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PHA 332 > MSK ANATOMY > Flashcards

MSK ANATOMY Flashcards

1
Q

define arthralgia

A

term used to describe joint pain when the joint appears normal onexamination

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2
Q

define arthritis

A

term used when there is evidence of joint inflammation (swelling, deformity or an effusion)

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3
Q

what should be done with a person presenting with joint pains/

A

the history and examination must assess:–the distribution of the joints affected (symmetrical or peripheral)–the presence of morning stiffness (common in inflammatory arthropathies)–aggravating and relieving factors–past medical history and family history

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4
Q

where could pain around a single joint arise from?

A

rom the joint itself (articular problem) or from structures surrounding the joint (periarticular problem)

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5
Q

define enthesitis

A

(inflammation at the site of attachment of ligaments, tendons and joint capsules) e.g. tenosynovitis (sheath surrounding tendon), bursitis and tendonitis are all causes of periarticular pain

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6
Q

what are causes of large joint monoarthritis?

A

osteoarthritis, gout, pseudogout, trauma and septic arthritis

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7
Q

what are more prevelant- non- inflam or inflam diseases?

A

non-inflam

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8
Q

who are MSK diseases seen more in?

A

women- associate with ageing

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9
Q

what is the most common MSK problem?

A

Osteoarthritis is the most common joint disorder, with knee involvement a major cause of disability
osteoprosisi is most common bone disorder

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10
Q

what are the 3 types of joint?

A

Fibrous: 2 bones united by fibrous tissue; immoveable
Cartilaginous: Bone(s) united by hyaline cartilage (synchondroses) / fibrocartilage (symphyses); limited movements
Synovial: synovial capsule, membrane and cavity; moveable

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11
Q

what are the types of fibrous joints?

A

sutures
syndesmoses
gomphoses

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12
Q

what is the difference between primary and secondary symphsis?

A

Primary/ synchondrosis : Bone(s) united by hyaline cartilage, limited movements Examples: costochondral joints,1st
Sternochondraljoint, growth plate.

Secondary/ symphysis: 2 bone ends covered with hyaline cartilage with a disc of fibrocartilage in between, limited movements
Examples: all midline symphyses–intervertebral,pubis.

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13
Q

what are the different types of synovial joints?

A

atypical- articular surface covered with fibrocartliage

typical- articular surface covered with hyaline cartliage

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14
Q

what are the 6 features that typical synovial joints are characterised by?

A
  1. The bone ends involved are covered by hyaline cartilage
  2. Surrounded by a joint capsule
  3. Encloses a joint cavity
  4. Capsule reinforced externally/internally byligaments
  5. Lined by synovialfluid
  6. Joints are capable of varying degrees ofmovement
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15
Q

what is in a synovial joint?

A
  1. Articularcartilage
  2. Joint (synovial)cavity
  3. Capsule
  4. Synovial fluid
  5. Ligaments
  6. Nerves
  7. Blood vessels
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16
Q

what are the 6 types of synovial joints?

A 
plane
pivot
saddle
ball & socket
hinge
ellipsoid / condyloid
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17
Q

what are the movements assoicated with ball and socket joints?

A

monoaxial
biaxial
multiaxial

18
Q

what is joint stability?

A

This refers to the resistance offered by various musculoskeletal tissues that surround a skeletal joint, and is affected by a number of factors:•joint shape•ligaments•tendons and muscles

19
Q

whats an example of a ball and socket joint?

A

shoulder and hip

-shoulder has greater movement due to the bone being more shallow

20
Q

what is an exmple of a hinge+ pivot/ bicondylar joint?

A

elbow and knee

21
Q

what is osteoarthritis?

A
  • painful and stiff joints; most common type ofarthritisin the UK
  • Imbalance between mechanical wear of the articular cartilage (degeneration) and its repair
  • leads to inflammation and degradation (disordered repair –bone spurs).•Inflammation leads to further joint degradation (rather than repair).
22
Q

what are the predisposing factors of OA?

A
  • Female sex
  • Increasing age (time tears at the joints)
  • Obesity (heavy loading on the joints)
  • occupation
  • Joint trauma (accelerates joint erosion)
  • Family historyExplain
23
Q

what causes OA?

A

degradation of cartilage and remodelling of bone
•degradation of cartilageandremodellingof bonedue to:
•an active response ofchondrocytesin the articular cartilage •inflammatory cells in the surrounding tissues.

24
Q

what does LOSS stand for- OA?

A

L-loss of joint space,
O-osteophytes / formation of bone spurs
S-Sub-articular sclerosis –increased bone density at points on contact,
S-subcondralcysts

25
Q

what is the upper extremity of OA?

A
  • Heberdennodes -osteophytes (bone spurs) at the Distal Interphalangeal joints.
  • Bouchard nodes -osteophytes (bone spurs) at the Proximal Interphalangealjoints.•Sparing of wrists, elbows, and shoulders.
26
Q

what is the lower extremity of OA?

A
  • Affects the hips and knees.

* Spine; affects the lower lumbar and cervical vertebrae

27
Q

how does GOUT present?

A

usually the big toe, but it can be in other joints in the feet, hands, wrists, elbows or knees
•hot, swollen, red skin over the affected joint

28
Q

what is GOUT?

A

a type of arthritis where crystals of uric acid form inside and around joints that causes sudden, severe joint pain

29
Q

what is Gouty tophi?

A

subcutaneous deposits of uric acid under the skin –DIP

30
Q

what joints are affected by GOUT?

A

base of big toe and thumb, wrist, DIP , knees and ankles

31
Q

what are the pre-disposing factors of GOUT?

A

It’s more common in men (3 x more) over 40•Overweight / obese
•High purine diet: diet: beer, sugar-sweetened beverages, high purine such as liver, shellfish, or anchovies)
•alcohol consumption
•have high cholesterol, high blood pressure, kidney problems, osteoarthritis or diabetes
•take medicines such as diuretics (water tablets), or medicines for high blood pressure (such as ACE inhibitors)
•have had surgery or an injury
•Family history

32
Q

what is scleroderma?

A

•Autoimmune, inflammatory, fibrotic CT disease

33
Q

what is the underlying cause of scleroderma?

A

an overproduction and accumulation of collagen

34
Q

what does scleroderma cause?

A

results in hard, thickened areas of skin and sometimes problems with internal organs and blood vessels.

35
Q

what are the types of scleroderma?

A
  • localised scleroderma– just affects the skin (morphoea and linear)
  • Morphoea- discoloured, tight and shiney patches of skin anywhere on body, itchy,
  • Linear– thickened skin occurs in lines on face, scalp, arms, legs; can affect underlying muscle and bone

Systemic sclerosis– may affect blood circulation and internal organs as well as the skin

36
Q

what can systemic sclerosis affect?

A

This can cause a range of potentially serious problems if heart, lungs, GI tract and kidneys affected by fibrosis and inflammation (SOB, hypertension and pulmonary hypertension(high blood pressure in the lungs).

37
Q

what are the visible symptoms of systemic sclerois?

A

Calcinosis in digits and Raynard’s as a result of damage to peripheral blood vessels

38
Q

what are the causes of cleroderma?

A
  • Auto-immune system problems; 15-20% percent of cases also has symptoms of another autoimmune disease, such as rheumatoid arthritis, lupus or Sjogren’ssyndrome
  • Genetics
  • Environmental triggers; viral exposure, medicines , chemical exposure (e.g. silica dust)
39
Q

who is scleroderma more common in?

A

3x more likely in women

40
Q

what is ehlers-Danlos syndromes?

A

a group of rare inherited conditions that affect connective tissue
it increases range if joint movement
causes stretchy skin
fragile skin that breaks/ bruises easily

41
Q

what are the types of EDs?

A
  • Hypermobile EDS (hEDS) is the most common type.
  • Classical EDS (cEDS)is less common than hypermobile EDS and tends to affect the skin more.
  • Vascular EDS (vEDS)is a rare type of EDS and is often considered to be the most serious and potentially life threatening.
42
Q

what is the differences between EDs caused by?

A

caused by gene defects which weaken connective tissue.
•Depending on the type of EDS, the faulty gene may have been inherited from 1 parent or both parents.
•Can be a result of a spontaneous genetic mutation

PHA 332 (42 decks)

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