Unit 2 STRX Flashcards

1
Q

Boundaries of the axilla

A

Anterior Wall - Pectoralis major, pectoralis minor, clavipectoral fascia

Medial Wall - Serratus anterior, ribs 1-4

Posterior Wall - Scapula, Teres Major, Subscapularis, Latissimus dorsi

Lateral Wall - Intertubercular Sulcus of Humerus

Apex - Cervicoaxillary canal, 1st rib, clavicle, scapula

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2
Q

What are the contents of the axillary sheath?

Which of these are most anterior?

A

Cords of the brachial plexus, axillary artery, axillary vein, fat, lymphatics

Axillary vein

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3
Q

How many parts does the Axillary a. have and what are the borders that separate them?

A

3 parts

Subclavian a. |inferior border of 1st rib| Axillary a. part 1

Axillary a. part 1 |Pec minor (proximal border)| Axillary a. part 2

Axillary a. part 2 |Pec minor (distal border)| Axillary a. part 3

Axillary a. part 3 |inferior border Teres Minor| Brachial a.

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4
Q

Name the parts of the Axillary artery and their corresponding branches

A

Part 1 - Superior thoracic a

Part 2 - Thoracoacromial trunk, Lateral thoracic a.

Part 3 - Anterior and Posterior Circumflex, Subscapular
Subscapular –> Circumflex scap and thoracodorsal a.

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5
Q

What is the origin of the Axillary v?

A

Basilic and Brachial veins

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6
Q

What major vein drains into the axillary vein?

A

Cephalic v

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7
Q

What nerves come from the Roots of the Brachial plexus?

A

Dorsal Scapular n (C5)
Phrenic n (C5)
Long thoracic n (C5-C7)

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8
Q

What nerves come from the Trunks of the Brachial Plexus?

A

Suprascapular (C5-C6)
N to Subclavius (C5-C6)

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9
Q

What nerves come from the Divisions of the Brachial Plexus?

A

None

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10
Q

What nerves come from the Cords of the Brachial Plexus?

A

Lateral: Lateral Pectoral (C5-7)

Posterior: Upper subscapular (C5-6)
Lower subscapular (C5-6)
Thoracodorsal (C6-8)

Medial: Medial Pectoral (C8-T1)
Medial cutaneous of the arm (T1)
Medial cutaneous of the forearm (C8)

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11
Q

What are the Terminal Branches of the Brachial Plexus?

A

Musculocutaneous (C5-C7)
Median (C5-T1)
Axillary (C5-6)
Radial (C5-T1)
Ulnar (C8-T1)

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12
Q

What is this a common sign of?

A

winged scapula - C5, C6, C7 Long thoracic n. injury

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13
Q

Describe the common signs of Erb’s Palsy and the nerves associated with it

A

Arm hanging by their side and medially rotated
Forearm extended and pronated - “Waiter’s tip hand”

Damage to the upper plexus (C5-C6)

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14
Q

Pt presents with this symptom, along with supinated forearm. What has been damaged?

A

Lower plexus (C8-T1)

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15
Q

Identify what nerve dysfunction causes these signs as well as Ape Hand and Wrist Drop

A

Ulnar Claw - Distal ulnar n
Hand of Benediction - Proximal Median n
Median Claw - Distal Median n
“OK” guesture - Proximal Ulnar n
Ape Hand - Distal Median n
Wrist drop - Radial n

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16
Q

The epidermis arises from ___________ while the dermis arises from ______________

A

Ectoderm
Mesoderm

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17
Q

Identify the layers of the _________

A

Epidermis

Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Stratum Basale

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18
Q

What are Keratohyaline granules and their function?

A

Granules that contain filaggrin that promote keratin fiber cross-linking

Creates impermeable barrier in stratum corneum to prevent pathogen crossing

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19
Q

What are Odland bodies and their function?

A

Granules that release glycophospholipid-rich contents (via exocytosis) into intercellular spaces of stratum granulosum around individual keratinocytes

Makes epidermis impermeable to water loss from skin

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20
Q

What type of cells are in the epidermis and what are their functions?

A

Merkel cells - oval shaped mechanoreceptors that detect light touch

Langerhans cells - first defense, dendritic immune cells that destroy pathogens and use Birbeck granules for antigen presentation to T-regulatory cells

Melanocytes - produces melanin which is packed into melanosomes –> sent to keratinocytes through cytoplasmic projections

Keratinocytes - form protective layer on epidermis (stratum corneum)

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21
Q

What are the layers of the dermis and what are they composed of?

A

Papillary layer - loose connective tissue

Reticular layer - dense connective tissue

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22
Q

List the sensory receptors found in the dermis and their functions

A

Meissner corpuscles - light touch receptors in the papillary layer

Pacinian corpuscles - phasic receptors - deep pressure, vibration

Ruffini endings - tonic receptors - pressure (skin stretch), deformations within joints

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23
Q

Identify the structure indicated

A

Pacinian corpuscle

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24
Q

Differentiate acanthosis from ancatholysis

A

Acanthosis is hyperplasia of the stratum spinosum

Acantholysis is the breakdown of desmosome attachment (in the stratum spinosum)

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25
Q

Differentiate dyskeratosis from spongiosis and parakeratosis

A

Dyskeratosis are cells coming apart and show hyperpigmented nuclei

Spongiosis is when there is intercellular edema pushing cells apart

Parakeratosis is abnormal keratin production and maturation

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26
Q

Identify the structure indicated by the yellow arrows.

By the blue arrows.

A

Langerhans cells

Cytoplasmic projections

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27
Q

Interpret the histological findings and the skin abnormality

A

Nodule

The mass is in the epidermis and dermis, and it’s raising the epidermis more superficially

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28
Q

Interpret the histological findings and the skin abnormality

A

Pustule

Abundance of dead neutrophils in the epidermis

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29
Q

Interpret the histological findings and the skin abnormality

A

Vesicle or Bulla - size unknown

Histology shows intraepidermal fluid-filled space that appears unstained, with the layers of the epidermis separated from each other.

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30
Q

Interpret the histological findings and the skin abnormality

A

Erosion

Histology shows an incomplete loss of epidermis; the stratum spinosum and basal layer seem to be untouched.

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31
Q

Interpret the histological findings and the skin abnormality

A

Ulcer

Histology shows a complete loss of epidermis and partial loss of dermis; if it had been contained to the epidermis it would have been erosion

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32
Q

Interpret the histological findings and the skin abnormality

A

Acanthosis

Diffuse epidermal hyperplasia; pathology shows exaggerated rete ridges and dermal papilla

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33
Q

Identify the skin abnormality and it’s pathophysiology

A

Wheals

Brought on by type I hypersensitivity reactions - IgE responds to allergen and mediates mast cell degranulation, releasing potent vasodilators

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34
Q

Interpret the histological findings and the skin abnormality

A

Parakeratosis

Histology shows nuclei in the stratum corneum

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35
Q

Interpret the histological findings and the skin abnormality

A

Hyperkeratosis

Histology shows excessive hyperplasia of the stratum corneum

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36
Q

Identify the cells indicated by the red arrows

A

Eosinophils

Red staining

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37
Q

Identify the circled cells

A

Neutrophils

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38
Q

Interpret the histological findings and identify the skin abnormality

A

Spongiosis

Histology shows intraepidermal intercellular edema

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39
Q

Patient presents with small, lichenified, scaly mass.

Interpret the histological findings and explain the pathogenesis of the likely diagnosis

A

Actinic keratosis - squamous cell carcinoma precursor

Histology shows parakeratosis and dysplastic keratinocytes; the encircled section shows a keratinized pearl indicative of Actinic keratosis

Pathogenesis: DNA damage from UV rays results in mutations in p53 and/or RAS

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40
Q

Patient presents with macule.

Interpret the histological findings and identify the skin abnormality

A

Nevi

Histology shows linear pattern of melanocyte proliferation within epidermis

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41
Q

Patient presents with scaling.

Interpret the histological findings and explain the pathogenesis of the likely diagnosis

A

Psoriasis

Histology shows parakeratosis, hyperkeratosis, and acanthosis; loss of stratum granulosum; dilated capillaries; neutrophils in dermal papillae

Pathogenesis: Inheritable HLA-C, upregulation of CARD14, mutation in IL-12, or mutation in IL-23 –> leads to predisposition of keratinocyte production

Pathophysiology: Irritation/trauma activate inflammatory factors –> IL-23 stimulates CD4 T-cell differentiation–> release of IL17 –> binding of IL-17 to IL-17R on epithelial and stromal cells –> secretion of CXCL8 –> lead to neutrophil recruitment
Overall secretion of IL-17, TNF-a, IFN-y, IL-22 stimulates survival and proliferation

Sustained inflammatory response + predisposition of keratinocyte differentiation –> psoriasis

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42
Q

Patient presents with pearly telangiectatic papule.

Interpret the histological findings and explain the pathogenesis of the likely diagnosis

A

Basal cell carcinoma

Histology shows palisading arrangement of cells with elongated hyperchromatic nuclei around a nodule in stratum basale

Pathogenesis: DNA damage results in activation of SHH signaling pathway –> inhibits PTCH patched protein allowing SMO smoothened protein to detach –> SMO travels to nucleus and activates glioma-associated oncogene (GLI) transcription factors –> increased cell proliferation

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43
Q

Explain each step of the melanocytic nevus progression

A

A. Normal skin with scatted melanocytes
B. Junctional Nevus - nests of nevus cells along the epidermis-dermis junction
C. Compound nevus - nests of nevus cells within the dermis and along the epidermis-dermis junction
D. Dermal nevus - nests of nevus cells only in the dermis
E. Dermal nevus with neurotization - spindle-shaped cells in wave-like orientations that have lost their ability to produce melanin

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44
Q

Identify what stage of nevus progression this is and justify your findings

A

Junctional - nests of nevus cells along dermis-epidermis junction

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45
Q

Identify what stage of nevus progression this is and justify your findings

A

Compound - nests of nevus cells within the dermis and along the epidermis-dermis junction

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46
Q

Identify what stage of nevus progression this is and justify your findings

A

Dermal - nests of nevus cells only in the dermis

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47
Q

Identify what stage of nevus progression this is and justify your findings

A

Dermal with neurotization - spindle-shaped cells are seen in the dermis

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48
Q

Explain each step of the progression from dysplastic nevus to melanoma

A

A. Lentiginous melanocytic hyperplasia
B. Lentiginous junctional nevus
C. Dysplastic lentiginous compound nevus
D. Early melanoma
E. Advanced melanoma

49
Q

Identify what stage of dysplastic nevus –> melanoma progression this is and justify your findings

A

Dysplastic compound nevus

3 arrows show hyperchromatic, atypical nuclei
2 arrows show perinuclear halos
Double-headed arrow shows lamella fibrosis

50
Q

Identify what stage of dysplastic nevus –> melanoma progression this is and justify your findings

A

Early melanoma

Histology shows radial growth phase - horizontal spreading of melanoma in epidermis and dermis

51
Q

Identify what stage of dysplastic nevus progression –> melanoma this is and justify your findings

A

Advanced melanoma

Histology shows vertical growth phase - vertical spread of melanoma into dermis, subQ and possibly vasculature

52
Q

What are the borders of the triangular space of the shoulder region?

How does this differ from the triangular interval?

A

Triangular space borders:
Superior - Teres minor
Inferior - Teres major
Lateral - Long head of the tricep

Triangular interval borders:
Superior - Teres major
Medial - Long head of the tricep
Lateral - Surgical neck of the humerus

53
Q

What are the borders of the quadrangular space of the shoulder region?

A

Superior - Teres minor
Inferior - Teres major
Medial - Long head of triceps
Lateral - Surgical neck of humerus

54
Q

Explain the Empty Can test and what it’s testing for.

A

Testing for ruptured supraspinatus tendon

Pt places straight arm 90 degrees of abduction and 30 degrees forward flexion
Internally rotates the arm completely
Pt then resists examiners attempts to depress arm

55
Q

Identify the following structures

A

A. Suspensory Ligaments
B. Fat lobule
C. Lactiferous Sinus
D. Lactiferous Ducts
E. Pectoral Fascia
F. Retromammary space (bursa)

56
Q

What arteries supply blood to the breast?

What veins drain the breast?

A

Arteries:
Pectoral branch of the thoracoacromial trunk
Internal thoracic a.
Lateral mammary branches of lateral thoracic a.
Medial mammary branches of internal thoracic a.

Veins:
Axillary vein
Internal thoracic vein

57
Q

What nerves innervate the breast?

A

Lateral cutaneous branches of the 4th and 5th intercostal nerves

58
Q

What are the different pathways of lymph drainage from the nipple, areola, and mammary glands in the breast?

A

subareolar plexus –> parasternal –> bronchomediastinal

subareolar plexus –> pectoral –> central –> apical –> infraclavicular –> supraclavicular

subareolar plexus –> subscapular –> central –> …

Subareolar plexus –> abdominal

59
Q

What are the different pathways of lymph drainage from the skin of the breast?

A
60
Q

IM, orientation, and body part

A

Axillary radiograph of the left shoulder

61
Q

IM, orientation, body part

A

radiographic “Y” view of left shoulder/scapula

62
Q

What are the orientations of these X-rays?

A

Top: AP
Bottom: Lateral

63
Q

Compare and contrast these two imaging modalities.

A

Both are MRIs

Top is T-1 weighted
Bottom is T-2 weighted

64
Q

What structures are contained in the Triangular interval?

A

Radial n.
Deep radial a. (profunda a.)

65
Q

Which nerve provides sensory cutaneous innervation to the regions noted?

A

Pink - Radial n
Green - Musculocutaneous n
Yellow - Median n
Purple - Medial cutaneous n of the forearm
Blue - Ulnar n.

66
Q

How can you tell the difference between a myopathic injury from a neurogenic injury in a group of muscle tissue cells?

A

A neurogenic injury would show fiber type grouping after reinnervation –> nerves to cells die –> motor units around it take over those cells and reassign to that fiber type –> form groups of motor units instead of the randomly distributed

A myopathic injury would maintain the random distribution of motor units but would likely atrophy in groups, show inflammation, repair of damage portioned of cell

67
Q

What are the classic histological findings of Dermatomyositis, and the clinical presentation?

A

Perifascicular atrophy + inflammation of tissue cells

CP: Muscle pain, proximal muscle weakness (getting out of chairs, climbing stairs, picking up things), erythematous skin changes around eyes, red thickened skin on knuckles and knees

68
Q

How do you differentiate between Dermatomyositis and Polymyositis?

A

Similar musculoskeletal symptoms and presentation

Polymyositis doesn’t present with skin changes - diagnosis of exclusion

69
Q

How do X-linked Muscular Dystrophies result in the clinical presentations seen?

A

Loss of function mutation with DAG (dystrophin-associated glycoprotein)

DAG links sarcolemma to ECM –> transmits force out of actin/myosin in cell into ECM –> culminates contraction, prevents damage to cell during contraction

No DAG –> no link –> damage to cells faster than repair can keep up

70
Q

Explain the histological differences between skeletal, cardiac, and smooth muscle tissue

A

Skeletal muscle: latitudinal striations, multiple peripheral nuclei, elongated cells

Cardiac muscle: longitudinal striations, single central nucleus, intercalated disks

Smooth muscle: non-striated, homogenous pink background, single central nucleus, fusiform cells

71
Q

How is skeletal muscle developed and repaired?

A

Developed: mesoderm –> mesenchymal cells –> myoblasts –> myotubes –> differentiation to muscle fiber

Regeneration: satellites stem cells

72
Q

Function of the glenohumeral ligaments

A

Strengthen the anterior aspect of the joint capsule

73
Q

Function of coracohumeral ligament

A

Strengthens the joint capsule superiorly

74
Q

Structures and function of coraco-acromial arch

A

Coracoid process, acromion, coracoacromial ligament

Form protective arch that overlies humeral head, prevents superior displacement from glenoid cavity

75
Q

Blood supply and innervation of the glenohumeral joint

A

Anterior and posterior circumflex humeral a
Branches of suprascapular a

Suprascapular n
Axillary n
Lateral pectoral n

76
Q

Blood supply and innervation of the acromioclavicular joint

A

Suprascapular a
Thoraco-acromial a

Lateral pectoral n
Axillary n

77
Q

Grading of Acromioclavicular separation

A

Grade 1 - ligaments bruised/strained, no actual separation of joint

Grade 2 - Partial tear or stretching of AC ligaments with slight joint separation

Grade 3 - both AC ligaments and coracoclavicular ligaments are torn, clavicle and acromion completely separated

78
Q

What is the function of the transverse humeral ligament?

A

Hold the long head of the biceps tendon in place

79
Q

What is the location and function of the conoid ligament?

A

Attaches the coracoid process to the clavicle

Helps prevent dislocation of the acromioclavicular joint

80
Q

What is the function of the superior transverse scapular ligament?

A

Bridges the scapular notch and allows passage for the suprascapular nerve

81
Q

Function of the coracoacromial ligament

A

Prevents upward dislocation of the shoulder joint

82
Q

The three bones that make up the shoulder

A

Humerus, scapula, clavicle

83
Q

What is the name of the coracoclavicular ligament that connects the clavicle to the coracoid process?

A

Trapezoid ligament

84
Q

What type of joint is the glenohumeral joint?

A

Synovial

85
Q

Shoulder dislocations may injure what nerve, resulting in what sensory and motor dysfunctions?

A

Axillary nerve

Sensory loss of lateral part of upper arm

Motor loss of deltoid - difficulty abducting arm

86
Q

What structures limit elbow extension?

A

Olecranon fossa of the humerus and olecranon process

87
Q

What structures limit elbow flexion?

A

Coranoid process and coranoid fossa

88
Q

What structure keeps the head of the radius tight against the capitulum of the humerus while allowing for rotation to occur during pronation and supination?

A

Annular ligament

89
Q

The elbow joint is weakest ____________ and strengthened by _________

A

anteriorly and posteriorly

collateral ligaments on the sides

90
Q

“Golfer’s elbow” refers to…

A

Repetitive use injury, typically excessive ulnar deviation

irritation of the medial epicondyle leading to inflammation of the muscles originating from it

91
Q

“Tennis elbow” is caused by…

A

Repetitive use injury, typically excessive extension of the wrist

irritation of the lateral epicondyle leading to inflammation of the muscles originating from it

92
Q

What bones articulate in the radiocarpal joint?

A

Radius, scaphoid, lunate

93
Q

Which ligaments play a role in limiting movement at the CMC and IM joints of the hand?

A

Superficial and deep transverse metacarpal ligaments

94
Q

What is the clinical presentation of lymphangitis?

A

localized pain and muscle aches, red streaks along drainage channel, systemic symptoms

Risk of septicemia if not treated

95
Q

What are the boundaries and structures that run through the cubital fossa?

A

Lateral - brachioradialis
Medial - pronator teres
Floor - brachialis
Superior - imaginary line connecting epicondyles

Structures lateral to medial - TAN
Tendon of biceps brachii
Artery, brachial
Nerve, median

96
Q

The medial cubital vein is tributary to what vein?

A

Basilic v

97
Q

What nerve travels with the cephalic v at the level of the cubital fossa?

A

Lateral antebrachial cutaneous n

98
Q

What is the role of arrector pili in sweat glands?

A

Muscle that causes hair to become erect and compresses sebaceous gland which then secretes sebum into shaft

99
Q

What is the role of sebum secreted by sebaceous glands?

A

Protect and hydrate the skin

100
Q

Explain the significance of a BRAF mutation in melanoma

A

BRAF is a proto-oncogene caused by a missense mutation
- responsible for MEK phosphorylation

Gain of function mutation results in kinase activity 500x higher than normal –> uncontrolled proliferation

Most nevi are docile until UV radiation causes further mutations

101
Q

Explain the significance of a RAS mutation in melanoma

A

Gain of function mutation in RAS would cause unregulated phosphorylation of BRAF –> MEK –> MAPK/ERK –> melanocyte cell proliferation

102
Q

Clinical presentation: slowly progressive muscle weakness in distal extremities.

Muscle biopsy: patchy mononuclear inflammatory cells rich in CD8+ T cells, focal invasion of abnormal appearing myofibers, “rimmed vacuoles”

A

Inclusion body myositis

103
Q

What structures create the carpal tunnel?

A

Hook of hamate and pisiform
Trapezium and scaphoid

104
Q

What structures pass through carpal tunnel?

A

Median n
FPL
FDP x4
FDS x4

105
Q

What structures create the ulnar canal?

A

Pisiform, hook of hamate, pisohamate ligaments

106
Q

Explain how regeneration is different from scar formation

A

Regeneration is the complete restoration to a normal state by differentiated cells and stem cells

Scar formation occurs when there is severe damage and loss of progenitor cells; the damage is replaced by connective tissue

107
Q

What determines a tissues ability to repair itself?

A
  1. Type of tissue: labile, stable, permanent
  2. extracellular matrix integrity
  3. factors produced at site of injury: macrophages, stromal cells, etc
  4. Integrins
108
Q

How is liver regenerated?

A

Kupffer cells (liver macrophages) recruit cytokines by autocrine releasing TNF –> it paracrine releases IL6 to act on hepatocytes –> stimulates hepatocytes from G0 to G1 –> growth factors released from the injury site bind to hepatocyte receptors –> cell proliferation –> TGF-B initiates termination when there is enough

109
Q

What are the steps of scar formation?

A

Platelet – fibroblasts, macrophages, neutrophils

Eschar - granulation tissue, new blood vessels

Collagen scar

110
Q

Healing by first intention

A

24 hrs: Neutrophil accumulation
24-48: Epithelial cells close wound
3 days: neutrophils replaced by macrophages to clear debris; granulation tissue invades
5 days: neovascularization peaks; fibroblasts migrate/proliferate
2 weeks: decrease in leukocyte infiltrate
4 weeks: essentially normal epidermis

111
Q

Healing by second intention

A

Severe wound –> necrotic debris –> more inflammation –> more granulation tissue made of fibrin, plasma fibronectin, type III collagen –> loss of dermal appendages –> scar by end of 1 month

112
Q

Dupuytren’s Contracture pathophysiology and clinical presentation

A

Hypoxia of the muscle in the hand + HLA-T cell interaction –> inflammatory response –> fibroblasts proliferate –> fibromatosis (excessive ECM deposition) –> tissue fibrosis and thickening/shortening of palmar fascia

Presents as firm nodule on palm of hand proximal to metacarpophalangeal joint

113
Q

Achondroplasia pathophysiology and clinical features

A

AD mutation by gain of function FGFR3 gene

Defective FGFR3 gene –> continuous receptor stimulation by FGF –> inhibited chondrocyte proliferation –> decreased lengthening of bone during endochondral ossification

Clinical features
- disproportionately large heads, short stature, normal torso

114
Q

Osteogenesis imperfecta pathophysiolog

A

AD in COL1A1 or COL1A2 –> decreased formation of hydrogen and disulfide bonds between type I precollagen molecules –> decreased triple helix formation –> decreased synthesis of normal type I collagen –> impaired bone matrix formation

115
Q

Osteogenesis Imperfecta type I and type II clinical features

A

Type I - mildest, most common
- growth delay, skeletal deformities, brittle bones, blue sclerae, progressive hearing loss

Type II - most severe, usually fatal in first year of life
- multiple intrauterine fractures
- underdeveloped lungs

116
Q

Osteopetrosis pathophysiology and clinical features

A

gene mutation –> inability of osteoclasts to generate acidic environment –> decreased bone resorption –> overgrowth of bone with pathological bone composition

Clinical features
- recurrent fractures - bones dense but brittle from poor remodeling
- cranial nerve disorders
- pancytopenia

117
Q

Briefly distinguish between osteoporosis, osteogenesis imperfecta, and osteopetrosis

A

Osteoporosis: increased osteoclastic activity –> increased bone resorption

Osteogenesis imperfecta: inability of osteoclasts to generate acidic environment –> decreased bone resorption

Osteopetrosis: decreased osteoclastic activity –> bone overgrowth

118
Q

Difference between bull rider’s thumb and skier’s thumb

A

Bull rider’s thumb is a torn ulnar collateral ligament of the thumb

Skier’s thumb is a torn radial collateral ligament of the thumb