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First Aid > Musculo/Derm 2 > Flashcards

Musculo/Derm 2 Flashcards

1
Q

What is Spondylolisthesis?

A

Forward displacement of one vertebra over another

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2
Q

What is Spondylosis?

A

Degeneration of the spinal column

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3
Q

Spinal Stenosis occurs mainly due to?

A

Increasing age

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4
Q

What 3 processes occur in Spinal Stenosis?

A
  • Intervertebral discs shrink → narrows foramen
  • Facet joints rub against each other → arthritis → bone spurs
  • Ligamentum flavum hypertrophies
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5
Q

What posture narrows the lumbar canal?

A

Standing straight

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6
Q

Spinal stenosis causes what symptom?

A

Neurogenic Claudication

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7
Q

What is Neurogenic Claudication? What are 2 clinical features?

A
  • Leg pain with walking in spinal stenosis
  • Persists with standing, improves with stooped/flexed posture
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8
Q

What are the motor and sensory innervations of the Sciatic nerve (not including branches)?

A

Motor: Muscles of posterior thigh + Hamstring portion of adductor magnus
Sensory: No direct sensory functions

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9
Q

What are the 3 Hamstring muscles?

A

Biceps femoris (lateral), Semimembranosus, Semitendinosus

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10
Q

What are the 3 main functions of the Hamstring muscles?

A

Knee flexion, hip extension, hip rotation (minor)

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11
Q

What is Sciatica?

A

Clinical syndrome used to describe low back pain radiating along the path of the sciatic nerve (lumbar radiculopathy)

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12
Q

What is a common cause of Sciatica?

A

Herniated disk

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13
Q

What are 3 causes of Complete Sciatic neuropathy?

A
  • Hip fracture or dislocation
  • Hip replacement therapy
  • Prolonged compression (coma/bed rest)
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14
Q

Posterior hip dislocations commonly cause?

A

Sciatic neuropathy

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15
Q

Severe Sciatic neuropathy can lead to what symptoms?

A
  • Hamstring muscle weakness
  • Foot drop (common peroneal nerve)
  • Sensory loss in lower leg/foot
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16
Q

Herniated disc at L4/L5 lead to compression of which nerve?

A

Bottom, L5

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17
Q

What is the most common Radiculopathy Syndrome? This is usually due to?

A

L5, herniated disc at L4/L5

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18
Q

L5 nerve compression will cause what symptoms?

A
  • Back pain down lateral leg
  • Weak foot dorsiflexion, toe extension → Difficult walking on heels
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19
Q

What is the 2nd most common Radiculopathy Syndrome?

A

S1 nerve root

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20
Q

S1 Nerve compression leads to what symptoms?

A
  • Pain down back of leg
  • Weakness plantar flexion → Difficulty standing on toes
  • Ankle reflex lost
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21
Q

L5 nerve root compression mainly involves what nerve?

A

Common peroneal

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22
Q

S1 nerve root compression mainly involves what nerve?

A

Tibial nerve

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23
Q

L2/L3/L4 nerve roots compression mostly involves what nerve?

A

Femoral

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24
Q

L2/L3/L4 nerve roots compression lead to what symptoms?

A
  • Pain to anterior thigh and knee
  • Weak hip flexion and knee extension
  • Reduced knee (patellar) reflex
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25
Q

What is Lasègue’s sign?

A

Worsening back pain with straight leg raise

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26
Q

What are Major flexors of the hip joint?

A
  • Iliopsoas
  • Sartorius
  • Pectinius
  • Tensor fasciae latae
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27
Q

What are Major Extensors of the hip joint?

A

Gluteus maximus, Hamstrings: Semimembranosus, semitendinosus, Biceps femoris

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28
Q

What are Major Abductors of the hip joint?

A

Gluteus medius, Gluteus minimus

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29
Q

What are Major Adductors of the hip joint?

A
  • Adductor magnus
  • Adductor longus
  • Adductor brevis
  • Pectineus, gracilis
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30
Q

What are 4 muscles involved in External rotation of the hip joint?

A
  • Gluteus maximus
  • Obturator internus
  • Gemellus superior/inferior
  • Quadratus femoris
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31
Q

What are 7 muscles involved in Internal rotation of the hip joint?

A

Gluteus medius/minimus, Tensor fasciae latae, Adductor longus/brevis, Posterior head of adductor magnus, Pectineus

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32
Q

Superior Gluteal Nerve is derived from?

A

Sacral plexus (L4-S1)

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33
Q

Superior Gluteal Nerve supplies what 3 muscles?

A
  • Gluteus minimus/medius (abductors)
  • Tensor fasciae latae (flexor)
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34
Q

Superior Gluteal Nerve is sometimes injured by _____. What can be done to prevent this?

A
  • IM injection to buttocks
  • Inject in upper, outer quadrant to avoid injury
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35
Q

What is a classic finding of Superior Gluteal Nerve injury?

A

Trendelenburg sign

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36
Q

What is the Trendelenburg sign?

A

Weight bearing leg cannot maintain balance → Pelvis tilts with walking

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37
Q

What does the Inferior Gluteal Nerve supply?

A

Gluteus maximus

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38
Q

Inferior Gluteal Nerve injury presents with difficulty?

A

Standing from sitting position

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39
Q

Inferior Gluteal Nerve is rarely injured by?

A

Pelvic masses

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40
Q

Avascular Necrosis is common at the?

A

Femoral head

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41
Q

What is the most common complaint of Avascular Necrosis? What other symptoms are present?

A
  • Groin pain
  • Leg and thigh pain, difficulty bearing weight
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42
Q

Avascular Necrosis is often caused by?

A

Trauma (femoral head fracture)

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43
Q

What is the major blood supply to the Femoral head? What artery is it from?

A
  • Medial circumflex femoral artery
  • Femoral profunda artery
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44
Q

Damage to Medial circumflex femoral artery leads to?

A

Avascular necrosis

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45
Q

What are non-traumatic causes of Avascular necrosis?

A
  • Steroid therapy
  • SLE
  • Heavy alcohol consumption
  • Sickle cell anemia
  • Gaucher disease (lysosomal storage disease)
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46
Q

What is the most common hip disorder in adolescence?

A

Slipped Capital Femoral Epiphysis

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47
Q

What is Slipped Capital Femoral Epiphysis?

A

Fracture through growth plate → Slippage of overlying end of femur

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48
Q

Slipped Capital Femoral Epiphysis can lead to?

A

Avascular necrosis

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49
Q

What is Legg-Calvé-Perthes Disease? What is it caused by?

A
  • Idiopathic avascular necrosis in children
  • Abnormal blood flow
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50
Q

A muscle cell is also called?

A

Muscle fiber

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51
Q

Sacrolemma is the?

A

Plasma membrane of muscle cell

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52
Q

Sarcoplasmic reticulum is similar to what other structure?

A

Endoplasmic reticulum

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53
Q

Sarcoplasmic reticulum is important for?

A

Calcium storage

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54
Q

What is a T-tubule?

A

Invaginations of plasma membrane

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55
Q

What is a terminal cisternae?

A

Sarcoplasmic Reticulum near T-tubule

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56
Q

Muscle fibers are made up of?

A

Myofibrils (contractile structure)

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57
Q

What are sarcomeres?

A

Contractile structures within myofibrils

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58
Q

Sacromeres contains what 2 filaments?

A

Actin and myosin filaments

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59
Q

What forms the thick and thin filaments of sacromeres?

A

Thin: mostly actin, troponin, tropomyosin
Thick: Myosin

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60
Q

What are Z disks? What is the function?

A

Ends of sarcomeres, mechanical stability

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61
Q

Z disks contain what 2 filaments?

A

Vimentin and desmin

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62
Q

What tethers myosin to Z disks?

A

Titin

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63
Q

What is the I, A, and H band in a sarcomere contain? What is the M line?

A
  • I Band: Light band near Z disks, mostly actin
  • A Band: Between I bands, where actin and myosin overlap
  • H Band: Center of sarcomere, Myosin only
  • M line: Central proteins for alignment
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64
Q

What band in the sarcomere does not change with contraction?

A

A band

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65
Q

What are the 3 subunits of troponin? What is the function of each?

A

Troponin C: binds calcium
Troponin T: binds tropomyosin
Troponin I: inhibits myosin binding to actin

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66
Q

Muscle contraction is initiated via?

A

Calcium binding troponin

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67
Q

What blocks ‘binding groove’ for myosin?

A

Tropomyosin

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68
Q

What happens when Calcium binds troponin?

A

Conformational change in tropomyosin → exposes actin to myosin

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69
Q

Myosin bind ____ at rest?

A

ATP

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70
Q

What happens after myosin binds ATP in muscle contraction?

A

ATP hydrolyzed to ADP and Pi → assumes ‘cocked’ position → can bind to actin if Tropomyosin block is removed → ‘power stroke’ → myosin binds new ATP and detaches from actin

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71
Q

What is Excitation-Contraction Coupling?

A

Contraction occurs when cell depolarizes (action potential)

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72
Q

Neuron depolarization leads to what events in skeletal muscle contraction?

A

Presynaptic calcium entry into neuron → release of ACh → bind Nicotinic Acetylcholine Receptors on muscle cells → Na+ receptor opens → depolarization of muscle

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73
Q

What leads to the release of Calcium from SR after the sarcolemma is depolarized?

A

T tubules depolarize → conformational change of Dihydropyridine receptors → opens Ryanodine receptors on terminal cisternae (SR near T-tubule) → releases calcium → initiates contractions

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74
Q

What is the role of Dihydropyridine Receptors in skeletal muscle?

A

Proteins that span gap between T-tubule and SR, depolarization leads to conformational change which opens ryanodine receptors

75
Q

What is SERCA? What is the function?

A
  • Sarco/endoplasmic reticulum Ca2+-ATPase
  • Transfers Ca2+ from cytosol back into SR using ATP
76
Q

What are 2 drugs associated with Malignant Hyperthermia?

A

Succinylcholine, Halothane

77
Q

What is Malignant Hyperthermia? What is the underlying mechanism?

A
  • Rare, dangerous reaction to anesthetics
  • Abnormal ryanodine receptors causes excessive calcium release → consumption of ATP by SERCA → heat, muscle damage → ↑CK/K+ → Fever, muscle rigidity after surgery
78
Q

What is used to treat Malignant Hyperthermia?

A

Dantrolene

79
Q

What is the mechanism of Dantrolene?

A

Ryanodine receptor antagonist, block Ca2+ release from SR → relaxes muscle

80
Q

Slow twitch fibers are also called?

A

Red fibers

81
Q

What are 4 characteristics of Slow twitch fibers?

A
  • Have extra myoglobin (Resists fatigue)
  • More mitochondria = more oxidative phosphorylation
  • More fatty acid metabolism
  • Moderate glycolysis activity
82
Q

What muscles consist of more Slow twitch fibers?

A

Postural muscles (spine)

83
Q

Fast twitch fibers are also called?

A

White fibers

84
Q

Fast twitch fibers primarily metabolize?

A

Glucose and glycogen

85
Q

What muscles are mostly Fast twitch fibers?

A

Eye muscles

86
Q

What are 3 characteristics of Fast twitch fibers?

A
  • Increased activity of glycolysis enzymes
  • More glycogen storage
  • Less mitochondria
87
Q

What are differences between Cardiac muscle and Skeletal muscle?

A
  • Dyads vs Triads
  • Cardiac muscle is depolarized by pacemaker cells (SA node) and contain Gap junctions
  • Different action potential
88
Q

How is the Cardiac muscle action potential different from skeletal muscle?

A

Calcium influx via L-type calcium channels causes a plateau (Phase 2)

89
Q

Dihydropyridine receptors are what type of receptors?

A

L-type Ca+ Channels

90
Q

What are examples of dihydropyridine/non-dihydropyridine Ca+ channel blockers? Which are low/high affinity for dihydropyridine receptors?

A

Low affinity: Amlodipine, nifedipine
High affinity: Diltiazem, verapamil

91
Q

What is the importance of Dihydropyridine receptors in cardiac muscle?

A

Allows influx of calcium → triggers SR calcium release via ryanodine receptor (‘Calcium-triggered calcium release’)

92
Q

How do Cardiac muscle cells increase contractility?

A

Increase calcium entry into cell via L-type Ca channels

93
Q

What is the mechanism of Diltiazem and verapamil? What does this lead to?

A

Block L type calcium channels in cardiac myocytes → decreases contractility, slows conduction and lowers heart rate

94
Q

How does the Sympathetic Nervous system increase cardiac contractility?

A

β1 Receptors linked Gs proteins → activate adenylyl cyclase → increase cAMP/PKA → increase Ca into cell → increase contractility

95
Q

What is Lusitropy?

A

Myocardial relaxation

96
Q

Increase in Lusitropy always accompanies increase in?

A

Contractility (Faster contraction → faster relaxation)

97
Q

What mediates Lusitropy?

A

SERCA

98
Q

What is a key regulatory protein of Lusitropy? What is the role in regulation?

A
  • Phospholamban
  • Inhibits SERCA unless it is phosphorylated by beta adrenergic stimulation/PKA
99
Q

What is Phospholamban?

A

Key regulator protein of Lusitropy

100
Q

What are differences between smooth muscle cells and striated muscle?

A
  • Do not depend on action potential
  • Do not require membrane depolarization to contract
  • Slow, sustained contraction
  • Utilize Ca2+ differently
101
Q

Skeletal muscle is [thin/thick] filament regulated and Smooth muscle is [thin/thick] filament regulated.

A

Thin, thick

102
Q

What is modified to control contraction in Smooth muscle? What regulates contraction/tone?

A
  • Myosin light chain
  • MLC Phosphorylation
103
Q

MLC phosphorylation is regulated by what 2 proteins?

A

Myosin light chain kinase, Myosin light chain phosphatase

104
Q

Only [non-phosphorylated/phosphorylated] MLC interacts with actin.

A

Phosphorylated

105
Q

What is Calmodulin? What is the function?

A

Ubiquitous smooth muscle cell protein, binds calcium and activates MLC Kinase

106
Q

What are the 2 sources of Calcium for Smooth muscle cells?

A

SR and L-type Calcium channels that bind dihydropyridine (‘Dihydropyridine receptors’)

107
Q

What interacts with actin?

A

Only non-phosphorylated MLC interacts with actin.

108
Q

What is Calmodulin? What is its function?

A

Ubiquitous smooth muscle cell protein that binds calcium and activates MLC Kinase.

109
Q

What are the 2 sources of Calcium for Smooth muscle cells?

A

SR and L-type Calcium channels that bind dihydropyridine.

110
Q

What is the mechanism of Amlodipine, Felodipine, and Nicardipine? What is it used for?

A

L-type calcium channel blockers → less Ca → Vascular smooth muscle relaxation. Used in hypertension.

111
Q

What are the 2 major regulators of smooth muscle tone?

A

Calcium in cell and Myosin light chain phosphorylation.

112
Q

What are the 3 major 2nd messengers in smooth muscle?

A

cAMP, cGMP, IP3.

113
Q

What does cAMP in smooth muscle lead to?

A

MLK kinase inhibition → relaxation.

114
Q

What does cGMP in smooth muscle lead to?

A

MLC phosphatase activation → relaxation.

115
Q

What does IP3 in smooth muscle lead to?

A

Calcium release from SR → contraction.

116
Q

What is Nitric Oxide also called?

A

Endothelial derived relaxing factor.

117
Q

Nitric Oxide is synthesized from what amino acid? What cell?

A

L-arginine, Endothelial cells.

118
Q

What are 4 stimuli for increased production of Nitric Oxide?

A

Blood flow/shear stress, Acetylcholine, Bradykinin, Substance-P.

119
Q

What action does Nitric Oxide do in smooth muscle?

A

Activates guanylyl cyclase → increase cGMP → activates MLC phosphatase → smooth muscle relaxation.

120
Q

Acetylcholine and bradykinin work indirectly through what to cause smooth muscle relaxation?

A

Endothelial cells.

121
Q

What is the mechanism of Nitroglycerine? Uses?

A

Converted to NO in smooth muscle. Used for Angina and heart failure.

122
Q

Nitroprusside is a vasodilator used for?

A

Hypertensive emergency.

123
Q

What is the effect of G proteins (Gs, Gi, Gq) on smooth muscle? What is the mechanism?

A

Gs: increase cAMP → relaxation. Gi: decrease cAMP → contraction. Gq: increase IP3 → contraction.

124
Q

What does the periosteum contain?

A

Blood vessels and sensory nerves.

125
Q

Where is Trabecular bone found?

A

At the ends of long bones.

126
Q

What are Osteoclasts?

A

Specialized macrophages.

127
Q

What do Osteoclasts secrete?

A

Acid (H+) and proteases.

128
Q

What do Osteoblasts buried in bone matrix become?

A

Osteocytes.

129
Q

What does Bone Matrix contain?

A

Type I collagen and Hydroxyapatite (contains calcium and phosphorus).

130
Q

Bone Matrix is synthesized from?

A

Osteoblasts.

131
Q

Bone matrix is first synthesized as?

A

Osteoid: Non-mineralized bone matrix laid down by osteoblasts followed by mineralization.

132
Q

What modulates Bone turnover?

A

Signals from osteoblasts.

133
Q

What is RANK? What is its function?

A

Receptor expressed on surface of osteoclasts. Ligand binding leads to receptor synthesis of NF-kB → Osteoclast stimulation.

134
Q

What is RANK-L? What is its function?

A

Receptor expressed by osteoblasts, binds RANK → osteoclast stimulation.

135
Q

What is Osteoprotegerin (OPG)? What is its function?

A

Decoy receptor made by osteoblasts that binds RANK-L → prevents RANK binding.

136
Q

What is the role of M-CSF in bone turnover? It is secreted by what cells?

A

Stimulates osteoclasts. Secreted by osteoblasts.

137
Q

What are the 2 types of bone formation?

A

Endochondral ossification and Membranous ossification.

138
Q

When does Endochondral Ossification occur?

A

During embryogenesis.

139
Q

How do Long bones develop?

A

Via Endochondral Ossification.

140
Q

What begins Endochondral Ossification?

A

Hyaline cartilage ‘model’ → primary and secondary ossification centers grow toward each other → leaves area of cartilage that becomes the Epiphyseal plate (‘growth plate’).

141
Q

Where is the growth plate found?

A

Between Metaphysis and epiphysis.

142
Q

What occurs at the growth plate?

A

Chondrocytes grow toward epiphysis. Osteoblasts lay down matrix toward diaphysis.

143
Q

What is Woven and Lamellar bone?

A

Woven bone: first type of bone formed by osteoblasts, disorganized collagen fibers/weaker → later remodeled into lamellar bone. Lamellar bone: layered bone, organized, and stronger.

144
Q

When is woven bone seen in adults?

A

After injury.

145
Q

What does Membranous Ossification form?

A

Most flat bones (skull, facial bones).

146
Q

How does Membranous Ossification occur?

A

Matrix formed directly, osteoblasts lay down woven bone → remodeled to lamellar bone.

147
Q

What is the most common cause of dwarfism?

A

Achondroplasia.

148
Q

What gene mutation is associated with Achondroplasia?

A

FGFR3 gene mutation.

149
Q

What percentage of Achondroplasia cases are due to spontaneous mutation?

A

80%.

150
Q

What happens to babies with homozygous gene mutation for Achondroplasia?

A

They will die.

151
Q

What is the inheritance pattern of Achondroplasia?

A

Autosomal dominant.

152
Q

Achondroplasia occurs due to defective?

A

Endochondral ossification.

153
Q

What are Mucopolysaccharidoses? What are 2 examples?

A

Lysosomal storage disease. Hurler’s and Hunter’s syndrome.

154
Q

What do Hurler’s and Hunter’s syndrome lead to?

A

Inability to metabolize Heparan and dermatan sulfate.

155
Q

What happens to chondrocytes in Hurler’s and Hunter’s syndrome? What does this lead to?

A

Mucopolysaccharides accumulate in Chondrocytes → cell death. Leads to short stature and malformed bones.

156
Q

What are 3 osteoblast activity markers?

A

Alkaline phosphatase, Osteocalcin, Type I procollagen.

157
Q

What is Osteocalcin?

A

Major non-collagen protein in bone matrix.

158
Q

Type I procollagen is synthesized by what cells? What is it made of?

A

Osteoblasts. Made of 3 pro alpha chains.

159
Q

What is the function of Alkaline Phosphatase in bone?

A

Creates alkaline environment for calcium deposition.

160
Q

Where is Alkaline Phosphatase found?

A

In bone and liver.

161
Q

What stimulates osteoclasts?

A

Acidosis.

162
Q

What does continuous administration of PTH lead to?

A

Cortical bone resorption → ↑ serum calcium.

163
Q

What does low dose once daily bolus administration of PTH lead to?

A

Increase in Trabecular bone formation.

164
Q

What is the mechanism of Teriparatide? What is it used for?

A

Artificial PTH, used for Osteoporosis.

165
Q

Which cells contain PTH receptors?

A

Osteoblasts.

166
Q

What are 2 effects of estrogen on bone?

A

Increase bone density and close growth plate at puberty.

167
Q

What does estrogen induce?

A

Apoptosis of osteoclasts.

168
Q

What does estrogen increase/decrease in terms of bone related proteins?

A

Stimulates OPG synthesis, decreases M-CSF and RANK production.

169
Q

What occurs due to defective osteoclast activity?

A

Osteopetrosis.

170
Q

What are the 2 main forms of Osteopetrosis? Which is most severe?

A

Autosomal recessive (infantile) form: more severe. Autosomal dominant form: milder form, present in adolescence.

171
Q

What results from a mutation in carbonic anhydrase type II gene?

A

Infantile form of Osteopetrosis.

172
Q

What condition may a patient with Infantile form of Osteopetrosis also have?

A

Renal tubular acidosis.

173
Q

What is the autosomal dominant form of Osteopetrosis also called?

A

Albers Schönberg disease.

174
Q

What is the clinical presentation of Osteopetrosis?

A

Bones prone to fracture, excess bone → loss of bone marrow → Pancytopenia, enlarged liver and spleen (extramedullary hematopoiesis), excess bone in skull → cranial nerve compression (Vision loss, Deafness, Facial paralysis), Hydrocephalus.

175
Q

What is Osteopetrosis potentially curable with?

A

Bone marrow transplant.

176
Q

What is Rickets and Osteomalacia caused by? This leads to?

A

Low calcium or vitamin D intake leads to poor mineralization of osteoid.

177
Q

Where is osteoid found?

A

Area of new bone growth: Children = growth plates, Adults = bone turnover.

178
Q

What occurs to the bone in Rickets?

A

Growth plate thickens from osteoid accumulation, distorted bone growth, epiphyseal widening.

179
Q

What are clinical features seen in Rickets?

A

Genu Varum, Rachitic rosary: swelling at costochondral junctions, Craniotabes (soft skull).

180
Q

Where does Osteomalacia occur?

A

In areas of bone turnover (most often spine, pelvis, legs).

181
Q

What are 2 clinical features of Osteomalacia?

A

Bone pain/tenderness and fractures.

182
Q

What are 2 classic X-ray findings of Osteomalacia? What is it caused by?

A

Pseudofractures, Looser Zones. Caused by repaired stress fractures that are inadequately mineralized.

183
Q

What are common causes for Vitamin D deficiency?

A

Maternal deficiency during pregnancy, reduced sun exposure, fat malabsorption, liver and renal failure.

184
Q

What are 5 lab findings seen in Rickets and Osteomalacia?

A

Low Calcium, Low Vit D.

First Aid (18 decks)

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