Week 2 Flashcards
(108 cards)
1
Q
BONES
A
Provide structure, protect vital organs and play crucial role in mineral homeostasis
2
Q
Major cells: Osteoblast
A
(Bone forming)
3
Q
Major cells: Oseoclasts
A
{Resorptive (removal) cells}
4
Q
Major cells: Osteocyte
A
(Mature osteoblast) → mature bone cell
5
Q
Bones classed by shape
A
Long, flat, short (cuboidal) or irregular
6
Q
Bones classed by; other
A
Compact bone (cortical) and spongy bone (cancellous)
7
Q
BONE TURNOVER
A
- 5-7% recycled weekly and 0.5g enter/leave the adult skeleton every day
- Bones are constantly remodelled
- Mineralisation→ mineral deposition→ organic matrix
- Mineral resorption→ release of minerals→ blood
- Osteoblasts→ build bone {Hydroxyapatite crystals (calcium and phosphate)}
- Osteoclasts→ degrade (corrode) bone
8
Q
BONE FORMATION
A
- Ossification/Osteogenesis→ Bone formation, new bone material forms
- Bone formation begins in fetal life → cartilage or membranes grow into shape of bones
- Intramembranous ossification→ occurs in a limited number of bones→ bones are formed around a membrane that has been formed by mesenchymal cells
- Endochondral ossification→ more common process→ bones formed based on cartilage shape already established in fetus
- Bones grow, repair themselves and change shape in response to stress
- Mature bone repair or remodelling→ begins with production of organic matrix by bone cells
9
Q
Bone matrix
A
Consists of ground substances, collagen and other proteins that help bone formation and maintenance
10
Q
BONE REMODELLING: PHASE 1: ACTIVATION
A
A stimulus (drugs, hormone or physical stress) activates osteoclast production
11
Q
BONE REMODELLING: PHASE 2: RESORPTION
A
Osteoclasts gradually resorb bone; leaves elongated cavity (resorption cavity)
12
Q
BONE REMODELLING: PHASE 3: FORMATION
A
- New bone (secondary bone) is formed by osteoblasts lining the walls of resorption cavity
- Entire process of remodelling takes approx 3-4 months
13
Q
BONE REPAIR
A
- Bone remodelling→ useful for combatting physical stress or microscopic bone injuries
- Larger injuries→ need bone repair
- Bones heal in same stages as soft tissue injuries (but instead of scar tissue; a new bone is formed)
14
Q
STAGES OF BONE REPAIR (4)
A
- INFLAMMATION/ HAEMATOMA FORMATION
- PROCALLUS FORMATION
- CALLUS FORMATION
- REPLACEMENT OF CALLUS
15
Q
STAGES OF BONE REPAIR: INFLAMMATION/ HAEMATOMA FORMATION
A
- Initial phase; inflammatory cells move to site of injury
- A haematoma forms (blood collection outside of blood vessel due to injury)
16
Q
STAGES OF BONE REPAIR: PROCALLUS FORMATION
A
- Soft callus occurs where connective tissue stem cells and blood vessels move to the fracture
17
Q
STAGES OF BONE REPAIR: CALLUS FORMATION
A
- Toughened area→ arises due to woven components being deposited
18
Q
STAGES OF BONE REPAIR: REPLACEMENT OF CALLUS
A
Replacement of callus with true, new bone
19
Q
CALCIUM HOMEOSTASIS
A
- Regulated by 3 hormones: PTH, calcitonin, calcitriol
- Balance between dietary intake, urinary and fecal losses and exchanges between osseous bone tissue
20
Q
CALCIUM HOMEOSTASIS: PARATHYROID HORMONE (PTH)
A
- Secreted by chief cells
- Senses low Ca2+ in plasma→ secretes hormone to increase Ca2+ (decrease in phosphate)
- Will be sensed by the kidneys, bones, GIT
21
Q
CALCIUM HOMEOSTASIS: CALCITONIN (THYROCALCITONIN)
A
- Secreted by parafollicular cells of the thyroid gland
- Decrease Ca2+ in plasma (decrease phosphate, phosphate absorption is increased in GIT)
- Can be in response to eating too much calcium
- Will be sensed by the kidneys, bones (Not GI) Strongest effect on bone
22
Q
CALCIUM HOMEOSTASIS: CALCITRIOL (Vit D3, 1,25-dihydroxyvitamin D)
A
- Active hormone that is modified from absorbed vit D
- Kidney→ Increased reabsorption of calcium and phosphate
- GIT→ Increased absorption of calcium and phosphate
- Bone: Stimulates PTH increased reabsorption of calcium and decreased of phosphate
23
Q
FRACTURES: AETIOLOGY AND PATHOPHYSIOLOGY
A
- Fracture→ a break in bone (Any bone may break)
- Trauma and disease may cause a bone to break
24
Q
SIGNS AND SYMPTOMS OF FRACTURES
A
- Impaired or loss of function
- Unnatural alignment (deformity)
- Swelling
- Possible muscle spasm
- Tenderness and pain
- Bruising or discoloration around the break
- Impaired sensation
25
CLASSIFICATION OF FRACTURES: CLOSED
Bone is broken
| Skin isn’t broken
26
CLASSIFICATION OF FRACTURES: OPEN
- Bone broken and protruding through skin→ bone marrow exposed to external environment
- Risk of infection and osteomyelitis
27
CLASSIFICATION OF FRACTURES: GREENSTICK
- Bone is bent on one side with incomplete fracture on the other side
28
CLASSIFICATION OF FRACTURES: HAIRLINE
- Crack in bone, but bones remain aligned
29
CLASSIFICATION OF FRACTURES: COMMINUTED
Bone in 3 or more pieces
30
CLASSIFICATION OF FRACTURES: DISPLACED
Bones are out of anatomical alignment
31
CLASSIFICATION OF FRACTURES: IMPACTED
- Bone fragment is driven into medullary space or spongy bone of another
- Pressure/weight that causes break
- Impacts or crushes the rest of the bone
32
CLASSIFICATION OF FRACTURES: TRANSVERSE
Fracture is perpendicular to
33
CLASSIFICATION OF FRACTURES: OBLIQUE
Diagonal fracture, between linear and transverse
34
CLASSIFICATION OF FRACTURES: SPIRAL
Fracture spirals around axis of bone
35
COMMON FRACTURES; UPPER LIMB
- Clavicle
- Neck of humerus (usually in elderly)
- Shaft of humerus
- Radius/Ulna
- Thumb side of wrist
36
COMMON FRACTURES; LOWER LIMB
Femur
- Neck of femur
- Intertrochanteric fracture
- Shaft of femur
- Tibia and Fibula (common in young; motorcyclists)
- Bones of the toes or foot, or ankle
37
HEALING OF FRACTURES (4)
- Hematoma formation
- Soft callus formation
- Hard callus formation
- Bone remodelling
38
HEALING OF FRACTURES: Hematoma formation
Hematoma is converted to granulation tissue by invasion of cells and blood capillaries
39
HEALING OF FRACTURES: Soft callus formation
Deposition of collagen and fibrocartilage converts granulation tissue to a soft callus
40
HEALING OF FRACTURES: Hard callus formation
Osteoblasts deposit a temporary bony collar around the fracture to unit the broken pieces while ossification occurs
41
HEALING OF FRACTURES: Bone remodelling
Small bone fragments are removed by osteoclasts, while osteoblasts deposit spongy bone and then convert it to compact bone
42
HEALING OF FRACTURES: general info
- Uncomplicated fracture takes 8-12 weeks to heal
- Hard callus formation→ 4-6 weeks to form
- Callus persists for 3-4 months
- Remodelling→ original structure
43
Joints: Articulation and classification
- Articulation→ site where 2 or more bones are attached→ allows for movement bones don’t provide
- Joints classed on movement potential or structure
44
JOINTS: BASED ON MOVEMENT
- Synarthroses→ immovable joints
- Amphiarthroses→ Slightly movable joints
- Diarthroses→ Freely movable joints
45
JOINTS: BASED ON CONNECTIVE STRUCTURES
- Cartilaginous
- Fibrous
- Synovial
46
SYNOVIAL JOINTS
Largest group of joints found in the body (e.g. Hips, shoulders and knees)
47
SYNOVIAL JOINTS: ARTICULAR CARTILAGE
- Layer of hyaline cartilage that covers the facing surfaces of 2 bones
48
SYNOVIAL JOINTS: JOINT CAVITY
- Separates articular surfaces and filled with synovial fluid
49
SYNOVIAL JOINTS: SYNOVIAL MEMBRANES AND SYNOVIAL FLUID
- Lines capsule and secrete a substance that gives synovial fluid its viscous quality
- Lubricates the joint so the joint moves more freely
50
SYNOVIAL JOINTS: OUTER SLEEVE IS CALLED THE JOINT CAPSULE
- Fibrous connective tissue
| - Holds bones together and protects joints
51
WHAT IS CARTILAGE
- Part of skeletal system→ it is ‘pre-bone’ in mammals
- Some exceptions→ E.g. Clavicle (collarbone) isn’t preformed in cartilage and is directly formed as bone via ossification
- Gives body tensile strength→ strength with added movement
- Supplied nutritional needs by diffusion→ cartilage doesn’t contain blood vessels or nerves
52
CARYILAGE: CELL UNIT AND TYPES
- Cell unit→ chondrocytes
| - 3 types of cartilage→ Hyaline, Fibrocartilage and Elastic
53
SOFT TISSUE INJURIES: DISLOCATION (OR LUXACTION)
- Total and temporary loss of contact between articular cartilage
- Or displacement of one or more ends of articulating bones
- Occurs when extreme forces damage a ligament and permit 2 bones to separate
54
SOFT TISSUE INJURIES: SUBLUXATION
- Partial loss of contact between articular surfaces of 2 bone
- Disolacations must be restored to normal position then joint immobilised for healing of torn ligaments and tendons
55
SOFT TISSUE INJURIES: STRAIN
- Tear or injury to a tendon (strip or sheet of fibrous CT that attaches skeletal muscle to bone) or muscle
56
SOFT TISSUE INJURIES: SPRAIN
- Tear or injury to a ligament (band of fibrous CT that connects bone to bone or bone to cartilage)
- May occur as a result of a twisting or stretching action
57
SOFT TISSUE INJURIES: AVULSION
- Forcible detachment of a tendon, ligament, muscle or bone from its attachment site
58
SOFT TISSUE INJURIES: MYOGLOBINURIA
Release of myoglobin into bloodstream due to muscle damage/trauma
59
SOFT TISSUE INJURIES: SIGNS AND SYMPTOMS
- Usually painful and accompanied by soft tissue swelling
- Decreased range of motion
- Localised oedema
- Obvious deformity. E.g. Complete rupture of tendon, dislocation
- Total loss of function in severe sprain or strain
- Some may hear a ‘pop’ or ‘snap’ during injury
- Compromised blood supply
60
SOFT TISSUE INJURIES: TREATMENT
Rest , Ice, Compression , Elevation, Referral
61
MUSCLES
- Muscles→ Only contractile tissue in body and drives movement
- Attachment of muscles on bones→ provide series of levers above joints→ controls speed and strength of movement
- Each muscle fibre→ Single muscle cell; cylindrical & surrounded by membrane capable of excitation
- Classified by appearance or metabolic process
62
TYPES OF MUSCLE: APPEARANCE
- Red muscle→ contains oxygen-carrying protein myoglobin (red colour)
- White muscle→ Lacking myoglobin
63
TYPES OF MUSCLE: METABOLIC PROCESS
- Slow- twitch fibres depend on aerobic oxidative metabolism
- Fast-twitch fibres use anaerobic glycolytic pathway for rapid-energy conversion
- Further grouped into type 1 (red, slow twitch) and type 2 (white, fast twitch)
64
MUSCLE CONTRACTIONS
- For muscle to create movement in body→ signal must be sent telling muscle to contract or relax
- Signal transmitted via neuromuscular junction (where nerve fibre meets muscle cell)
- Motor unit→ Single motor neuron and muscle fibres connected→ may be considered functional unit of skeletal muscle
- Myofibrils→ Functional unit of muscle contraction
- Within each myofibril→ are sarcomeres (contractile units of muscle cell)
65
ACTION POTENTIAL: MUSCLES
- Muscle cells also have membrane potential→ makes resting muscle cell polarised
- When Acetylcholine (ACh) (a neurotransmitter) is bound to motor end plate→ it opens ion channels
- Allows Sodium and Potassium to pass through
- In this process→ More Sodium will diffuse than potassium diffusing out→ changing overall charge
- Results in depolarization of cell (interior of muscle cell becomes less negative
- This starts the action potential which spreads across muscle cell
- Change in charge in initial section changes permeability in adjacent areas (opens sodium ion channels)→ passes on reaction
- Once this passes→ sodium channels close and potassium channels open→ allows potassium ions to move out of cell
- Results in muscle returning to resting charge state (depolarised) → needs to occur before stimulation occurs again→ Ion concentration restored by sodium potassium pump
66
URIC ACID
- Forms ions and salts (urates and acid urates); normal product of metabolic breakdown of purine nucleotides
- Normally excreted in urine; defect in metabolism can lead to buildup of acid in blood
- High concentration→ forms insoluble crystals; deposited in connective tissue in body→ inflammation
67
METABOLIC JOINT DISEASE: GOUT SUMMARY
- Form of arthritis caused by too much uric acid in the bloodstream
- Increased uric acid→ insoluble crystals deposited in connective tissue in body→ inflammation→ gouty arthritis
68
METABOLIC JOINT DISEASE: GOUT RISK FACTORS
Age, genetic predisposition, excessive alcohol intake, obesity, meds, lead toxicity
69
METABOLIC JOINT DISEASE: GOUTPATHOPHYSIOLOGY
- Most uric acid (by product of protein metabolism) is eliminated from the body through the kidneys
- Crystallisation in synovial tissue (why this happens is unknown)
- Lower body temperatures at periphery of body
- Decreased albumin or glycosaminoglycan levels
- Changes in ion concentration and pH
- Trauma that promotes crystal precipitation
- Leads to inflammatory response in the joint- leads to tissue damage
70
METABOLIC JOINT DISEASE: GOUT SYMPTOMS
- Primary symptom→ severe pain, usually at night
- Affected area becomes hot, red and extremely tender and slightly swollen
- 50% of initial attacks are in the metatarsophalangeal joint of the big toe
- Other 50% elbow, heel, ankle, instep of foot, knee and wrist
71
METABOLIC JOINT DISEASE: GOUT TREATMENTS
- Anti-inflammatory drugs (NSAIDs)
- Anti-hyperuricemic drugs (e.g. allopurinol) are given to reduce serum urate concentrations
- Uricosuric drugs (e.g. Probenecid) to increase excretion of urate by blocking its reabsorption by kidney tubules
- Hydrocortisone may be injected into joint to relieve pain
- Ice may relieve inflammatory pain
- Low protein diet to decrease uric acid concentration
72
INFLAMMATORY AUTOIMMUNE DISEASE
- Inflammatory cells accumulate in the synovial fluid→ Synovial membrane thickens and puts pressure on venules which leads to focal hypoxia and metabolic acidosis
- Stimulates enzymes that degrade the articular cartilage→ Increased inflammation in surrounding ligaments and tendons→ Pannus formation (scar tissue over denuded area of synovial membrane)
73
ANKYLOSING SPONDYLITIS
- Chronic inflammatory joint disease→ Stiffening and fusion (ankylosis) of the spine and sacroiliac joints
- Begins late adolescence or early adulthood (peak incidence -20 years old)
- Cause unknown but genetic predisposition
- Affects point at which the tendons and ligament attach to bone
- Begins with inflammation of fibrocartilage, particularly in the vertebrae and sacroiliac joint
- Inflammatory cells infiltrate and erode fibrocartilage
- As repair begins, the scar tissue ossifies and calcifies; the joint eventually fuses (usually beginning with the sacroiliac joints and progressing up the vertebral column)
74
RHEUMATOID ARTHRITIS: SUMMARY
Inflamed joints due to autoantibodies
75
RHEUMATOID ARTHRITIS: CAUSE
Autoimmune, genetics, unknown
76
RHEUMATOID ARTHRITIS: SYMPTOMS
Joint pain, swelling, warm joints, affects organs, rheumatoid nodule, morning stiffness
77
RHEUMATOID ARTHRITIS: JOINTS OR BONES AFFECTED
Systemic synovial joints (fingers, feet, wrists, elbows, ankles, knees, shoulders, hips, cervical spine)
78
RHEUMATOID ARTHRITIS: DIAGNOSIS
Diagnostic criteria (rheumatoid factor in blood, imaging shows synovitis, presence of symmetrical arthritis, morning stiffness)
79
RHEUMATOID ARTHRITIS: TREATMENT
Hot/cold packs, anti-inflammatories, immunosuppression, corticosteroids, synovectomy
80
RHEUMATOID ARTHRITIS: DEMOGRAPHICS (AGE, GENDER)
Females 3:1, 20-60 years
81
OSTEOARTHRITIS: SUMMARY
Age related disorder of synovial joints leading to degradation of bone cartilage
82
OSTEOARTHRITIS: CAUSE
- Related to wear and tear, articular cartilage breaks down.
- Degradation faster than repair
- Bone spurs can develop and break off
83
OSTEOARTHRITIS: SYMPTOMS
Pain, stiffness, swelling, muscle wasting, deformity, use related pain relieved by resting
84
OSTEOARTHRITIS: JOINTS OR BONES AFFECTED
Weight bearing joints or commonly used joints
85
OSTEOARTHRITIS: DIAGNOSIS
Imaging (X-ray, CT, MRI)
| Arthroscopy
86
OSTEOARTHRITIS: TREATMENT
Rest, light exercise, analgesics, surgery, anti-inflammatories
87
OSTEOARTHRITIS: DEMOGRAPHICS
> 45 years, equal risk for men and women (men> women up to age 55)
88
OSTEOPOROSIS: SUMMARY
- Decreased bone mass due to loss of bone matrix
- More bone resorption than formation
- Porous bone (brittle and fragile)
89
OSTEOPOROSIS: CAUSE
Diet (decreased Ca2+, decreased Vit D, increased carbonated beverages/ alcohol)
Sedentary lifestyle,
Decreased estrogen
90
OSTEOPOROSIS: SYMPTOMS
Increased risk of fractures, bone fractures, kyphosis (outwards curvature of the spine)
Low body weight
91
OSTEOPOROSIS: JOINTS OR BONES AFFECTED
Mostly hip, femur and lower vertebrae, but can affect all bones
92
OSTEOPOROSIS: DIAGNOSIS
Dual energy X ray (DEXA)
| DEXA imaging showing reduced bone mass
93
OSTEOPOROSIS: TREATMENTS
No treatment- preventions:
| Increased Ca2+/Vit D, decreased alcohol, weight bearing exercise
94
OSTEOPOROSIS: DEMOGRAPHICS
> 55 years, more common in females (menopause)
95
OSTEOMALACIA: SUMMARY
Metastatic bone disease, causing bones to soften
96
OSTEOMALACIA: CAUSE
- Deficiency of Vit D leading to decreased absorption of Ca2+ from intestine
- Inadequate bone mineralisation
- Results from a defect in bone building process
97
OSTEOMALACIA: SYMPTOMS
- Skeletal deformities
- Soft bones, pain when weight bearing/ palpation of affected bone
- Muscle weakness
98
OSTEOMALACIA: JOINTS OR BONES AFFECTED
Affects all bones
99
OSTEOMALACIA: DIAGNOSIS
Palpation of bone (pain)
Vit D levels
Imaging
Bone biopsy
100
OSTEOMALACIA: TREATMENTS
Increased Vit D, Increased exposure to sun
101
OSTEOMALACIA: DEMOGRAPHICS
Those with low dietary vit D or low sun exposure, darker skin, obesity
102
MUSCULAR DYSTROPHY: SUMMARY
Group of genetic disorders that produce progressive degeneration and necrosis of skeletal muscle fibres and eventual replacement with fat and CT
103
MUSCULAR DYSTROPHY:
| CAUSE
- Skeletal muscles get replaced with fat and CT
- Muscle weakness leading to wasting
- Dystrophin (protein) connects cytoskeleton of a muscle fibre to surrounding
Types: DMD→ No dystrophin,
BMD→ Decreased dystrophin
104
MUSCULAR DYSTROPHY:
| SYMPTOMS
- Walking problems (Gower’s sign for DMD)
- Skeletal deformity
- Limited use of arms
- Impaired pulmonary function
- Muscle pain and stiffness
- Learning disabilities
105
MUSCULAR DYSTROPHY:
| BONES OR JOINTS AFFECTED
Proximal muscles
106
MUSCULAR DYSTROPHY:
| DIAGNOSIS
Serum muscle enzymes
Genetic screening
Muscle biopsy
Electromyography
107
MUSCULAR DYSTROPHY:
| TREATMENTS
Physical therapy, medication, surgery, assistive devices/support equipment
Outcome depends on type and prognosis of disease
108
MUSCULAR DYSTROPHY:
| DEMOGRAPHICS
More common in males (X-linked)
| DMD→ males only 1 in 3500
