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Block 4 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

How muscle can be affected after neural fibers are removed from the muscle?

A

Muscle atrophy

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2
Q

What is Spondylolisthesis?

A

Displacement of vertebra

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3
Q

What degeneration of cartilage between bones might lead to?

A

More bone rubbing leading to bone growth

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4
Q

Which part of vertebra are fused?

A

Coccygeal

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5
Q

Which vertebra do not have the intervertebral disk?

A

Atlas and axis

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6
Q

How many cervical nerves are there?

How many cervical vertebra are there?

A

8

7

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7
Q

What is the name of the hole that spinal cord is passing through?

A

Vertebral foramen

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8
Q

What forms neural arch?

A

Pedicle

Lamina

Body

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9
Q

What is the join between inferior and superior transverse proceeses of vertebra

A

azygoshypophyseal joint

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10
Q

Name the locations where nerves are exiting from spinal cord

A

Intravertebral foramen

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11
Q

What is the effect of anastetic injected in sacral hiatus?

A

Only affects spinal nerves not spinal cord

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12
Q

What artery passes through transverse foramen of cervical vertebra?

Exception?

A

Vertebral artery C1-6 not 7

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13
Q

Which vertebra can be felt on the back of the neck?

A

C7

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14
Q

What articular facets are connected to?

Which type of vertebra are they found in?

A

Ribs

Thoracic

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15
Q

Direction of superior/inferior articular proceses:

Cervical vertebra

Thoracic vertebra

Lumbar vertebra

A

Transverse plane

Frontal plane

Saggital plane

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16
Q

Would thicker or thinker disc allow more movement?

A

Thicker

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17
Q

What is found in all vertebra except atlas?

A

Body

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18
Q

What is the difference in shape of inferior vs. superior articular fovea?

What movement is allowed by superior articular fovea?

A

Superior is more concave

Front/back

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19
Q

Why spinal cord does not extend entire length of vertebral column?

A

It does not grow as much as vertrebral column

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20
Q

What is the special innervation of trapeizus muscle?

A

Innervated by CN XI

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21
Q

What is osteophytes?

A

a bony outgrowth associated with the degeneration of cartilage at joints

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22
Q

Components of axial skeleton

A

Skull

Vertebral column

Ribs

Sternum (not pelvis)

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23
Q

How many vertebra are there?

How many at each level?

A

7C, 12T, 5L, 5S, 4C

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24
Q

Which segment of vertebral colum belong to primary / secondary curvatures

A

Primary: thoracic & sacral

Secondary: cervical & lumbar

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25
Q

Name the parts of vertebra

A

BOdy

Pedicle

Lamina

Transverse process

Spinous process

Articular process

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26
Q

What is intervertebral foramen made of?

A

Inferior and superior vertebral notches

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27
Q

What is present on the lateral surface of each superior articular facet (muscle attachement)? – name it

A

Mammillary prossess

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28
Q

Name these two structures:

A

Posterior sacral foramina (anterior is behind)

Sacral Hiatus

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29
Q

Name the characteristics structure for each group of vertebra

A
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30
Q

Name the structures

A
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31
Q

Complete the table

A
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32
Q

What are the restrictions on movement of vertebral column?

A

Thickness of the intervertebral discs

Orientation of the articular facets

Attachements of ribs

Size, elasticsity, and orientation of muscle of th back and abdominal wall

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33
Q

Definition of pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

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34
Q

Defintion of

Actute Pain

Chronic Pain

A

Paid due to injury of tissues and activation of nocioceptors

Pain that extends beoynd the expected period of healing

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35
Q

Three general types of pain

A

Nociceptive pain (somatic pain / visceral pain)

Neuropathic pain (lesion or disease affecting the somatosensory system)

Mixen pain (cancers e.g. lung)

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36
Q

Two types of nociceptive pain

A

Arthritis (most common) : mechanical-osteoarthiritis & inflammatory-rheumatoid arthiritis

Low Back Pain

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37
Q

Examples of neuropathic pain

A

Herpes Zoster dormant in DRG -> Shingles and Post Herpetic Neuralgia (pain that could last for years)

Complex Regional Pain Syndrome (CRPS) - Involvement of sympathetic nervous system BPPS model (fire hand)

Central pain (pain associated with lesions of the CNS including spinal and central -opposite)

Phantom pain (stabbing, throbbing, burning)

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38
Q

Dependence vs. Addiction

A

Physical vs. Psychological

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39
Q

What fibers carry the pain signals?

Characteristics?

Location?

A

C-fiber and Ad-fiber

Heretogenous, unmylenated

Sking, muscle, joints, and viscera

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40
Q

Two types of sensitization

Location of central?

A

Primary / peripheral

Central (Lamina V)

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41
Q

What receptor triggers pain and exaple of molecule that binds to it?

How voltage gated sodium channels can be inhibited?

What voltage channels promote propagation of pain signals? Medications?

A

TRPV1 receptor / Capsaicin

Local Anasthetics and Lidoderm patches

N-type calcium channels

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42
Q

What is

Hyperalgesia

Allodynia

A

Hyperalgesia – heightened sense of pain to noxious stimuli

Allodynia – pain resulting from normally painless stimuli

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43
Q

What is the location when synapse of primary afferent neurons?

A

substantia gelatinosa

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44
Q

What tract carries pain signal?

A

Spinalthalamic tract (STT)

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45
Q

How pain is regulated?

A

Spinoreticular neurons have targets in medulla and brainstem

Spinomesencephalic neurons have targets midbrain and periaqueductal grey (PAG)

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46
Q

Where are all sensory system send to?

A

Thalamus

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47
Q

Two pathways of pain signals from thalamus to cerebrum

A

Lateral pain system -> Cerebral coretex (localization and intensity)

Medial pain system -> Limbic System

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48
Q

What is gate control theory (of melzack and wall)

A

Jamming pain signals (rubbin or massaging injured parts of body in order to achieve pain relief)

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49
Q

What can cause central sensitization

A

high intensity or prolonged stimuli such as occur with nonneuronal tissue injury and inflammation

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50
Q

Difference between:

Spondylolysis

Spondylolisthesis

A

Scotty Dog (Scotty Dog=fracture of pars interarticularis)

Displacement of vertebra

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51
Q

Ligaments that prevent flexion in spinal column?

Ligmanets that prevent extension in spinal column?

Importance?

A

Anteior Longitidinal Ligament = largest

Posterior Longitidinal Ligament = prevent disk herniation

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52
Q

What ligament on atlas surrounds dens?

What is the connection between skull and dens?

A

Cruciate ligament

Alar ligament

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53
Q

Parts of intervertebral disk

A

Annulus fibrosis = fibrocartilage thinner posteriorly

Nucleus pulposis= gelatinous fore

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54
Q

Where do spinal nerves exit in cervical region?

Where do spinal nerves exit in thoracic/lumbar/sacral region?

What nerve gets pinched?

A

Above same number vertebra

Below same number verebra

One number below

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55
Q

Spinal Meninges

A
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56
Q

What is the name of collection of fibers below the spinal cord?

Where does the spinal cord end?

A

Cauda equina

L2

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57
Q

Artery that runs in back/front of spinal cord?

What supplies these arteries?

A

Posterior / Anterior spinal

Posterior radicular artery / anterior medullary artery

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58
Q

Where is the Adamkiewicz artery located (level)?

A

T8-L2

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59
Q

What is Anterior Spinal Artery Syndrome?

A

Loss of blood flow to a spinal cord

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60
Q

Importance about venous drainage in vertebral column?

A

Conntected to both brain and prostatic venous plexus (prostate cancer metastasize to the CNS).

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61
Q

On what level are the dimples?

On what level is the iliac crest?

A

On L4/L5

Dimples on S2

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62
Q

Back muscles

A
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63
Q

Three groups of intrinsic back muscles

A

Spinotransverse (superficial)
Erector spinae (intermediate)
Transversospinae (deep)

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64
Q

What innervates back muscle?

A

Dorsal rami

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65
Q

What is the relationship between the direction of the muscle and vertebra turn?

Oblique

Transversospinal

A

Same side

Opposite side

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66
Q

Another name for spinotransverse

A

Splenius (superficial)

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67
Q

What are the three erector spinae muscle?

A

Spinalis

Longissimus

Ileocostalis

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68
Q

Two components of splenius group

A

Capitis and Cervicis

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69
Q

Transversospinae muscle group members

A

Semispinalis spanning 6-8 vertebrae

Multifidus spanning 3-5 vertebrae

Long rotators spanning 2

Short rotators spanning 1

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70
Q

What is the most powerful extender of the head

A

Semispinalis capitis (transversospinae muscle)

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71
Q

Microfailure

A
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72
Q

Yield Point

Failure Point

Elastic Region

Plastic Region

A
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73
Q

Isotropy

Anisotropy

Orthotropy

A

Mechanical properties independent of direction of stress

Mechanical properties different in all directions of loading

Mechanical properties symmetric within two planes

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74
Q

Hysteresis

A

The dependence of the output of a system not only on its current input, but also on its history of past inputs

Cyclic loading leads to smaller difference between loading and unloading curves

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75
Q

How multiple cycle of load affects failure strength?

A
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76
Q

Condition?

A

Stress Fracture

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77
Q

Stress vs. Strain curve

Brittle / Ductile material

A
78
Q

Wolff’s Law

A

Bone remodels in response to stress placed on it

79
Q

Which portion of the bode is responsible for hematopoiesis?

A

Proximal/distal

80
Q

Trabecular bone vs. cortical bone properties?

A

Trabecular: lower ultimate stress, ductile

Cortical bone: high ultimate stress brittle

81
Q

Weakest axis for loading on the bone?

A

Transverse

82
Q

Viscoelastic

How bone is affected at low and high frequency?

A

Sensitive to strain rate and duration of applied loads

Low frequency = ductile

High frequency = britle

83
Q

If force is applied over long period time then what happens to strain?

What changes if strain is maintained over long period?

A

Strain increases (creep)

Required stress decreases (stress relaxation)

84
Q

What is toughness?

A

Energy absorbed before ultimate failure

85
Q

Ductility

A

Ultimate strain substantially larger than yield strain

86
Q

Senile Osteoporosis symptoms / gender

Postmenopausal Osteoporosis

A

Both geneder / Both compact & trebecular

Female / Trabecular bone

87
Q

How vertical trabeculae are effected with aging?

A

Reduction in vertical trabecula disproportionally
Reduction in thickness of trabeculae
Increase in length of trabeculae

88
Q

How modulus relates to density?

A

2^n

power-law function of density

89
Q

How bone reacts to aging?

A

Density decreases

Cortical thicknes decreases

Diameter increases

90
Q

What are the main component of tendon?

Substructures?

A

Type I Collagen (Also water IIIm tenocytes, proteoglycans)

Tripple Helix -> Microfibril -> Fibrils -> Fascicles -> Tendon

91
Q

Stress vs. Strain curve regions for tendon

Regions?

A

Toe Region: uncrimping of collagen fibers

Linear Region: slope is elastic modulus of tendon

Failure Region: permanent stretching

92
Q

Ligament vs. Tednon

A

Ligament has less % collagen

More ground substance and type III collagen

Less longitudinal organization

93
Q

Tendon Insertion Into Bone

4 Zonez

A

Zone I:parallel collagen fibers
Zone II: unmineralized fibrocartilage
Zone III: mineralized fibrocartilage
Zone IV: Cortical Bone

94
Q

How tendon strength is affected with age?

How ligament strength is affected with age?

A

Increases to maturity then stays the same

It increases with age

95
Q

How steroid affect strength?

A

Corticosteroids reduce failure load

Estrogens reduce collagen production (e.g. pubic symphysis laxity)

96
Q

What collagen fibers are found in articular cartilage?

A

Type II

97
Q

What is responsible for 90 percent of load transmitted in cartilage ?

A

Flow Dependent Rate of Creep

rest: Flow Independent (friction between long chains)

98
Q

Which cartilage does not have perichondrium?

Which cartilage does not go through calcification?

A

Fibrocartilage

Elastic cartilage

99
Q

Function of:

Hyaline cartilage

Elastic cartilage

Fibrocartilage

A

Resistance to compression

Flexible support

Resist deformatin

100
Q

Two types of matrix in hyaline cartilage

A

Teritorial matrix

Interteritorial matrix

101
Q

Does hyaline cartilage have a lot of water? Why?

Evenly distributed?

Importance in development?

A

Yes (aggrecam)

No

Model for skeleton development

102
Q

Zones of Articular Cartilage

Direction of fibers

A

Tangential layer = parallel to join surface

Transitional zone = oblique

Radial zone = perpendicular

Calcified cartilage =

103
Q

Is there perichondrium at articular cartilage?

A

No

104
Q

What is the stain for elastin fibers?

A

Verhoeff (type II are masked by stain)

105
Q

What is the difference in mitosis between elastic cartilage and hyaline cartilage?

A

Mitosis occurs in elastic chondrocytes (more cells in cartilage)

106
Q

What is the arrangement of cells in fibrocartilage?

What does it connect?

A

Parallel columns of chondrocytes

Dense connective tissue and hyaline cartilage

107
Q

Where do chondroblast come from?

What gives rise to cartilage proper?

What produces perichondrium?

A

Mesenchymal cells

Chondroblasts

Fibroblasts

108
Q

What is the tissue that makes perichondrium?

What are the two layers of perichondrium?

A

Inner chondrogenic layer

Outer fibrous layer

109
Q

Two types of growth in cartilage?

Which cartilage?

A

Appositional

Hyaline and Elastic Cartilage

Chondrogenic cells -> Chondroblasts

Most of the growth in newly formed cartilage

Interstitial

All

Only growth in cartilage that do not have perichondrium

Epiphyseal plate

110
Q

Components of the bone

3 organic components 35%

1 inorganic component 65%

A

Type I collagen

Proteoglycans (compressive strength)

Multi-adhesive glycoproteins

Hydroxyapatite crystals (calcium+phosphate)

111
Q

Location of osteoblasts?

Location of osteocytes?

Location of bone lining cells?

Location of osteoclasts?

A

periosteum (inner)

endosteum

lining of Haversian canal

Lacuna

Cells that remain on the surface with no active growth

Bonemarrow

112
Q

What hormone targets osteoclasts?

What hormone inhibits osteoclasts?

A

PTH

Calcitonin

113
Q

Types of bones classification based on their shape

A

Long

Short

Flat

Irregular

114
Q

What structures are present in spongy bone and what are absent?

A

Lamellae present

Osteons absent

115
Q

What are the three blood supplies to long bones?

Characteristics

A

Nutrient arterial system

High pressure from major systemic arteries

Enter through nutrient foramina

Supply medullary cavity and 2/3 cortex via haversian system

Metaphseal-epiphyseal system

Arises from periarticular vascular plexus

Periosteal system

Low pressure

1/3 of cortex

116
Q

Blood supply to large irregular, short, and flat bones

A

receive blood supply from periosteum and often large **nutrient arteries **

many anastomosis

117
Q

Where is lymphatic drainage in bones?

A

Periosteum and absent in medulla

118
Q

What is and where is the nerve supply to the bone?

A

Periosteal = sensory (some are pain)

Medulla = vasomotor

119
Q

Two ways that bone is formed?

Which type of bones are formed by these proceses?

A

Intramembranous - flat and irregular

Endochondral - short and long

120
Q

Intramembranous Bone Formation

Trabeculated spongy bone formation

A

Mesenchymal cells differentiate into osteoblasts

Secretion of bone matrix

Formation of spiculates and trabeculate (random orientation of collagen)

Calcification

Trapping

Osteocytes

121
Q

What is subperiosteal bone collar?

What is periosteal bud?

A

Produced by osteoblasts allow blood vessels to come in to cartilage

Enters the cartilage

122
Q

Growth of Long bone (zones)

A

Epiphyseal cartilage

Reserve Zone

Proliferative Zone

Hypertrophic Zone

Vascular invasion Zone

123
Q

Where are only one epiphyseal plates present at?

A

metacarpals

metatarsals (proximal 1st and distal 2nd-5th)

clavicles

ribs.

124
Q

What ypes of myosin is involved in heart contraction?

cell division?

vescile transport?

A

cardiac

II

V

125
Q

What is similar in all myosins?

What makes myosins different?

A

Motor

Tail

126
Q

What happens if myosin is broken

II

V

VI & VII

A

Muscle myopathies (cell division)

Griscelli Synrome (melanosome transport - hypopigmentations and neurological defects))

Hearing loss (organization of actin-filled stereocilia)

127
Q

Structure of myosin II

A

Dimer

Actin binding site

Active site

Regulatory domain

Essential domain

128
Q

What is special about myosin IV?

A

It is minus-end directed

129
Q

Myosin-actin cycle

A

ATP binding causes head release

ATP->ADP+P causes confromational change

Release of phosphate allows binding back to the new site

Release of ADP causes power stroke

130
Q

What is the difference between myosin II and V?

Neck?

Duty?

Function?

Functional Units?

A

Long 6IQ / Short 2IQ

50% / 10%

Organelle motor / Muscle contraction

Two heads / ~20 heads

131
Q

What connects myosin fibers together?

A

Hydrophobic tail region

132
Q

Function of:

CapZ and tropomodulin

Z disc

Titin

Nebulin

A

Keep filaments length constant

has a-actinin that joins sacromeres

mantains thick filament position

sets the length of the thin filament

133
Q

Where does the regulation occur in:

Skeletal and cardiac muscle?

Smooth muscle?

A

Thin filament

Thick filament (Myosin Light Chain Kinease/Phosphatase calcium dependent)

134
Q

What affects the muscle ability to generate force and contract?

A

Myosin isofroms

Frequency of stimulation

Number of motor units stimulated

Degree of strech (Frank-Starling relationship)

Whether muscle is allowed to shorten (Force-velocity relationship)

135
Q

Isomatric vs. isotonic muscle contraction

A
136
Q

Mutations to MyHC IIa (MYHC2)

Disease?

Features?

Pathogenesis?

A

Disease: Muscle Myopathy.

Clinical Features: Muscle Weakness. Atrophy near shoulders, back, hand and thigh muscles. Muscle weakness.

Pathogenesis: Mutations primarily to SH1 Helix in myosin. Thought to alter actin-myosin ATPase activity.

137
Q

Mutations to embryonic MyHC (MYH3):

Disease?

Features?

Pathogenesis?

A

Disease: Distal arthrogryposis. Freeman-Sheldon Syndrome, Sheldon-Hall Syndrome.

Clinical Features: Joint contractures with predominant distal involvement.

Pathogenesis: Mutations in troponin I, troponin T, tropomyosin, perinatal myosin and embryonic myosin. Thought to disrupt sarcomere development.

138
Q

Mutations to B-Cardiac myosin (MyHC7):

Disease?

Features?

Pathogenesis?

A

Disease: Laing myopathy.

Clinical Features: Weakness of ankle dorsiflexion and “hanging big toe”.

Pathogenesis: Mutations are in the LMM region of Myosin. Thought to disrupt myosin filament formation or disrupt interactions with myosin binding proteins like titin.

139
Q

What two cardiovascular diseases can be caused by myosin mutations?

Pathogenesis

A

familial hypertrophic cardiomyopathy (FHC) and dilated cardiomyopathy (DCM). \

FHC mutations enhance myosin force generation

DCM mutations decrease myosin force generation

140
Q

What is the effect of ___ on Ca++ levels?

Parathyroid hormone (PTH)

Fibroblast growth factors 23 (FGF23)

Vitamind D

Calcitonin

RANKL (receptor activator of nuclear kappaB ligand)

M-CSF: macrophage colony stimulating factor

OPG: osteoprogenin

A

PTH Increases plasma Ca++ concentration: activation of vit D in kidneys, stimulate osteoclasts (and osteoblasts)

FGF23: inhibition of activation of vit D in kidneys

Vit D: inhibits PTH secretion, calcium absorption and deposition

Promotes osteoclasts differentiation

Promotes osteoclasts differentiation

Inhbits osteoclasts differentiation

141
Q

What type of hormone is PTH?

What is required for PTH to function?

A

Peptide 84 amino acids

1-34 amino acids

142
Q

How PTH is regulated? (three ways)

A

Calcium sensitive receptors

Calcium sensitve protease (limit PTH product)

Vit D receptor

143
Q

Effects of Parathyroid hormone?

* little clinical use

A

Mobilizes bone calcium

Decreases renal excretion of calcium

Stimulates Vitamin D3 synthesis

Promotes phosphate excretion

144
Q

Vit D biosynthesis

A
145
Q

Calcitriol (Vitamin D)

Effects?

A

Stimulates absorption of calcium and phosphate in the intestine and the mobilization of calcium from bone.

146
Q

Fibroblast growth factor 23

Effects?

Where is it produced?

How is it inactived?

Mutations in this site leads to?

What is the production stimulated by? inhibited?

A

inhibits 1,25(OH)2D production and inhibits phosphate reabsorption in the kidney

Osteoblasts and osteocytes in bone

At RXXR site

Hypophosphatemic rickets (autosomal dominant)

1,25(OH)2D01 / dentin matrix protein DMP1

147
Q

Application of calcitonin?

A

Hypercalcemia associated with neoplasams

148
Q

Glucocorticoids effect on bone regulation?

Uses?

Prolonged use?

A

Antagonize Vit-D intestinal calcium transport & stimulate renal calcium excretion, block bone formation

Hypercalcemia associated with lymphomas and granulomatous disease (sarcoidosis) where 1,25(OH)2D is elevated

Ostoporesis

149
Q

How estrogen affects bone mass?

A

Decreases PTH action

Increases 1,25[OH]2D levels with no direct effects

Bone remodling (receptors present in bone)

150
Q

What is osteoporosisis? Accelerated by?

What is osteomalacia? Children? Adults? Cause?

A

Reduced quantity of bone / Loss of ovary, drugs (e.g. corticosteroids), lifestyle

Lack of mineralization / Rickets / Bone pain & fractures / Vit Deficiency

151
Q

Pagets disease?

Results?

Pathology?

A

Abnormal bone production (bone pain, skeletal deformity, neurological complications)

Osteolytic, osteoblastic, and quiescent (excessive bone resorption and formation)

152
Q

How osteoporosis is diagnosed?

A

Dual-energy X-ray absorptiometry (DEXA or DXA)

-1 to -2.5 osteopenia

below -2.5 osteoporosis

153
Q

Selective Estrogen Receptor Modulators (SERMs)

e.g. Tamoxifen and Raloxifene

Speficicity?

Mechanism?

A

Tissue specifc

Competitive inhibition of a-receptors and agonist in b-estrogen receptors

154
Q

Tamoxifen

Mechanism?

Affects osteoporosis? Lipids?

Risk?

Side effects?

A

Blocks estrogen receptor

No (has some antiestrogenic effects), No

Endometrial cancer

Hot flashes, nausea, vomiting

155
Q

Raloxifene

Affects osteoporosis?

Estrogenic activity?

Lipids?

Side effects?

A

Yes (first aproved treatment)

Yes

Decreases total cholesterol

Thromboembolic events (similar to estrogens) hot flashes and leg cramps

156
Q

Bisphosphonates

Molecular structure?

Mechanism?

Can be given continously?

Effectiveness?

Not combine with what diet?

Side effects?

A

Analogs of pyrophosphate – Designed to mimic pyrophosphate (P-O-P structure replaced by P-C-P).

Reduce osteoclasts (48 hours), block transformation of calcium phosphate into hydroxyapatite (preventing dissolution)

2 week off

Increase bone density by 4-9% over first 3 years

Milk products, food or Ca2+ supplements

Heartburn, nausea, and abdominal pain

157
Q

Denosumab

Mechanism?

Contraindications?

Side effects?

A

Denosumab inhibit the maturation of pre-osteoclasts into osteoclasts and therefore prevents bone resorption. Denosumab mimics the actions of osteoprogenin, an endogenous RANKL inhibitor that is decreased in patients with osteoporosis.

Hypocalcemia

Increased UTI and respiratory infections, rashes, joint pain, eczema

158
Q

Tibolone

Teriparatide (PTH analog)

A

C-19 steroid with weak hormonal properties

Effective

159
Q

Hypercalcemia

Treatment?

A

Loop diuretics secrete Ca2+

Biphosphates IV

Cinacalcet a calcium sensor mimetic

160
Q

Name the structures

A
161
Q

Epidermis

Embryological origin?

Regeneration time?

What time of the day the division occurs?

Steps in life of keratinocytes?

A

Ectoderm

30days

Night

Mitosis, differentiation (keratinization), cell death, exfoliation

162
Q

Five layers of the skin

A

Stratum basale

Stratum spinosum

Stratum granulosum

Stratum lucidum

Stratum corneum

163
Q

Stratum Basale

What connections do keratinocytes have?

Intermediate filament? Change in amount?

Other cells?

A

Desmosomes and hemidesmosomes

Cytokeratin, increases toward surface

Melanocytes and Merkel’s cells

164
Q

Stratum Spinosum

Thickness?

Bundles of cytokeratin?

Shape?

Other cells?

A

Several layers

Tonofibrils

Langerhans cells and melanocytes

165
Q

Mitotically active layers

A

Stratum Basale and Spinosum

Malpighian layer

166
Q

Stratum Granulosum

Contain what structures?

Insulation?

Formation of keratin?

A

Lamellar bodies, membrane-less keratohyalin granules, and bundles of tonofilaments (cytokeratin)

Lamellar bodies fues with PM and release GAGS and phsopolipids to ECM

Keratohyalin has histidine and cystine rich proteins binding to tonofilaments. This convers cells to conified cells (first step in keratinization)

167
Q

Stratum Lucidum

Present in what type of skin?

Staining?

Keratin type?

A

Thick only

Acidophilic

Contains immature keratin (eleidin)

168
Q

Stratum Corneum

Cell charactersitics?

A

Dead, platelike, enucleated keratinocytes containing mature keratin

169
Q

Psoriasis

A

Accelerated keratinocyte mitosis in stratum basale and spinosum

Turnover (one week instead of 4 weeks); leads to thickening of epidermis

170
Q

Langerhans’ Cells

Origin?

Function?

Characteristic molecule?

Location?

Where are they present?

A

Bone marrow (MNP)

APC

Birbeck’s Granules rodlike or racket-shaped

Stratum spinosum

oral, esophageal, rectal and vaginal epithelium as well as thymus

171
Q

Merkel’s Cells

Layer?

Origin?

Structures?

Where are found the most?

Function?

A

Stratum basale

Neural crest cells

Desmosomes and tonofilaments

Thick skin

Sensory mechnoreceptors

172
Q

Melanin

Contribution to?

Origin?

Layer?

Have desmosomes?

Enzymes?

Why different skin colors?

A

Skin, eye, hair color, freckles

Neural crest

Stratum basale 10-25%

No

Tyrosinase, an UV-sensitive enzyme involved in melanin synthesis

Not related to number but activity

173
Q

Mature melanin granules

Where does melanin initially go to?

Location of accumulation?

Removal of melanin?

Protective role

A

Injected into keratinocytes

Around nuclei

Attacked by lysozomes (over a few days)

Absorption of free radicals

174
Q

Two layers of dermis?

Structures present?

A

Papillary Layer (superficial)

Dermal papillae

Meissner’s corpuscules (fine touch)

Type III and type VII collagen bindin to epidermis

Reticular Layer

follicles, sweat, and sebaceous glands

dense irregular connective tissue

elastic fibers and collagen type 1

175
Q

Hypodermis

Thicknes variations?

Type of tissue?

Really thick hypdermis name?

Another name?

A

nutritional status, level of activity, body region and gender

Loose ct and adipose tissue

Panniculus adiposus

Subcutaneous fascia

176
Q

Sensory Receptors

A

Meissner corpuscule

Merkel cells

Free nerve endings

Ruffini end organ (pacinian corupuscle pressure)

Peritrichial nerve ending

177
Q

Thick vs. Thin skin

A
178
Q

Hair and Arrector Pili Muscle

What layers form these structures?

What is hair follicle composed of?

Any hair follicles formed after birth?

A

Both epidermis and dermis

Shaft and bulb

No

179
Q

Sebaceous gland

Types?

Where does it empty?

Health problems associated with them?

When do they form?

What the baby is slippery?

When become inactive/active?

A

Hair dependent and independent

Into the neck of hair follicle

acne

6th moth in utero

vernix caseosa

At birth / at puberty

180
Q

Eccrine Sweat gland

Shape?

Secretory unit?

Ducts lining?

Type of secretion?

Sensitive to?

Function?

A

Simple coiled ubular gland

Dark, celar, and myoepithelial cells

Stratified cuboidal epithelium (modification sweat by absorbing, electrolytes, excreting ions, urea, and lactic acid)

Merocrine

Heat and nervous stress

Thermoregulatory and excretion (urea, ammonia)

181
Q

Hyperhidrosis

What is it?

Location?

Treatment?

A

Excessive sweating

Hands

1.antiperspirants 2.Iontophoresis 3.drugs 4. surgery for axillary glands

182
Q

Apocrine Sweat Gland

Location?

Function?

When activated?

Sensitive to?

A

Specialized sweat glands in axilla, areola of the niple, and perianal region of Moll, ceruminous (Wax) glands of the ear

Vestigial scent glands

Puberty

Hormonal, emotional, and sensory NOT heat

183
Q

Sunburn

Effect on keratinocytes?

Melanocytes?

Langerhans?

Dermal changes?

A

Lose alignment, flatten, obtain nuclear inclusion

Melanocytes enlarge, increase in number, and migrate to higher levels of epidermis

Reduceing antigen presenting capability

Less elastic, leaky vasculature, increase in mast cells

184
Q

Actinic keratosis

What is it?

Progression to?

Colors?

Which part of the body does it present?

A

Pre malignant condition of thick, scaly, or crusty patches of skin.

Squamous cell carcinoma / or dissapear (1/2 will go away if not exposed to sun damage)

Vary

scale or crust is dry, rough

Part that is exposed to the sun

185
Q

Skin cancer
Characteristics?

Basal cell carcinoma

A
186
Q

Melanoma

Initial apparance?

Common location

A

usually appears as dark brown or black mole like lesions

upper back in men and legs in women

187
Q

ABCD

for melanoma

A

A: asymmetry- one side or half does not look like the other

B: border irregularity

C: color-black, or much darker than patient’s other moles, often with red, white or blue areas.

D: diameter > 6 millimeters

188
Q

What is kyphosis?

What is lordosis?

A

Kyphosis

Abnormal increase in thoracic curvature (thoracic wedge fracture; osteoporosis; loss of heigh)

Lordosis

Abnormal increase in lumbar curvature (obesity; compensatiory lordsis)

189
Q

What is scoliosis?

A

Abnormal lateral curvature

190
Q

Steele’s rule of 3

A
191
Q

Hangman’s fracture

A
192
Q

Hyperextension injury

A

Block 4 (4 decks)

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