysis (by myosin ATPase) into ADP + Pi re-energizes ('cocks') myosin head.
180
What is the mechanism of muscle relaxation?
Cytoplasmic Ca2+ removed by SERCA pump (requires ATP) back into SR; tropomyosin re-blocks actin sites.
181
What is the function of T-tubules?
Propagate muscle AP deep into fiber.
182
What is the DHP receptor?
Located on T-tubule membrane, activated by AP, mechanically linked to RyR.
183
What is the Ryanodine receptor (RyR)?
Ca2+ release channel on SR, opened by DHP activation.
184
What is the source of Ca2+ release?
Sarcoplasmic Reticulum (SR) is muscle's internal Ca2+ store, releases into sarcoplasm.
185
What is a Single Twitch?
Single AP → brief contraction + complete relaxation.
186
What is Twitch Summation?
Repeated stimulation before full relaxation → stronger contraction (elevated Ca2+).
187
What is Complete (Fused) Tetanus?
High-frequency stimulation, no relaxation → smooth, maximal sustained contraction (steadily high Ca2+).
188
What is Optimal Sarcomere Length (L$_o$)?
Length at which maximal active tension can be generated due to maximal filament overlap.
189
What is the Force-Velocity Relationship?
Inverse relationship between force generated and velocity of shortening.
190
When does max velocity of shortening occur?
Occurs with zero load.
191
When does max force (load) occur?
Occurs with zero velocity (isometric contraction).
192
What is an isometric contraction?
Muscle generates tension but does not change length.
193
What is an eccentric contraction?
Muscle lengthens while still generating force (e.g., lowering a weight slowly).
194
What mechanisms vary force production?
* Motor unit recruitment * Frequency of stimulation (summation/tetanus) * Sarcomere length * Fiber type/thickness * Fatigue
195
What is a Motor Unit?
A single motor neuron and all the muscle fibers it innervates.
196
What is Motor Unit Recruitment (Size Principle)?
Smaller motor units (Type I) recruited first for low force; larger units (Type IIa, then IIx) recruited as more force is needed.
197
Why is the Size Principle important?
Smaller motor neurons have lower excitation thresholds, fire first.
198
What are Slow-Oxidative (Type I) Fibers?
Slow speed, high fatigue resistance, oxidative metabolism (many mitochondria, high myoglobin → red), low force, recruited first.
199
What is the function of Slow-Oxidative (Type I) Fibers?
Postural.
200
What are Fast-Glycolytic (Type IIx) Fibers?
Fast speed, low fatigue resistance, anaerobic glycolysis (few mitochondria, low myoglobin → white), high force, recruited last.
201
What is the function of Fast-Glycolytic (Type IIx) Fibers?
Burst power.
202
What is the Creatine Phosphate System?
Provides rapid ATP burst, lasts 8-10 seconds.
203
What is the Lactic Acid System (Anaerobic)?
Provides ATP for 1-3 minutes, produces lactate and H+, contributes to fatigue.
204
What is ATP crucial for?
* Myosin detachment * Re-cocking * SERCA pump (Ca2+ reuptake) * Na-K pump
205
What are the causes of fatigue?
Buildup of H+, Pi, ADP inhibiting cross-bridge cycling and slowing velocity.
206
What is the primary blood supply to the femoral head?
Medial Circumflex Femoral Artery (branch of Deep Femoral Artery) ## Footnote Damage to this artery can lead to avascular necrosis of the femoral head.
207
What are the major venous drainage pathways of the thigh?
Great Saphenous Vein (superficial) & Femoral Vein (deep) ## Footnote Profunda Femoris Vein drains into Femoral Vein, crucial for DVT understanding.
208
Which muscles are innervated by the femoral nerve (L2, L3, L4) motor function?
Quadriceps Femoris, Sartorius, Pectineus, Iliacus ## Footnote Mnemonic: 'Fear Quaking Iliac Sartorius Pain' (Femoral, Quadriceps, Iliacus, Sartorius, Pectineus).
209
What is the cutaneous innervation provided by the femoral nerve?
Anterior thigh sensation
210
Which muscles are innervated by the obturator nerve (L2, L3, L4) motor function?
Most Adductor muscles (Longus, Brevis, Magnus, Gracilis), Obturator Externus ## Footnote Adductor Magnus has dual innervation: Obturator Nerve AND Tibial Nerve (L4 component).
211
What is the cutaneous innervation provided by the obturator nerve?
Medial aspect of thigh sensation
212
What is considered the strongest hip flexor?
Iliopsoas (Iliacus + Psoas Major) ## Footnote Inserts on Lesser Trochanter.
213
What is unique about the rectus femoris compared to other quadriceps heads?
Only quadriceps head that crosses the hip joint and flexes the hip
214
What are the main knee extensors?
Quadriceps Femoris (all four heads) ## Footnote Innervated by Femoral Nerve (L2, L3, L4).
215
What is the primary innervation for adductor muscles?
Obturator Nerve (L2, L3, L4)
216
What are the characteristics of the gracilis muscle?
Most superficial and medial adductor, inserts on Pes Anserinus
217
What is the function of hip flexors during gait?
Crucial for preswing and initial/mid-swing phases to advance the limb
218
What role do quadriceps play in gait?
Vital for loading response, preventing knee collapse, initiating extension
219
What is the superior boundary of the femoral triangle?
Inguinal Ligament ## Footnote Mnemonic: SAIL
220
What is the medial boundary of the femoral triangle?
Adductor Longus muscle ## Footnote Mnemonic: SAIL
221
What is the lateral boundary of the femoral triangle?
Sartorius muscle ## Footnote Mnemonic: SAIL
222
What forms the floor of the femoral triangle?
Iliopsoas and Pectineus muscles ## Footnote Mnemonic: SAIL
223
What are the contents of the femoral triangle (lateral to medial)?
NAVEL: Nerve (Femoral), Artery (Femoral), Vein (Femoral), Empty space (Femoral Canal w/ Lymphatics) ## Footnote Mnemonic: SAIL
224
What does the femoral sheath contain?
Femoral Artery, Femoral Vein, Femoral Canal (Lymphatics) ## Footnote Does NOT contain the Femoral Nerve.
225
What are the boundaries of the adductor canal (Hunter's/Subsartorial)?
Anterior/Lateral: Vastus Medialis; Posterior: Adductor Longus/Magnus; Medial/Roof: Sartorius
226
What does the adductor canal contain?
Femoral Artery, Femoral Vein, Saphenous Vein, Nerve to Vastus Medialis
227
What is the significance of the adductor hiatus?
Femoral Artery passes through Adductor Magnus to become Popliteal Artery ## Footnote Prime site for compression.
228
What is the function of the MCL (Tibial Collateral Ligament)?
Resists valgus stress (lateral force, pushes knee inward) ## Footnote Often injured together with the medial meniscus.
229
What is the function of the LCL (Fibular Collateral Ligament)?
Resists varus stress (medial force, pushes knee outward) ## Footnote Separated from the lateral meniscus.
230
What is the function of the ACL (Anterior Cruciate Ligament)?
Prevents tibia from sliding anteriorly relative to femur ## Footnote Commonly torn in sports.
231
What is the function of the PCL (Posterior Cruciate Ligament)?
Prevents tibia from sliding posteriorly relative to femur ## Footnote Stronger, less commonly injured than ACL.
PCOM DO (2025-)
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