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2nd Year Medicine > MSK > Flashcards

MSK Flashcards

1
Q

Largest type of tissue in human body?

A

Muscle

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2
Q

Striated muscles? (2)

A

Skeletal + cardiac

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3
Q

What causes striations?

A

Myosin + actin

  • Myosin = dark thick filaments
  • Actin = light thin filaments
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4
Q

Skeletal muscle innervation? Cardiac muscle? Smooth muscle?

A
  • Skeletal muscle = somatic NS

* cardiac + smooth = ANS

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5
Q

Differences between skeletal and cardiac muscle? (4)

A

Skeletal muscle

  • Neurogenic initiation of contraction
  • Neuromuscular junction
  • No gap junction
  • Ca++ entirely from SR

Cardiac

  • Myogenic (pacemaker) initiation of contraction
  • No neuromuscular junction
  • Gap junctions
  • Ca++ from ECF and SR (CICR)
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6
Q

What is the neurotransmitter at neuromuscular junction?

A

Acetylcholine

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7
Q

Skeletal muscle fibres organised into? What is this?

A

Motor units

* Motor unit = single alpha motor neuron + skeletal muscle fibres it innervates

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8
Q

Number of muscle fibres per motor unit?

A
  • Muscles which serve fine movements (e.g. external eye muscles, facial expression, hand) have fewer fibres per motor unit
  • In muscles where power is more important than precision = more muscle fibres
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9
Q

Levels of organisation in skeletal muscle?

A
  • Whole muscle -> muscle fibre (= one muscle cell) -> myofibril -> sarcomere (functional unit)

Myofibril and sarcomeres made up of myocin and actin

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10
Q

How are skeletal muscles attached to skeleton?

A

Tendons

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11
Q

Functional units of muscle?

A

Sacromeres

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12
Q

Zones of the sarcomere? (4)

A
  • A-band = thick filaments along with portions of thin filaments that overlap in both ends of thick filaments
  • H-Zone = lighter area within middle of A-band where thin filaments don’t reach
  • M-Line = extends vertically down middle of A-band within the centre of H-zone
  • I-Band = consists of remaining portion of thin filaments that do not project in A-band
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13
Q

What is the definition of a functional unit?

A

the smallest component capable of performing all the functions of that organ

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14
Q

Where is sacromere found?

A

Between 2 z-lines

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15
Q

Muscle tension?

A

Produced by sliding of actin filaments on myocin filaments

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16
Q

Force generation depends on?

A

ATP-dependent interaction between myosin + actin

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17
Q

ATP only required for muscle contraction? Ca++?

A

ATP is required for both contraction & relaxation

* Ca++ is required to switch on cross bridge formation

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18
Q

Excitation contraction coupling?

A

process where surface action potential results in activation of the contractile structures of the muscle fibre

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19
Q

When is Ca++ released in skeletal muscle fibres? What are T-tubules?

A

In skeletal muscle fibres Ca2+ is released from the lateral sacs of the sarcoplasmic reticulum when the surface action potential spreads down the transverse (T)-tubules
* T-tubules are extensions of the surface membrane that dip into the muscle fibre

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20
Q

Explain process of muscle contraction + relaxation

A
  • Acetylcholine released by motor neurone and binds to receptors
  • Action potential generated and travels down transverse T-tubules
  • AP in T-tubules triggers Ca++ release from SR
  • Ca++ binds to troponin-tropomyosin to reveal cross-bridge binding site
  • Cross bridge formed between myosin and actin
  • Ca++ actively taken up by SR when AP dissipates
  • When Ca++ no longer bound to troponin/tropomyosin, binding site is blocked again and myosin detaches from actin
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21
Q

Motor units? Motor unit recruitment? How can muscle fatigue be prevented?

A
  • Motor units = allow simultaneous contraction of muscle fibres
  • Motor unit recruitment = stronger contraction achieved by stimulation of more motor units
  • Muscle fatigue can be prevented via asynchronus motor unit recruitment during submaximal contractions
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22
Q

What does tension developed by each contracting muscle fibre depend on?

A
  • frequency of stimulation
  • length of muscle fibre
  • thickness of muscle fibre
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23
Q

How are stronger contractions in skeletal muscle brought about?

A

If restimulate muscle fibre before it has relaxed, 2nd twitch added on to first twitch resulting in summation

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24
Q

Tetanus contraction? Can this phenomenon occur in cardiac muscle?

A

Muscle fibre stimulated so rapidly that it does not relax at all between stimuli resulting in MAXIMAL SUSTAINED CONTRACTION

  • NO, as long refractory period prevents generation of tetanic contractions
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25
Q

What is the approximate optimal length of skeletal muscle?

A

In the body the resting length of skeletal muscle is approximately its optimal length (not the same for cardiac muscle)

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26
Q

Contractile component of skeletal muscle? Elastic component skeletal muscle?

A
  • Contractile = sarcomeres

* Elastic = tendon/connective tissue

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27
Q

2 types of skeletal muscle contraction?

A
  • Isotonic contraction: used for (1) body movements and for (2) moving objects. Muscle tension remains constant as the muscle length CHANGES
  • Isometric contraction: used for (1) supporting objects in fixed positions and for (2) maintaining body posture. Muscle tension develops at CONSTANT muscle length
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28
Q

Differences between different types of skeletal muscle fibres? (3)

A
  • enzymatic pathways for ATP synthesis
  • resistance to fatigue - muscle fibres with greater capacity to synthesise ATP are more resistant to fatigue
  • activity of myosin ATPase - determines speed at which energy is made available for cross bridge cycling i.e. the speed of contraction
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29
Q

ATP production in skeletal muscle? (3)

A
  • Oxidative phosphorylation (main source when O2 present)
  • Transfer of high energy phosphate from creatine Phosphate to ADP
  • Glycolysis (main source when O2 is not present)
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30
Q

3 types of skeletal muscle fibre?

A
  • Slow oxidative type I fibres (also known as slow-twitch fibres) - prolonged, low work aerobic activities e.g. maintenance of posture, walking
  • Fast oxidative (Type IIa) fibres (also known as intermediate-twitch fibres) - both aerobic and anaerobic metabolism, prolonged moderate work activities e.g. jogging
  • Fast glycolytic (Type IIx) fibres (also known as fast-twitch fibers) - anaerobic metabolism, short-term high intensity activities e.g. jumping
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31
Q

Reflex action?

A

stereotyped response to a specific stimulus - simplest form of coordinated movement

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32
Q

Stretch reflex?

A

simplest monosynaptic spinal reflex

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33
Q

What kind of mechanism is stretch reflex?

A

Stretch reflex is negative feedback that resists passive change in muscle length to maintain optimal resting length of muscle

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34
Q

Why is stretch reflex important?

A

helps maintain posture e.g. while walking

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35
Q

Receptor for stretch reflex? Process?

A

sensory receptor is the muscle spindle and is activated by muscle stretch

  • stretching muscle spindle increases firing in afferent neurons
  • afferent neurons synapse in the spinal cord with the alpha motor neurons (efferents) that innervate the stretched muscle
  • Contraction of stretched muscle
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36
Q

What is required for stretch reflex other than contraction of affected muscle?

A

Relaxation of antagonist muscle

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37
Q

Spinal segment and peripheral nerve involved in knee jerk reflex? Ankle jerk? Biceps jerk? Brachioradialis? Triceps jerk?

A
  • Knee jerk (L3, L4) - femoral nerve
  • Ankle jerk (S1, S2) - tibial nerve
  • Biceps jerk (C5, C6) - musculocutaneous nerve
  • Brachioradials (C5, C6) - radial nerve
  • Triceps jerk (C6, C7) - radial nerve
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38
Q

What are muscle spindles? Other name? Ordinary muscle fibres?

A
  • Collection of specialised muscle fibres
  • Intrafusal fibres
  • Ordinary = extrafusal fibres
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39
Q

Where are muscle spindles found? Features?

A

Found in belly of muscles and run parallel to extrafusal muscle fibres
* Have sensory nerve endings called annulospiral fibres

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40
Q

Efferent supply to muscle spindles? Function?

A

Gamma motor neurons
* y neurons adjust level of tension in muscle spindles to maintain their sensitivity when muscle contracts

Intrafusal fibres DO NOT contribute to overall strength of contraction!!!

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41
Q

Causes of intrinsic muscle disease? (5)

A
  • Genetic e.g. muscular dystrophy, myotonia, congenital
  • Inflammatory e.g. polymyositis
  • Non-inflammatory e.g. fibromyalgia
  • Endocrine e.g. cushing
  • Toxic e.g. alcohol
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42
Q

Ix neuromuscular disease? (5)

A
  • Electromyography (muscular activity via APs)
  • nerve conduction studies
  • muscle enzymes
  • inflammatory markers
  • muscle biopsy
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43
Q

Features of skeletal muscle fibres? (3)

A
  • Striated
  • Unbranched
  • Multinucleate (nuclei are at periphery of fibre)
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44
Q

Muscle fibre arrangement? Connective tissue supporting skeletal muscle tissue?

A
  • Muscle fibres grouped into bundles called fascicles (muscle contains several fascicles)
  • connective tissue that surrounds the muscle as a whole is called the epimysium
  • connective tissue around a single fascicle is the perimysium
  • connetive tissue around a single muscle fibre is the endomysium
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45
Q

What do thousands of sarcomeres placed end-to-end form? How far does a single sarcomere extend?

A

A myofibril

* sarcomere extends from one Z line to the next

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46
Q

Why are skeletal muscles striated?

A

Striations are an optical illusion – myofibril dark and light bands held in registry

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47
Q

3 types of skeletal muscle fibres?

A
  • Type I (“RED” fibres): slow contracting fibres that depend on oxidative metabolism -abundant mitochondria and myoglobin, resistant to fatigue and produce less force.
  • Type IIA: intermediate - relatively fast contracting, but are also reasonably resistant to fatigue
  • Type IIB (WHITE fibres): fast contracting fibres that depend on anaerobic metabolism - few mitochondria and myoglobin, fatigue easily and produce greater force
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48
Q

Features of cartilage? (4)

A
  • Semi-rigid and Deformable
  • Permeable
  • Avascular
  • Cells nourished by diffusion through the extracellular matrix
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49
Q

Features of bone? (3)

A
  • Rigid
  • Not Permeable
  • Cells within bone must be nourished by blood vessels that pass thru the tissue
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50
Q

Cells found in cartilage? Organisation?

A

chondrocytes (chondroblasts when immature)

* Chondrocytes held within extracellular matrix called lacuna

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51
Q

Hyaline ECM composed of?

A

1) 75% water
2) 25% organic material.
* 60% Type II collagen. Type II collagen differs from type I collagen (e.g. tendon) - it is finer and instead of aggregating into linear bundles it forms a 3D meshwork
* 40% proteoglycan aggregates. Proteoglycan aggregates are made up of GAGs (keratan sulfate and chondroitin sulfate) bound to a core protein and hyaluronan

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52
Q

Types of cartilage? (3)

A
  • Hyaline cartilage (blue) - most common form of cartilage
  • Elastic cartilage (yellow): very flexible
  • Fibrocartilage (white): hybrid between tendon and hyaline cartilage i.e. bands of type I collagen + rows of chondrocytes surrounded by ECM
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53
Q

Sites of hyaline cartilage? (5)

A
  • Articular surfaces
  • Tracheal rings
  • Costal cartilage
  • Epiphyseal growth plates
  • Precursor in fetus to many bones
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54
Q

Functions of bone?

A
  • Support
  • Levers for movement
  • Protection of internal organs
  • Calcium store: >95% calcium found in bone + constant exchange of calcium between bone and blood
  • Haemopoiesis: only the axial and limb girdle skeleton is involved in blood production
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55
Q

Composition of bone? (4)

A
  • 65% bioapatite (form of calcium phosphate - mostly hydroxyapatite)
  • 23% collagen
  • 10% water
  • 2% non-collaged proteins
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56
Q

Structure of bone? (2)

A
  • outer shell of dense cortical bone makes up the shaft (diaphysis)
  • Cancellous/trabecular bone at ends of bone (epiphyses)
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57
Q

How do blood vessels travel through bone?

A
  • Haversian canal + volkman’s canal
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58
Q

Difference in structure of trabecular and cortical bone?

A
  • bone cells and matrix are similar in compact and trabecular bone
  • main difference is the presence of spaces (marrow cavities) adjacent to trabecular bone

BOTH TYPEs aRE LAMELLAR!!! (made up of layers)

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59
Q

Cement lines?

A

lines that are visible surrounding the osteon

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60
Q

What does trabecular bone often lack? Why?

A

lacks Haversian canals

* the struts are thin so the osteocytes can survive from contact with the marrow spaces

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61
Q

Bone cells? (4)

A
  • Osteoprogenitor cells: reserve cells that can differentiate into osteoblasts
  • Osteoblasts: bone forming cells (lots of RER and mitochondria)
  • Osteocytes: bone cell trapped within bone matrix
  • Osteoclasts: large multinucleated cells - bone resorption
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62
Q

Process of bone remodelling?

A

CUTTING CONE

  • osteoclasts ‘drill’ into the bone forming a tunnel
  • a blood vessel will grow into the tunnel bringing osteoblasts which line the tunnel and begin laying down new lamellar bone
  • This process continues until only the space of a Haversian canal remains
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63
Q

What is the collection of osteoclasts and osteoblasts that participate in bone remodelling called?

A

basic multicellular unit or BMU

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64
Q

How do osteoblasts produce bone?

A

Secrete OSTEOID: collagen, glycosaminoglycans (GAGs), proteoglycans
* this then becomes mineralized over time

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65
Q

What is the mineral of bone made up of?

A

calcium phosphate crystals, particularly hydroxyapatite

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66
Q

Osteoclast origin and morphology?

A
  • Derived from macrophage line of cells

* Several will fuse to form a single giant cell

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67
Q

Differences between lamellar and woven bone?

A

During development or following a break, rather than having collagen fibres orientated all in one direction like lamellar bone, the collagen fibres are laid down in a haphazard fashion - WOVEN BONE

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68
Q

Adult osteomyolitis?

A

Inflammation of bone and medullary cavity, usually in long bones

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69
Q

Places where osteomyolitis is most common?

A
  • Vertebral osteomyolitis
  • Diabetic foot infection
  • Post-traumatic infection
  • Prosthetic joint infection
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70
Q

Most common pathogen in osteomyolitis?

A

staph aureus

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71
Q

Dx osteomyolitis?

A

GOLD STANDARD is bone biopsy!

Via percutaneous sample or deep surgical culture

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72
Q

Tx osteomyolitis?

A

Tx: debridement + antibiotics

Not an emergency, wait for culture results before beginning treatment

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73
Q

Risk factors for osteomyolitis? (6)

A
  • Open fractures
  • Diabetes/ Vascular insufficiency
  • Haematogeneous osteomyelitis
  • Vertebral osteomyelitis
  • Prosthetic joint infection
  • Specific hosts and pathogens
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74
Q

s/s osteomyolitis?

A

Rubor, tumor, dolor, functio laesa

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75
Q

How does infection occur in bone?

A

Bone is highly resistant to infection – infection only occurs with necrosis + high inoculum

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76
Q

How long does osteomyolitis tx take?

A

6 weeks

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77
Q

Open fractures? Tx? Clinical clues of osteomyolitis with open fracture? Pathogens?

A
  • Contiguous infection
  • Tx: debridement, fixation + soft tissue cover
  • Clinical clues = non-union + poor wound healing
  • Ax: staph aureus + aerobic gram -ve bacteria
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78
Q

Diabetes/venous insufficiency? Dx? Tx?

A
  • Contiguous infection that is often polymicrobial
  • Dx: Bone biopsy
  • Tx: debridement and antimicrobials
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79
Q

Mild diabetic foot ulcer tx?
Moderate? Severe?

How about patients with penicillin allergy?
MRSA?

A
  • Mild: Fluclox
  • Mod: fluclox + metronidazole
  • Severe: fluclox, gentamicin + metronidazole

Penicillin allergy

  • Mild = doxycycline/co-trimoxazole
  • Mod = doxycycline + metronidazole OR co-trimoxazole + metronidazole
  • Severe = vancomicin, gentamicin + metronidazole
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80
Q

Tx acute osteomyolitis (i.e. when cannot wait for culture)? What about for patients with penicillin allergy?

A

Fluclox + gram -ve and anaerobic cover

* allergy = sub fluclox for vanco

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81
Q

Mild MRSA tx? Mod? Severe?

A
  • Mild = Doxycycline or co-trimoxazole
  • Mod = vancomycin
  • Severe = vancomycin + gram -ve cover
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82
Q

Duration of tx for mild diabetic foot sepsis? Mod? Severe?

Osteomyolitis?

A
  • mild = 7 days
  • mod = 7 days
  • severe = 7-10 days (14 days if s.aureus bacteraemia)
  • osteomyolitis = 6 weeks
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83
Q

Is vancomycin given orally?

A

NEVER switch a person from IV vancomycin to ORAL vancomycin (unless topical treatment for c.diff) as it is NOT absorbed systemically

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84
Q

Why is oral doxycycline normally given as oral switch from fluclox?

A

fluclox = big pill 4 x a day

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85
Q

Likely colonisers in culture i.e. not causative organism?

A

Pseudomonas, klebsiella, epidermidis

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86
Q

Epidemiology haematogenous osteomyolitis? (5)

A
  • Prepubertal children
  • PWID
  • Central lines
  • dialysis
  • elderly
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87
Q

Organisms involved in PWID haematogenous osteomyolitis? (2)

A
  • Strep + staph

* unusual pathogens = pseudomonas, candida, eikenella corrodens (needle lickers), mycobacterium

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88
Q

Organisms involved in dilaysis patients with haematogenous osteomyolitis? (2)

A
  • Staph aureus (most common)

* aerobic gram -ve’s

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89
Q

Most common site for haematogenous osteomyolitis?

Unusual sites to be aware of?

A
  • most common = femur

* Unusual sites = osteitis pubis + clavicle

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90
Q

Unusual patients that are prone to haematogenous osteomyolitis?

A
  • Sickle cell
  • Gaucher’s disease
  • SAPHO and CRMO
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91
Q

Pathogens involved in sickle cell osteomyolitis? Where does it commonly affect?

A
  • Salmonella + staph aureus

* Long bones

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92
Q

Gaucher’s disease? Most commonly affects? Pathogens involved?

A
  • Lysosomal storage disorder (can mimic bone crisis)
  • Often affects tibia
  • Staph aureus
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93
Q

S/s SAPHO (adults) + CRMO (kids)? (3) Most common sites? Dx?

A
  • Fever, weight loss, malaise
  • Chest wall, pelvis + spine
  • Dx = lytic lesions seen on x-ray + raised inflammatory markers
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94
Q

Vertebral osteomyolitis? Most common pathogen?

A

Vertebral osteomyolitis = spondylodiscitis (disc space infection)
* staph aureus

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95
Q

Risk factors vertebral osteomyolitis? (6)

A

Mostly haematogenous

  • Epidural abscess/psoas abscess
  • PWID
  • IV infection
  • GU infection
  • Skin infection
  • post-operative
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96
Q

s/s vertebral osteomyolitis? (5)

Dx? (2)

A
  • <50% have fever, <50% have raised WCC, insidious pain, neurological signs, infammatory markers
  • Dx: Can have someone with vertebral osteomyolitis who has no fever, normal WCC – so MRI important!! Also biopsy
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97
Q

Biopsy for vertebral osteomyolitis? Why is biopsy carried out?

A
  • First biopsy = 40% yield
  • Second biopsy = 80% sensitivity

Important as empiric antibiotics should be avoided

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98
Q

Tx vertebral osteo? (2)

When is MRI repeated in vertebral osteo? (3)

A
  • Drainage of large psoas/epidural abscesses
  • Antimicrobials for 6 weeks minimum

MRI repeated only if

  • Unexplained increase in inflammatory markers
  • Increasing pain
  • New signs/ symptoms
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99
Q

Vertebral TB also known as? S/s? Why does epidemiology matter?

A

= Pott’s disease
* often NO systemic symptoms i.e. no cough

Epidemiology MATTERS

  • In kids, check reduced receptors for IFN-gamma, IL 12
  • In adults over HIV test
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100
Q

Risk factors for prosthetic joint infection? (4)

What is a common indication of infection in prosthetic joints?

A
  • Rheumatoid arthritis
  • Diabetes
  • Malnutrition
  • Obesity

Dehiscing of wound

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101
Q

Difference between planktonic and sessile bacteria? Pathogens in prosthetic joint infection? (6)

A 
Planktonic = bacteraemia
Sessile = biofilm
* Staph aureus, epidermidis, propionibacterium (rarely strep + entero)
* Gram -ve i.e. E.coli
* Fungi
* Mycobacterium
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102
Q

Tx PVL-producing staph aureus?(3)

A

Fluclox, clindamycin, linezolid etc

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103
Q

Dx prosthetic joint infections? (4)

A
  • Culture - tissue sample
  • Blood culture
  • CRP
  • Radiology
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104
Q

Prosthetic joint infection tx? (3)

A
  • removal of prosthesis and cement
  • antibiotics at least 6 weeks
  • re-implantation of joint after aggressive antibiotic therapy
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105
Q

Tx staph epidermidis in prostehtic joint infection?

A

Vancomycin

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106
Q

Septic arthritis?

Ax septic arthritis? (4)

A

Inflammation of the joint space caused by infection

  • Wound
  • Haematogenous
  • Spread from osteomyolitis in adjacent bone
  • Infection in adjacent soft tissues i.e. cellulitis
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107
Q

Bacteria involved in septic arthritis? (5)

A
  • Staph aureus
  • Strep
  • Coag neg staph - if prosthetic joints
  • Neisseria gonorrheae - if sexually active
  • Haemophilus influenzae - in young children
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108
Q

s/s septic arthritis? Dx?

A 
* Severe pain, red, hot, swollen, pus, limited movement
Dx:
* Culture joint fluid
* Blood culture if fever
* exclude crystals (microscopy)
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109
Q

Septic arthritis tx?

A
  • Presumptive tx to cover staph aureus = fluclox
  • If <5 y/o add ceftriaxone for H.influenzae

(adjust when organisms confirmed)

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110
Q

Viral arthritis?

A
  • Hep B, alphavirus, rubella, parvovirus
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111
Q

Pyomyositis? Ax? (3)

A

Muscle inflamamtion caused by infection

  • Staph aureus!! most common
  • Immunosuppressed = psuedomonas, strep, enterococcus
  • Clostridial infection contaminated wounds
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112
Q

Tetanus? Pathogen?

A

Toxin-mediated illness caused by clostridium tetani

* Gram +ve strictly anaerobic rods = produce SPORES that live in soil etc

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113
Q

s/s tetanus? Incubation peroid?

A

Neurotoxin causes spastic paralysis, lock jaw, sadonic smile

* 4 days - weeks

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114
Q

Tx tetanus? (5)

A
  • Surgical debridement
  • Anti-toxin
  • Supportive measures.
  • Penicillin/Metronidazole
  • Booster vaccination
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115
Q

Ix fresh tissue lesions?

A
  • Cytogenetic studies - karyotyping, FISH

* Molecular genetic studies

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116
Q

Karyotype? Advantages and disadvantages?

A

Karyotype = culture cells then arrest during cell division

  • adv = overview of chromosome structure
  • dis = will NOT detect small lesions, issue with quality of cells
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117
Q

FISH use?

A

Useful for known translocations

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118
Q

Immunohistochemistry process?

A

place pigment on antibody with specific target protein - any pigment staining means the protein is present

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119
Q

Benign connective tissue lesions? (5)

A
  • common = ganglion cyst, giant cell tumour, fibromatosis

* rare = fibrous cortical defect, fibrous dysplasia

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120
Q

Ganglion cyst? Common site?

Histo?

A

Not a true cyst (no epithelial lining), causes degenerative change within connective tissue

  • Common site = wrist (found near joint capsule or tendon)
  • Histo = space with myxoid (mucous) material, inflammatory changes
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121
Q

Superficial fibromatoses e.g.? (4)

A
  • Dupuytren’s
  • Knuckle pads
  • Plantar
  • Penile - peyronie’s
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122
Q

Dupuytren’s epidemiology? Ax?

A
  • Older males

* Idiopathic but associated with alcohol

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123
Q

Deep fibromatosis? E.g? Ax?

A

Different than superifcial fibromatosis

  • Mesenteric or pelvic DESMOID tumours
  • Associated with Gardner’s syndrome (FAP)
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124
Q

Giant cell tumour e.g.? (3)

A
  • Pigmented villonodular synovitis – large joints
  • Giant cell tumour of tendon sheath – digits
  • Giant cell tumour of bone
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125
Q

Tx giant cell lesions? (2)

A
  • GC tendon sheath = small nodules that are easily excised (rarely recur)
  • PVNS - more destructive and diffuse, more difficult to excise and often recur
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126
Q

Angiolipoma? s/s?

A
  • Vascular lipomas

* Unlike other lipomas they are painful, usually multiple and peripheral

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127
Q

benign mesenteric tumours? (5)

A

ANGEL

  • Angiolipoma
  • Neuroma (pinched nerve)
  • Glomus tumour (nail beds)
  • Eccrine spiradenoma (skin adnexal tumour)
  • cutaneous leiomyoma (of erector pilae)
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128
Q

Leiomyomas?

A

Smooth muscle tumours (v common)

* Leiomyosarcomas are uncommon however

129
Q

Rhabdomyomas? Epidemiology?

A

Skeletal muscle tumours = very rare

* Cardiac is limited to paediatric age group

130
Q

Types rhabdomyosarcoma? (3)

A
  • Embryonal = childhood (deletion Xp11.15)
  • Alveolar = young adults (PAX translocation t2:5)
  • Pleomorphic (rarest) = young adults (IHC = positive MYOD1 and myogenin)
131
Q

Cartilage lesions? E.g.?

A

Benign lesions are common

  • Enchondroma - digits
  • Chondromyxoid fibroma
132
Q

Benign bone lesions? (3)

A
  • Simple osteoma – cranial bones
  • Multiple – Gardner’s syndrome
  • Osteoid osteoma and osteoblastoma
133
Q

Osteosarcoma epidemiology? Dx? (2)

A
  • Usually children = long bones
  • Radiology = CODMAN’S TRIANGLE
  • Any malignant tumour that produces osteoid is an osteosarcoma until proven otherwise
134
Q

Ewing’s sarcoma epidemiology? Location? Features? (3)

A

CHildren + adolescents

  • Often long bones but can appear in any bony location
  • Destructive, rapidly growing + highly malignant!!
135
Q

Ax Ewing’s sarcoma? Histo appearance?

A
  • Genetic abnormalities = t(11;22)(EWs-FLI1)

* Small round blue cell tumours

136
Q

Nodular fasciitis? Features? (3)

A

Pseudosarcoma

* Any age group, rapid growth, small

137
Q

Nodular fasciits histo features? (5)

A

Hard to differentiate from sarcoma

  • Chaotic appearance
  • Pseudocytic spaces
  • Large atypical cells
  • Frequent mitoses
  • Haemorrhage
138
Q

Myositis ossificans?Location?

A

Abnormal bone growth caused by trauma

* Big muscles - e.g. gluteus, quadriceps

139
Q

Ewing’s sarcoma?

A

A malignant tumour of endothelial cells in the marrow. Most cases occur between the ages of 10 and 20. It may be associated with fever, raised inflammatory markers and a warm swelling and may be misdiagnosed as osteomyelitis

140
Q

Types of joint? (3)

A
  • Synovial - bones separated by cavity containing synovial fluid + unites by fibrous capsule
  • Fibrous - doesn’t allow any movement e.g. skull
  • Cartilaginous - allow limited movement e.g. intervertebral discs, pubic symphysis, costochondral joints
141
Q

Explain structure of synovial joint (3)

A
  • inner aspect of fibrous capsule is lined with synovial membrane
  • synovial membrane is vascular connective tissue with capillary networks and lymphatics
  • synovial membrane contains synovial cells (fibroblasts) which produce synovial fluid
142
Q

Types of synovial joint? (2)

A
  • Simple = one pair of articular surfaces e.g. metacarpopharyngeal joint
  • Compound = more than one pair e.g. elbow joint
143
Q

What extra-articular surfaces support joints? (3)

A
  • Ligament
  • Bursa
  • Tendon
144
Q

Role of joints during purposeful motion?

A
  • Stress distribution
  • Stability (shape of articular surface, ligaments and synovial fluid contribute)
  • Joint lubication = cartilage interstitial fluid, synovium, synovium-derived lubricin
145
Q

What is synovium derived from?

A

Hyaluronic acid (mucin)

146
Q

Functions of synovial fluid? (5)

A
  • Lubricates Joint
  • Facilitates joint movement - reduces friction
  • minimises wear-and-tear of joints via lubrication
  • Aids in nutrition of articular cartilage
  • Supplies chondrocytes (cartilage cells) with O2 and nutrients and removes CO2 and waste products
147
Q

Is synovial fluid a static pool?

A

NO, it is continuously replenished and absorbed by the synovial membrane

148
Q

What gives synovial fluid a high viscosity?

A

hyaluronic acid (mucin) produced by the synovial cells (viscosity varies with joint movement however)

149
Q

Other than hyaluronic acid, what else synovial fluid contain? (2)

A
  • Uric acid - derived by dialysis of blood plasma

* Mononuclear leucocytes

150
Q

How does viscosity and elasticity of synovial fluid change during joint movement? When does this become defective?

A

Rapid movement is associated with decreased viscosity and increased elasticity
* These properties of synovial fluid become defective in a diseased joint e.g. in osteoarthritis

151
Q

Normal colour of synovial fluid? When does it turn red?

A
  • Colourless

* Red = traumatic synovial tap + haemorrhagic arthritis

152
Q

Normal WBCC of synovial fluid? When does WBC count increase?

A
  • Normal = <200 WBC/mm3, neutrophils <25/mm3

* Increases in inflammatory and septic arthritis

153
Q

Viscosity, colour, clarity, WCC, and neutrophil count of normal synovial fluid? Inflammatory synovial fluid? Septic synovial fluid?

A
  • Normal = high viscosity, colourless, transparent, <200 WBC, <25 neutrophil
  • Inflammatory = low viscosity, straw to yellow, translucent, 2000 - 75,000 WBC, >50 neutrophil
  • Septic = variable viscosity, variable colour, opaque, >100,000 WBC, >75 neutrophil
154
Q

Articular cartilage usually?

ECM made up of?

A

Hyaline

* ECM = water (70%), type II collagen (20%), proteoglycans (10%)

155
Q

Function of water in cartilage? Collagen? What happens to % of water and collagen as we age?

A
  • Water = maintains resiliency of tissue, nutrition + lubrication
  • Collagen = cartilage architecture + tensile stiffness and strength
  • Both collagen and water decrease with age
156
Q

Highest concentration of proteoglycans found? Composed of? Function?
What happens to proteoglycans as we age?

A
  • Highest conc = middle and deep zone
  • Composed of glycosaminoglycan e.g. chondroitin sulphate
  • Function = load-bearing
  • Decreases as we age
157
Q

ECM total cartilage volume?

What is responsible for the synthesis, organisation, and degradation of ECM?

A
  • ECM = >98% total cartilage volume

* CHONDROCYTES

158
Q

How does cartilage receive nutrients if it is avascular?

What is the rate of ECM degradation in normal joints?

A
  • Chondrocytes receive nutrients via SYNOVIAL FLUID

* In normal joints, the rate of ECM degradation doesn’t exceed the rate at which it is replaced

159
Q

How do chondrocytes degrade ECM?

A

Metalloproteinase proteolytic enzymes e.g. collagenase and stromelysin

160
Q

Catabolic and anabolic factors of ECM turnover?

A

Catabolic
* Stimulate proteolytic enzymes + inhibit proteoglycan synthesis via TNF-a and IL-1

Anabolic
* Stimulate proteoglycan synthesis and block effects of IL-1 via tumour growth factor-B and insulin-like growth factor-1

161
Q

Markers of cartilage degradation?

A
  • Serum and synovial keratin sulphate - increased levels indicate cartilage breakdown (level increases with age and patients with osteoarthritis)
  • Type II collagen in synovial fluid - increased levels indicate cartilage breakdown, useful in evaluating cartilage erosion e.g. in osteoarthritis and rheumatoid arthritis!!
162
Q

Problems with joint? (4)

A
  • Cartilage and synovial function deteriorate with age and wear and tear causing OSTEOARTHRITIS
  • Synovial cell proliferation and inflammation cause rheumatoid arthritis
  • Deposition of salt crystals e.g. uric acid can cause gouty arthritis
  • Injury and inflammation to periarticular structures causes soft tissue rheumatism e.g. injury to the tendon causes tendonitis
163
Q

Features of osteoarthritic joint? (6)

A
  • Thickened capsule
  • Cyst
  • Sclerosis in subchondral bone
  • Fibrillated cartilage
  • Synovial hypertrophy
  • Osteophyte formation
164
Q

Processes in the physiology of pain?

A
  • Transduction: translation of noxious stimulus into electrical activity at the peripheral nociceptor
  • Transmission: propagation of pain signal as nerve impulses
  • Modulation: modification/hindering of pain transmission in the nervous system e.g. by inhibitory neurotransmitters like endogenous opioids
  • Perception: Conscious experience of pain (physiological and behavioural responses)
165
Q

Wha are nociceptors? What kind of neurones are they?

A
  • Nociceptors are specific primary sensory afferent neurones normally activated by intense noxious stimuli (e.g. mechanical, thermal or chemical)
  • first order neurones that relay information to second order neurones in the CNS
166
Q

Nociceptive pathway?

A
  • Activated by noxious stimuli
  • Synapses with second order neurone in dorsal root ganglion
  • Second order neurones ascend in spinal cord in anterolateral system to the thalamus
  • Spinothalamic tract = involved in pain perception (location, intensity)
  • Spinoreticular tract = involved in autonomic responses to pain
  • From thalamus, third order neurones carry impulse to primary sensory cortex
167
Q

What neurotransmitters are delivered across synapse by nociceptors?

A

Substance P + neurokinin A

168
Q

Subtypes of nociceptors? (2)

A
  • a-delta fibres (thinly myelinated) = respond to noxious mechanical and thermal stimuli. Mediate ‘first’, or fast, pain
  • C-fibres (unmyelinated) = respond to all noxious stimuli (POLYMODAL). Mediate ‘second’, or slow, pain
169
Q

Sensations caused by a-delta fibres? C-fibres?

A
  • ad-fibres = quick high intensity pain, stabbing sensations

* C-fibres = slow lower intensity pain, burning, throbbing, aching sensations

170
Q

Inflammatory pain caused by?

How is pain activated?

A

Immune system
* mediators released at the site of inflammation - Causes heightened pain sensitivity to noxious stimuli (hyperalgesia) and pain sensitivity to innocuous stimuli (Allodynia)

171
Q

Neuropathic pain caused by? E.g.?

A

damage to neural tissue
e.g. compression neuropathies, peripheral neuropathies, central pain (following stroke or spinal injury), postherpetic neuralgia, trigeminal neuralgia, phantom limb

172
Q

Dysfunctional pain? E.g.?

Tx? Difference between pathological pain (neuropathic + dysfunctional) and other types of pain??

A

In dysfunctional pain there is no identifiable damage or inflammation

  • fibromyalgia, irritable bowel syndrome, tension headache, temporomandibular joint disease, interstitial cystitis
  • Sometimes tx by drugs not originally developed for pain e.g. antidepressants
  • Pathological pain is NOT adaptive!! It is maladaptive
173
Q

What is referred pain caused by?

A

convergence of nociceptive visceral and skin afferents upon the same spinothalamic neurons at the same spinal level

174
Q

IPEX syndrome? Caused by?

A

Autoimmune disease

* mutation in the FOXP3 gene, which is essential for the development of CD4+ regulatory T cells

175
Q

Class I MHC? Class II MHC?

A

Class I = expressed by all nucleated cells

Class II - APCs

176
Q

What are most (if not all) autoimmune diseases associated with?

A

Genetic polymorphisms in HLA region (MHC molecules)

177
Q

Other than genetics, what factors also play a role in autoimmune disease?

A

Sex hormones!
* Females more at risk of certain autoimmune diseases (alteration of course of some autoimmune diseases during pregnancy)

Environmental factors

  • Molecular mimicry - non-self antigens look identical to self
  • Intercurrent infections - immune responses can cause autoimmune reactions
  • Tissue damage - release of previously hidden self-antigens
  • Superantigens - bacterial superantigens can activate auto-reactive T cells (e.g. TSS)
178
Q

What are many autoimmune diseases driven by? E.g.?

A

Hypersensitivity reactions

  • Type II = Goodpasture’s syndrome, rheumatic fever, myasthenia gravis
  • Type III = SLE
  • Type IV = rheumatoid arthritis
179
Q

Examples of autoimmune diseases that affect musculoskeletal system?

A
  • Rheumatoid arthritis
  • Myasthenia gravis
  • Scleroderma
  • Polymyositis
  • Lupus
180
Q

Myasthenia gravis? Main cause?

A

Autoimmune neuromuscular disorder characterized by severe muscular weakness and progressive fatigue
* auto-reactive antibodies (auto-IgG) bind with acetylcholine receptors on muscle cells

181
Q

Epidemiology MG? (3)

A
  • ANy age
  • Thymic tumour (10% cases) - 90% unknown cause
  • Genetic predisposition i.e. HLA mutation
182
Q

Clinical manifestations MG? (5)

A
  • May first appear during pregnancy, postpartum or after anaesthetic agents
  • Fatigue
  • Muscle weakness: eyes, face, mouth, throat + neck
  • In advanced stage all muscles are weak
183
Q

What is early onset MG with AChR antibodies associated with?

A

increased adaptive immune responses in the thymus

thymic follicular hyperplasia with lymphoid follicles and germinal centres

184
Q

Pathophysiology of MG?

A
  • CD4+ T cells activated by AChR subunits expressed by thymic epithelial cells
  • Effector TH cells stimulate auto-reactive B cells to produce anti-AChR antibodies
  • Thymic myoid cells are attacked by these antibodies, and release AChR-immune complexes
  • These complexes activate other antigen presenting cells, perpetuating the response
  • AChR antibodies block binding of endogenous ACh to the receptors, leading to defects in nerve impulse transmission at the NMJ
  • Complement system activated leading to destruction of muscle endplate
185
Q

What does activation of compliment cascade result in in MG?

A

formation of the membrane attack complex (MAC) and localized destruction of the postsynaptic membrane

186
Q

MG tx? (4)

A
  • Anti-cholinesterase
  • Immunosuppression e.g. corticosteroids, Eculizumab
  • Plasmapheresis
  • Thymectomy
187
Q

Rheumatoid arthritis clinical manifestations?

A
  • Inflammatory change in synovial membrane
  • Fever
  • Leukocytosis
  • Anorexia
  • Hyperfibinogenaemia
188
Q

Pathogenesis rheumatoid arthritis?

A
  • Genetic, epigenetic + environmental factors: HLA-DR4, smoking, increased in post-partum + breastfeeding
  • Type IV hypersensitivity
189
Q

Tx RA? (6)

A
  • Methotrexate
  • Sulpasalazine
  • Hydroxychlorquinine
  • Leflunomide
  • Gold, penacillamine, ciclosporin A
  • Anti-TNF e.g. Infliximab
190
Q

Osteoarthritits?

A

Articular cartilage loss

191
Q

Risk factors OA? (10)

A
  • Elderly
  • Female
  • Obesity
  • Previous injury
  • Muscle weakness
  • Acromegaly
  • Joint inflammation
  • Crystal deposition in cartilage
192
Q

Pathogenesis OA? (5)

A
  • Mechanical damage
  • Imbalance of: cytokines, growth factors, PGE2, free radicals, proteolytic enzymes
  • Destroction of chondrocytes
  • Bone remodelling
  • Reduced synovial fluid viscosity
193
Q

Ax OA? (2)

A
  • Idiopathic

* Secondary - previous injury, rheumatoid arthritis etc

194
Q

Does osteoarthritis affect spine?

A

Yes can affect whole spine unlike RA which can only affect C1, C2

195
Q

S/s OA? (2)

A
  • Pain - worse on activity, relieved by rest

* Stiffness - morning stiffness lasts <30 mins

196
Q

o/e OA? (4)

A
  • Crepitus
  • Joint swelling -Bony enlargements due to osteophytes
  • Joint tenderness
  • Joint effusion
197
Q

S/s hands OA? (2)

A
  • Bony enlargements at DIPs (Heberdens nodes) and PIPs (Bouchards nodes)
  • Squaring of hand

(RA tends not to affect DIPs!!)

198
Q

s/s knee OA? (3)

A
  • Osteophytes, effusions, crepitus and restriction of movement
  • Genu varus or valgus
  • Bakers cyst
199
Q

s/s OA hip? (2)

A
  • Restricted movement

* Pain may be felt in groin or radiating to knee

200
Q

s/s OA spine?

A
  • Cervical – pain and restriction of neck movement
  • Lumbar – Pain on standing or walking
  • osteophytes can cause spinal stenosis if encroach on spinal canal or pinch the nerve root
201
Q

Radiological features OA? (4)

A
  • Loss of joint space
  • Subchondral sclerosis
  • Subchondral cysts
  • Osteophytes
202
Q

Kellgren-Lawrence Radiographic Grading Scale of Osteoarthritis?

A
  • Grade 0-No radiographic findings of osteoarthritis
  • Grade 1- Minute osteophytes of doubtful clinical significance
  • Grade 2 - Definite osteophytes with unimpaired joint space
  • Grade 3 - Definite osteophytes with moderate joint space narrowing
  • Grade 4 - Definite osteophytes with severe joint space narrowing and subchondral sclerosis
203
Q

Tx osteoarthritis?

A

Non-pharmalogical
* Physio, weight loss

Pharmacological

  • analgesia e.g. paracetamol
  • NSAIDs
  • Pain modulations e.g. tricyclics
  • Steroids

Surgical

  • Joint replacement
  • Arthroscopic washout
204
Q

Gout?

A

Inflammation in the joint triggered by uric acid crystals

205
Q

> 0.42 uric acid?

A

Hyperuricaemia = no longer soluble

206
Q

Causes of hyperuricaemia? (2)

A
  • Increased urate production - enzyme defects, psoriasis, cancer, ALCOHOL, high dietary purine intake (e.g. red meat, seafood)
  • Reduced urate excretion - renal impairment, HF, hypothyroidism, diuretics, cytotoxics e.g. cyclosporin
207
Q

Epidemiology gout?

A
  • Males > females

* Elderly (rare before menopause in women)

208
Q

Acute gout?

A
  • Usually monoarthropathy:- 1st MTP > ankle > knee
  • Settles in about 10 days without treatment
  • Settles in about 3 days with treatment
  • Abrupt onset, often overnight
  • May have normal uric acid during acute attack
209
Q

chronic tophaceous gout?

A
  • Chronic joint inflammation
  • Often diuretic associated
  • High serum uric acid
  • Tophi
  • May get acute attacks
210
Q

Ix gout? (5)

A
  • Raised inflammatory markers
  • Serum uric acid raised (may be normal during acute attack)
  • Synovial fluid - polarising microscopy shows needle shaped NEGATIVELY birefringent crystals
  • Renal impairment (may be cause or effect)
  • Xrays
211
Q

Tx acute gout? Long term?

A

Acute
* NSAIDs, colchicine, steroids

Long term (2-4 weeks after acute attack)
* allopurinol, febuxostat
212
Q

calcium pyrophosphate deposition disease epidemiology? Where does it affect? 2 types?

A

Commoner in elderly (chondrocalcinosis increases with age)
* Affects fibrocartilage - knees, wrists, ankles

2 types
* Calcium pyrophosphate and calcium hydroxyappatite crystals

213
Q

CPPD attacks due to? Appearance of crystals?

A
  • calcium pyrophosphate crystals (pseudogout)

* Calcium pyrophosphate crystals- rhmboid shaped, POSITIVELY birefringent

214
Q

Tx pseudogout? (4)

A
  • NSAIDs, colchicine, steroids, rehydration
215
Q

What causes “Milwaukee shoulder”?
Epidemiology?
Tx? (4)

A

Hydroxyapatite crystal deposition in or around the joint

  • Females, 50-60 years
  • NSAIDs, steroid injection, physiotherapy, arthroplasty
216
Q

Soft tissue rheumatism? Features?

A

pain that is caused by inflammation/damage to ligaments, tendons, muscles or nerve near a joint rather than the bone or cartilage
* Pain should be confined to specific site e.g. shoulder, wrist etc (more generalised soft tissue pain – consider fibromyalgia)

217
Q

Commonest area for soft tissue pain? e.g.? (5)

A

Shoulder!

  • Adhesive Capsulitis
  • Rotator cuff tendinosis
  • Calcific tendonitis
  • Impingement
  • rotator cuff tears
218
Q

Joint hypermobility syndrome epidemiology? Predisposing conditions?

A
  • F > M

* Marfan’s syndrome, ehlers danlos syndrome

219
Q

Hypermobility s/s? Tx?

A
  • Arthralgia, premature osteoarthritis

* Tx: physiotherapy

220
Q

Rheumatoid athritis? Epidemiology?

A

symmetrical inflammatory arthritis affecting mainly the peripheral joints (spine is NOT affected!!! Only C1, C2)
* Women:men 3:1

221
Q

Main structure involved in RA? Effect on structure?

A

Synovium

* Synovial inflammation causes bone erosion and damage (due to activation of osteoclasts)

222
Q

Pannus? Pro-inflammatory cytokines involved in RA?

A

hypervascular inflammed synovium associated with RA

* TNF-a, IL-1, IL-6

223
Q

Early RA?

A

<2 yrs since symptom onset

224
Q

Criteria for RA? (4)

A
  • Morning stiffness >1 hr.
  • Arthritis of 3 or more joint areas.
  • Arthritis of hand joints.
  • Symmetric arthritis.
225
Q

Dx RA? (3)

A
  • Bloods - anaemia of chronic disease (normocytic), raised platelets, CRP, plasma viscosity, autoantibodies
  • Imaging - xray, US, MRI
  • Positive compression test in MCP and MTP joints
226
Q

s/s RA? (7)

A
  • PIP, MCP, wrist, MTP synovitis
  • Tenosynovitis (tendinous inflammation)
  • Trigger figer
  • Bilateral carpal tunnel
  • Polymyalgia rheumatica.
  • Palindromic rheumatism.
  • Poor grip strength
227
Q

Auto-antibodies RA?

A
  • Rheumatoid factor(Rheumatoid IgM)-
  • Antibodies to cyclic citrullinated peptide(Anti-CCP antibodies)
228
Q

DAS28 scoring?

A

For RA

  • > 5.1 = active disease
  • 3.2 - 5.1 = moderate disease
  • 2.6 - 3.2 = low disease activity
  • <2.6 = remission
229
Q

Tx RA? (3)

A

Start with aggressive tx then gradually withdraw tx

  • NSAIDs
  • steroids (NOT used on their own - in combo with DMARDs!!)
  • DMARD
230
Q

DMARDs? (5)

A

DIsease-modifying anti-rheumatic drugs

  • Methotrexate (DRUG OF CHOICE)
  • Sulfasalazine
  • Hydroxychloroquinone (does not prevent erosions!!)
  • Leflunomide
  • Gold, penicillamine, azathioprine
231
Q

DMARD combo? Risk of methotrexate?

A

MTX + SASP + HCQ

* risk of pneumonitis with methotrexate

232
Q

Risks associated with DMARDs? (3)

A
  • Bone marrow suppression = infection
  • Impaired liver function
  • Pneumonitis in case of methotrexate
233
Q

Biologic agents for RA? (5)

When should biologic agents for RA be administered?

A
  • Anti TNF = inflixumab
  • T cell receptor blocker = abatacept
  • B cell blocker = rituximab
  • Anti-Il 6 = tocilizumab
  • JAK 2 inhibitor = tofacitinib

Failure to respond to 2 DMARDs (inc. methotrexate) + DAS28> 5.1
Methotrexate therapy is co-prescribed!!

234
Q

Spondylarthropathy?

A

inflammatory arthritides characterized by involvement of both the spine and joints, principally in genetically predisposed (HLA B27 positive) individuals

235
Q

HLA B27?

Used in dx?

A

Associated with Ankylosing spondylitis, Reactive arthritis, Crohn’s disease, uveitis

  • Not a useful screening or Diagnostic test unless patients also have symptoms
  • because 1/5 people have mutation but most don’t have disease
236
Q

Types of spondyloarthritis? (4)

A
  • Ankylosing Spondylitis
  • Psoriatic Arthritis
  • Reactive Arthritis
  • Enteropathic Arthritis
237
Q

Mechanical vs inflammatory back pain?

A
  • Mechanical- worsened by activity, typically worst at end of day, better with rest
  • Inflammatory- worse with rest, better with activity, significant early morning stiffness (>30 minutes)
238
Q

Features of spondylarthropathies? (4)

A
  • Sacroiliac and spinal involvement
  • Enthesitis: inflammation at insertion of tendons into bones eg Achilles tendinitis
  • Inflammatory arthritis
  • Dactylitis (“sausage” digits)- inflammation of entire digit (not just 1 joint)
239
Q

Extra-articular features of spondylarthropathies? (4)

A
  • Ocular inflammation (uveitis, conjuntivitis)
  • Mucocutaneous lesions
  • Rare Aortic incompetence or heart block
  • No rheumatoid nodules
240
Q

Ankylosing spondylitis?
Hallmark??
Epidemiology?

A

Chronic systemic inflammatory disorder that primarily affects the spine

  • HALLAMRK = sacroiliac joint involvement!! (v rare to have small joint involvement unlike RA)
  • Men > women, young adults
241
Q

s/s ankylosing spondylitis? (6)

Dx? (3)

A
  • Back pain
  • Enthesitis
  • Uveitis
  • Cardiovascular involvement (aortic regurgitation)
  • Fibrosis upper lung lobes
  • amyloidosis

Dx

  • Examination - occiput to wall, chest expansion, schober test
  • Bloods - CRP, HLA B27
  • X-ray - sacroiliitis, syndesmophytes, “bamboo” spine
242
Q

Ankylosing spondylitis vs osteoarthritis? (5)

A

AS

  • Bone density reduced in late disease
  • Shiny corners
  • Syndesmophytes
  • Fusion (bamboo spine)

OA

  • Normal bone density
  • Reduced joint space
  • Subchondral sclerosis
  • Sunchondral cyst
  • Osteophytes
243
Q

What is the preferred imaging technique for AS?

A

MRI - can detect AS earlier than x-rays

Can detect bone marrow oedema and enthesitis!!

244
Q

Psoriatic arthritis? s/s? (5)

A

Inflammatory arthritis associated with psoriasis (rheumatoid factor negative!)

  • Sacroiliitis (often asymmetric)
  • Nail pitting/oncholysis
  • Dactylitis
  • Enthesitis
  • Eye disease
245
Q

5 subgroups of psoriatic arthritis? (5)

A
  • Confined to distal interphalangeal joints (DIP) hands/feet
  • Symmetric polyarthritis (similar to RA)
  • Spondylitis (spine involvement) with or without peripheral joint involvement
  • Asymmetric oligoarthritis with dactylitis
  • Arthritis mutilans
246
Q

Dx psoriatic arthritis? (2)

A
  • Bloods - CRP, negative RF

* X-ray - whiskering, “pencil in cup”, osteolysis, enthesitis

247
Q

Reactive arthritis? Most common infections? Epidemiology?

A

Arthritis in response to infection etc characterised by inflammatory synovitis from which organisms CANNOT be cultured!!

  • Urogenital e.g. chlamydia
  • Enterogenic e.g. salmonella

Epidemiology

  • Equal sex distribution
  • Young adults
  • HLA B27 positive
248
Q

Reiter’s syndrome?

A

Form of reactive arthritis

Traid: urethritis, conjunctivitis/uveitis, arthritis

249
Q

s/s reactive arthritis?

A
  • fever
  • Asymmetrical arthritis
  • Enthesitis
  • Mucocutaneous lesions: keratodema blenorrhagica, circinate balanitis, painless oral ulcers, hyperkeratotic nails
250
Q

Dx reactive arthritis? (3)

A
  • Bloods - CRP, HLA B27
  • Cultures - blood, urine, stool (NOT SYNOVIAL FLUID)
  • x-ray
251
Q

Enteropathic arthritis?

s/s?

A

Associated with inflammatory bowel disease eg. Crohn’s, Ulcerative colitis

  • GI symptoms
  • Uveitis
  • arthritis in several joints, esp knees, ankles, elbows, and wrists
  • pyoderma gangrenosum
  • Enthesitis
  • Oral- apthous ulcers
252
Q

Dx enteropathic arthritis? (5)

A
  • Upper and lower GI endoscopy with biopsy showing ulceration/ colitis
  • Joint aspirate- no organisms or crystals
  • Raised inflammatory markers- CRP, PV
  • X ray/ MRI showing sacroiliitis
  • USS showing synovitis/ tenosynovitis
253
Q

Tx of spondylarthropathies? (look back if cant remember subgroups) - 6

Non-pharmacological tx? (2)

A
  • NSAIDs
  • Corticosteroids
  • Topical steroid eyedrops
  • DMARDs (methotrexate etc)
  • Anti-TNFa (biologics) – only in severe disease
  • Secukinumab (anti-Il7) only for PSA and AS

Non-pharma

  • Physiotherapy
  • Occupational therapist
254
Q

Vasculitis?

Mortality rate of untreated small vessel vasculitis?

A

inflammation of blood vessels

* Untreated small vessel vasculitis can have mortality rate of 90% after 2 years

255
Q

Ax vasculitis?

A
  • Primary vasculitis - inflammatory response that targets vessel walls and has no known cause (possibly autoimmune)
  • Secondary vasculitis - infection, drug, toxin, inflammatory disorder, cancer
256
Q

Pathogenesis vasculitis?

A
  • Dendritic cells activate T cells and release cytokines that cause vascular inflammation
  • T cells activate macrophages
  • Macrophages release mediators that cause vascular inflammation, endothelial damage, disruption of elastic lamina, intimal hyperplasia
257
Q

Classifications of vasculitis? (4)

A
  • Medium-vessel vasculitis - Kawasaki disease, polyarteritis nodosa
  • Immune complex small-vessel vasculitis - cytoglobunemic vasculitis
  • ANCA-associated smell vessel vasculitis - microscopic polyangitis
  • Large vessel vasculitis - takayasu vasculitis, giant cell arteritis
258
Q

S/s vasculitis? (5)

A
  • Depends on which vessel it affects
    HOWEVER
    Systemic symptoms like fever, malaise, weight loss and fatigue are common to ALL vasculitides
259
Q

Ax large vessel vasculitis?
Epidemiology?
Hallmark?

A
  • Takayasu arteritis and giant cell arteritis
  • Epidemiology: TA = <40 years, female, Asian
    GCA = >50 years, typically causes temporal arteritis
  • Granulomatous infiltration of walls of large vessels
260
Q

s/s large vessel vasculitis? (3)

A
  • Bruit (mostly carotid artery)
  • Blood pressure difference of extremities
  • Claudication
261
Q

Temporal arteritis? Associated with? s/s? (4)

Biggest risk??

A

Common in giant cell arteritis
* Associated with polymyalgia rheumatica

S/s

  • Unilateral temporal headache
  • scalp tenderness
  • jaw claudication
  • Temporal arteries prominent with reduced pulsation

Risk of blindness due to ischaemia of the optic nerve!!

262
Q

Ix large cell vasculitis? (3)

A
  • Bloods - ESR, plasma viscosity and CRP raised
  • Temporal artery biopsy (remember that “skip lesions” occur so biopsy may be negative)
  • MR angiogram or PET CT
263
Q

Tx large cell vasculitis?

A

40 - 60 mg prednisolone

264
Q

Small vessel vasculitis divided into? (2)

Types of small vessel vasculitis? (3)

A
  • ANCA associated vasculitis (AAV) and ANCA negative

Types

  • Granulomatosis with polyangiitis (Wegener’s granulomatosis) - granulomatous inflammation of respiratory tract, associated with necrotising glomerulonephritis
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) - eosinophilic granulomatous inflammation of respiratory tract, associated with asthma
  • Microscopic polyangiitis - necrotising vasculitis with immune deposits, associated with necrotising glomerulonephritis
265
Q

Ax ANCA associated vasculitis? (4)

A
  • Bacteria: Staph aureus, E.coli
  • Genetic: HLA, CD226
  • Environmental: silica
  • Drugs: propylthiouracil, hydralazine
266
Q

Granulomatosis with polyangiitis (GPA) epidemiology?

A
  • Europeans
  • Males > females
  • Adults
267
Q

s/s GPA? (6)

A
  • ENT = sinusitis, nasal crusting, epistaxis, mouth ulcers, otitis media + deafness, nose bleeds, saddle nose due to cartilage ishaemia
  • Resp = pulminary infiltrates, cough, haemoptysis, cavitating nodules on CXR
  • Skin = purpura!!! ulcers
  • Renal = necrotising glomerulonephritis (microhaematuria)
  • NS = mononeuritis multiplex, sensorimotor polyneuropathy, CN palsies
  • Eyes: conjunctivitis, uveiis, retinal artery occlusion
268
Q

Difference between Granulomatosis with polyangiitis (GPA) and Eosinophilic granulomatosis with polyangiitis (EGPA)?

A

EGPA = late onset asthma and a high eosinophil count

269
Q

s/s EGPA? (6)

A
  • Asthma
  • Eosinophilia > 10%
  • Paranasal sinusitis
  • Pulmonary infiltrates
  • Purpuric rash
  • Mononeuritis multiplex or polyneuropathy
270
Q

Immunology AAV? (3)

ANCA patterns? (2)

A
  • Anti-Neutrophil Cytoplasmic Antibodies (ANCAs) auto-antibodies against antigens in the cytoplasm of neutrophil granulocytes
  • Immunofluoresence used to detect ANCA and can differentiate ANCA patterns i.e. cANCA+ PR3 (GPA) and pANCA + MPO (MPA and EGPA)
271
Q

Tx AAV? (3)

A
  • Localised/early systemic = methotrexate + steroids
  • Generalised/systemic = cyclophosphamide + steroids
  • Refractory unresponsive to steroids + cyclo) = IV immunoglobulins + rituximab
272
Q

Prognosis AAV? (2)

A
  • Untreated = fatal

* Treated = 5 yr survival 90%

273
Q

Henoch-schonlein purpura (HSP)?

A

acute immunoglobulin A (IgA)–mediated disorder

* vasculitis involving small vessels of skin, GI tract, kidneys, joints (RARELY lungs and CNS)

274
Q

Epidemiology HSP? Ax?

A
  • Children 2-11

> 75% patients have preceding URTI, pharyngeal or GI infection
* GAS most common!!

275
Q

S/s HSP? (5)

A
  • Purpuric rash
  • Colicky abdominal pain
  • Bloody diarrhoea
  • Jont pain + swelling
  • Renal symptoms (50%)
276
Q

HSP tx?

A
  • Usually self-limiting (tends to resolve in 8 weeks)

* MUST perform urinalysis to screen for renal involvement!!

277
Q

Main causes of myopathy? (7)

A
  • Inflammatory - polymyositis
  • Endocrine disorders - cushing’s
  • Electrolyte disorders - hypokalaemia
  • Metabolic myopathies
  • Drugs and toxins
  • Infections - pyomyositis
  • Rhabdomyolysis
278
Q

Inflammatory myopathies? (2)
Epidemiology?
Risk?

A

Polymyositis + dermatomyositis

  • Female > male, adults
  • Increased incidence of malignancy
279
Q

Histology inflammatory myopathy? Ax?

A
  • Histo: necrosis, inflammatory cell infiltrate

* Ax = idiopathic (unknown)

280
Q

s/s inflammatory myopathies?

A

MUSCLE WEAKNESS

  • usually symmetrical, proximal muscles
  • Often specific problems eg difficulty brushing hair, climbing stairs
281
Q

Dermatomyositis? Other organs involved in inflammatory myopathies? (6)

A
  • Cutaneous disease - gottrons sign, heliotrope rash, shawl sign
  • ILD
  • Dysphagia
  • Myocarditis
  • Fever
  • Weight loss
  • Raynauds
282
Q

Risk factors for inflammatory myopathies? (4)

A
  • Other medical problems : thyroid disease, diabetes
  • Drugs : steroids, statins
  • Family history
  • Social : alcohol, illicit drug use
283
Q

Ix inflammatory myopathies?

A
  • Bloods - CK, inflammatory markers, autoantibodies
  • Electromyogrphy
  • Muscle biopsy (gold standard)
  • MRI
284
Q

Tx inflammatory myopathies? (6)

A
  • Glucocorticoids
  • Azathioprine
  • Methotrexate
  • Ciclosporin
  • IV immunoglobulin
  • Rituximab
285
Q

Polymyalgia rheumatica associated with? s/s? (7)

A

Temporal arteritis/Giant cell arteritis

  • Shoulder and hip ache (usually symmetrical)
  • Morning stiffness
  • Fatigue
  • Anorexia + weight loss
  • Fever
  • Limited movement
  • Muscle strength is normal
286
Q

Tx polymyalgia rheumatica?

A

Steroids

higher dose steroids for temporal arteritis

287
Q

Fibromyalgia associated with inflammation? s/s? (6)

A

NO!!

  • Pain (worse with exertion)
  • Swelling
  • Fatigue and poor sleep
  • Pins and needles
  • Headaches
  • IBS
288
Q

Connective tissue disease? e.g? (7)

A

NOT diseases of connective tissue!!
Spontaneous over activity of the immune system involving auto-antibodies (can lead to organ failure and death)

  • SLE
  • Sjogren’s syndrome
  • Systemic sclerosis
  • Dermatomyositis
  • Polymyositis
  • Mixed Connective Tissue Disease
  • Anti-phospholipid syndrome
289
Q

SLE? Epidemiology? (2)

A

Systemic autoimmune disease that can affect any part of the body

  • Females > males
  • Asians, afro-Americans, afro-caribbeans (uncommon in African blacks)
290
Q

Ax SLE? (4)

A
  • Genetic
  • Environmental
  • Hormonal - oestrogen (HRT)
  • Immunological
291
Q

Pathogenesis SLE?

A
  • Increased and defective apoptosis
  • Necrotic cells release nuclear material which act as auto-antigens
  • B and T cells are stimulated
  • Autoantibodies are produced
292
Q

How does SLE lead to renal disease?

A

Deposition of immune complexes in mesangium (neutrophils attack immune complexes)

293
Q

Clinical criteria SLE?

A
  • Mucocutaneous - oral/nasal ulcers, cutaneous disease, non-scarring alopecia
  • Musculoskeletal - arthritis
  • Serositis
  • Renal
  • Neurological
  • Haematological - haemolytic anaemia, leukopenia, thrombocytopenia
294
Q 
General s/s SLE? (5)
Mucocutaneous? (6)
Musculoskeletal? (3)
Serositis? (4)
Renal? (2)
Neurological? (4)
Haematological? (5)
A

General
* Fever, malaise, anorexia, weight loss, fatigue

Mucocutaneous
* Photosensitivity, malar rash, discoid lupus erythematosus, subacute cutaneous lupus, mouth ulcers, alopecia

MSK
* Non-deforming arthritis (poly), deforming arthropathy (Jaccoud’s arthritis), myopathy (weakness, myalgia)

Serositis
* Pericarditis, pleurisy, pleural effusion, pericardial effusion

Renal
* Proteinuria >500mg in 24 hrs, red cell casts

Neurological
* Depression, migrains, seizures, neuropathy (e.g. mononeuritis multiplex is a peripheral neuropathy)

Haematological
* Lymphadenopathy, lymphopenia, leukopenia, haemolytic anaemia, thrombocytopenia

295
Q

Anti-phospholipid syndrome?

s/s? (5)

A

Production of antiphospholipid auto-antibodies (associated with other autoimmune conditions esp SLE)!!!

  • Venous + arterial thrombosis
  • Recurrent miscarriage
  • Livido reticularis
  • Thrombocytopenia
  • Prolonged APTT
296
Q

Ix SLE? (10)

A
  • Antinuclear antibodies - ANA, anti-double stranded DNA, anti-Ro, anti-Sm, anti-RNP
  • Anti-phospholipid antibodies = anti-cardiolipid antibody, lupus anticoagulant, anti-beta 2 glycoprotein
  • CXR
  • Pulmonary function test
  • CT chest
  • Urine protein quantification
  • Renal biopsy
  • ECHO
  • Nerve conduction studies
  • MRI brain
297
Q

In a patient with SLE which of the following features would make you most suspicious of a disease flare?

A. Increasing fatigue levels
B. Raised CRP
C. Positive ANA
D. Fall in C4 level
E. More frequent headaches
A

D. Fall in C4 level

* C3/C4 levels NEGATIVELY correlate with disease activity

298
Q

How can SLE disease activity be monitored? (5)

A
  • Anti-dsDNA level positively correlates with activity
  • C3/C4 levels negatively correlate with activity
  • Urine examination
  • FBC
  • Blood biochemistry
299
Q

Tx SLE? (5)

A
  • NSAIDs
  • Anti-malarials e.g. hydroxychloroquine (useful for arthritis, skin manifestations)
  • Steroids (low dose for skin rashes/arthritis/serosisits, mod doses for resistant serositis, haematologic issues, high dose for severe haematological issues, renal disease and major organ involvement)
  • Immunosuppressants - azathioprine, methotrexate, cyclophosphamide
  • Biologics - anti-CD20 (rituximab), anti-Blys (belimumab)
300
Q

When to suspect autoimmune disease? (8)

A
  • Arthralgia/arthritis
  • Muscle pain/muscle weakness
  • Photosensitivity
  • Raynaud`s phenomenon
  • Sicca symptoms(dry eyes/mouth/throat/vaginal dryness) in the absence of other causes
  • Dysphagia, shortness of breath
  • Neurological symptoms
  • Recurrent pregnancy losses/unprovoked thrombosis/pregnancy complications
301
Q

When is Raynaud’s associated with autoimmune disease?

Tx?

A 
Primary = teenagers, no autoimmune disease, benign
Secondary = adults, underlying autoimmune disease (if ulcers or gangrene, usually secondary)

Tx

  • Vasodilators - CCB
  • For ulcers = iloprost, botox injections
302
Q

Systemic sclerosis? Types?

A

Used to be called scleroderma (skin thickening)

2 types

  • Diffuse cutaneous systemic sclerosis (dsCC) - skin involvement on extremities above AND below elbows and knees (plus face + trunk)
  • Limited cutaneous systemic sclerosis (lsCC) - skin involvement on extremities ONLY BELOW elbows and knees (plus face)
303
Q

Pathogenesis systemic sclerosis?

A

Environment + genetics!

  • Antigen detected
  • Endothelial cell stimulation
  • Chronic inflammation
304
Q

Systemic sclerosis symtpoms? (5)

A

CREST

  • Calcinosis - calcium deposits in skin
  • Raynaud’s
  • Esophageal dysfunction - acid reflex and decreased motility
  • Sclerodactyly - thickening and tightening of skin on fingers and hands
  • Telangiectasias - dilation of capillaries causing red marks on surface of skin

Also pulmonary + Renal complications!!

  • Pulmonary fibrosis + pulmonary hypertension
  • Scleroderma renal crisis
305
Q

Antibodies in systemic sclerosis? (5)

A
  • Anticentromere
  • Antitipoisomerase
  • Anti-RNA polymerase
  • Anticardiolipin antibodies
  • Anti-Scl-70
306
Q

Tx systemic sclerosis? (6)

A
  • Yearly ECHO and PFTs
  • Treat Raynaud`s and digital ulcers
  • Treat reflux with PPi (ranitadine)
  • Immunosuppression
  • Pulmonary hypertension- prostacyclin analogues, endothelin receptor antagonists, PDE5 inhibitors.
  • Tight control of blood pressure - ACE INHIBITORS
307
Q

Sjogren’s syndrome? Main features?

A

Characterised by lymphocytic infiltration of exocrine glands

* Keratoconjunctivitis sicca, vaginal dryness, difficulty swallowing, extreme thirst, dry mouth (tooth decay)

308
Q

S/s Sjogren’s? (5)

A
  • Blepharitis
  • Salivary gland inflammation
  • Tooth decay
  • Lymphoma
  • Dry cough
  • Multisystem involvement
309
Q

Dx Sjogren’s? (5)

A
  • Usually ANA positive
  • If antibodies negative, salivary gland ultrasound and biopsy
  • high ESR/plasma viscosity
  • Raised IgG
  • Cytopaenias
310
Q

Tx Sjogren’s?

A
  • Artificial tears, salivary supplements, vaginal lubricants
  • Good dental hygiene-strong fluoride toothpaste-e.g.Duraphat
  • Hydroxychloroquine for fatigue and arthralgia
  • Immunosuppression for major organ involvement.
311
Q

What pattern does psoriatic arthritis normally follow?

A

an asymmetrical oligoarthritis

312
Q

What are mixed connective tissue diseases?

A

Mixed connective tissue diseases are conditions which feature symptoms also seen in other connective tissue diseases

These include:
Raynauds phenomenon
Arthralgia/arthritis
Myositis
Sclerodactyly
Pulmonary hypertension
Interstitial lung disease (ILD)

They are associated associated with anti-RNP antibodies!!

313
Q

Difference between polymyositis and dematomyositis?

A

Polymyositis is an idiopathic inflammatory myopathy that causes symmetrical, proximal muscle weakness. Dermatomyositis is clinically similar but also has typical cutaneous manifestations

314
Q

How to differentiate between polymyositis and polymyalgia rheumatica?

A
  • Polymyositis = weakness

* Polymyalgia rheumatica = pain + stiffness

315
Q

Spondylosis?

A

intervertebral discs lose water content with age resulting in less cushioning and increased pressure on the facet joints leading to secondary OA

316
Q

Once suspect cauda equina syndrome?

A

Urgent MRI

317
Q

Tx carpal tunnel? (2)

A

Non-operative treatment

  • wrist splints at night to prevent flexion
  • Injection of corticosteroid

Surgical treatment
* Carpal tunnel decompression

318
Q

Tests for carpal tunnel? Cubital tunnel?

A

Carpal

  • Tinel’s test (percussing over the median nerve)
  • Phalen’s test (holding the wrists hyper‐flexed)

Cubital

  • Tinel’s test
  • Froment’s test
319
Q

Cubital tunnel syndrome?

A

compression of the ulnar nerve (paraesthesiae in the ulnar 1½ fingers)

2nd Year Medicine (24 decks)

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