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Flashcards in MSK week 1 Deck (160):
1

Three types of muscles and their description

Skeletal- voluntary- striated- somatic nervous system
Cardiac-involuntary-striated- autonomic nervous system
Smooth- involuntary- non-striated-autonomic nervous system

2

What makes up a motor unit?

One alpha neurone and all the muscle fibres (cells) it supplies.

3

What determines whether it is a fine movement or a powerful movement?

Fine movements will have fewer muscle fibres to each alpha neurone than a powerful movement will have.

4

What are the differences between skeletal and cardiac muscle?

Skeletal muscle- neurogenic initiation of contraction
-neuromuscular junctions are present
-no gap junctions
-Calcium entry is entirely from the sarcoplasmic reticulum

Cardiac
-myogenic initiation of contraction
-no neuromuscular junctions
-Gap junctions present
-Calcium from ECF and sarcoplasmic reticulum.

5

What do muscles consist of? (break it down into the cells etc)

Muscle- muscle fibres- myofibril (specialised intracellular structure) - sarcomeres (functional unit)

6

What is contained within a sarcomere?

The myosin and actin filaments that cross over to produce contraction. They are called collectively cytoskeletal elements.

7

Describe the process of an action potential causing muscle contraction.

Action potential arrives at the synapse and acetyl choline is transported across it. The action potential is then initiated in the muscle fibre and it travels along it and down the T tubule. This causes calcium release from the lateral sacs of the sarcoplasmic reticulum.
The calcium then binds to troponin meaning tropomyosin moves out of the way and an actin and myosin cross bridge can form (process powered by ATP)

8

How is contraction ended?

The action potential stops firing therefore calcium is reabsorbed by the sarcoplasmic reticulum. This means tropomyosin moves back into its blocking position and contraction ceases.

9

What are myofibrils?

Each muscle cell contains several of these. It is the contractable intracellular unit.

10

What is a sarcomere?

The functional unit of the muscles

11

Where are sarcomeres found?

Between two Z lines.

12

What is the M line?

The line down the middle of the A band and H zone.

13

What is the H zone?

Space where only thick filaments are.

14

What is the I band?

Space where only thin filaments are.

15

What is the A band?

The area of overlapping thick and thin filaments.

16

Gradation of skeletal muscle tension depends on two factors?

Number of muscle fibres contracting (more motor units=stronger contraction)
Tension developed by each contracting muscle fibre (influenced by length of muscle fibre and thickness of muscle fibre)

17

What is motor unit recruitment?

Recruiting more motor units to increase the strength of a contraction.

18

Describe tetanus

A muscle twitch lasts longer than the action potential for it. Therefore if you summate action potentials you can cause the muscle twitch to become stronger. Tetanus is a muscle fibre that is being constantly stimulated without time to relax to produce maximal muscle contraction.

19

When can maximal tetanus occur?

When a muscle is at its optimal length before contracting.

20

Two types of skeletal muscle contractions

Isotonic contraction- e.g. moving objects and body movements. Length of muscle fibre changes but muscle tension stays the same.
Isometric contraction e.g. supporting objects in a fixed position. Length of fibre stays the same but muscle tension changes.

21

What are the differences between skeletal muscles?

Enzymatic pathways for ATP synthesis
Resistance to fatigue- some have many mitochondria, some have few.
The activity of myosin ATPase- determines the speed at which energy is made available for cross bridging.

22

Describe the metabolic pathways that supply ATP in a muscle fibre

Transfer of a high energy phosphate from creatine phosphate to ADP. Immediate source of ATP.
Oxidative phosphorylation (main source when oxygen is present)
Glycolysis (main source when oxygen is not present)

23

Three types of skeletal muscle fibres

Slow oxidative (type 1) fibres
Fast oxidative (type 2a) fibres
Fast glycolytic (type 2b) fibres

24

Describe slow oxidative fibres

Used for prolonged relatively low intensity aerobic activities e.g. walking, maintaining posture.

25

Describe fast oxidative fibres

Used for moderate exercise. They are an intermediate between the other two. Examples are jogging.

26

Describe fast glycolytic fibres

Used for intense, short term exercise in anaerobic conditions e.g. jumping

27

What is a reflex action?

A stereotyped response to a specific stimulus. It is the simplest form of co-ordinated movement

28

What is a stretch reflex?

Negative feedback that resists passive change in muscle length to obtain optimal resting length.

29

What is the sensory receptor involved in a stretch reflex?

Muscle spindle

30

Describe the stretch reflex

By stretching the muscle you stretch the spindle cell, this increases firing of afferent neurons. These synapse within the spinal cord with the alpha motor neurones (efferent limb) that innervate the stretched muscle. This results in muscle contraction.

31

Describe muscle spindles

Collection of specialised muscle fibres known as intrafusal fibres. Located within the belly of the muscle and run parallel to ordinary fibres.

32

What is special at muscle spindles nerve supply?

They have their own nerve supply of gamma neurones that adjust the level of tension in the muscle spindles to maintain their sensitivity.

33

Three types of joints

Fibrous, cartilaginous and synovial.

34

Describe fibrous joints

Bones united by fibrous tissue
Hard, not-moveable joints e.g. in the skull.

35

Describe cartilaginous joints

Bones united by cartilage.
Allow limited movement. e.g. chostochondrol joints, intervertebral discs.

36

Describe synovial joints

Bones separated by a cavity containing synovial fluid and united by a fibrous capsule.

37

What is the purpose of a synovial membrane

It has the vascular supply, it contains synovial cells (which secrete synovial fluid)

38

What are the articular surfaces of synovial joints covered in?

Hyaline cartilage.

39

What is the function of articular cartilage?

Low friction lubricating surface. Helps to prevent wear and tear to joints.
Distributes contact pressure to subchondral bone.

40

Describe the extracellular matrix of cartilage

Contains water (70%), collagen (20%)and proteoglycans (10%)
Synthesised, organised, degraded and maintained by chondrocytes.
Articular cartilage is avascular and it receives its nutrients and oxygen from synovial fluid.

41

In normal joints, rate of ECM ...... does not exceed

Degradation does not exceed rate at which it's replaced.

42

What happens to cartilage with age?

Water content decreases. Composition of proteoglycans changes. Type 2 collagen decreases.

43

How is water distributed within the cartilage?

Unevenly- 80% is near the articular surface.

44

What is the function of water within the cartilage?

Helps to maintain the resiliency of the tissue and contribute to the nutrition and lubrication.

45

Where is the highest concentration of proteoglycans in cartilage?

highest in middle and deep zones of the cartilage.

46

What is the role of proteoglycans in cartilage?

Compressive properties and load bearing.

47

What is the role of collagen in cartilage?

Maintains cartilage architecture and provides tensile strength and stiffness.

48

Catabolic and anabolic factors of cartilage matrix turnover

Catabolic- stimulate proteolytic enzymes and inhibit proteoglycan synthesis. TNF alpha and IL-1.

Anabolic- stimulate proteoglycan synthesis and counter the effects of IL-1. TNF beta and insulin-like growth facor-1.

49

What is released by chondrocytes to have a negative impact on extracellular matrix components

Metallo-proteinase enzymes e.g. collagenase

50

Markers of cartilage degradation

Increased levels of serum and synovial keratin sulphate. (level increases with age and with OA)
Type II Collagen in synovial fluid (indicate cartilage breakdown)

51

What are the functions of synovial fluid?

Lubricate joint- facilitates movement
Minimises wear and tear
Supplies chondrocytes with O2 and removes CO2.

52

General characteristics of synovial fluid

Continuously replenished and absorbed by the synovial membrane.
Highly viscous (mainly due to presence of hyaluronic acid)
Viscosity varies with joint movement.

53

How are constituents of synovial fluid derived?

Uric acid- dialysis of blood plasma.

54

Does synovial fluid contain cells?

Normally very few mononuclear leukocytes.

55

What changes in synovial fluid can occur?

Changes in viscosity and elacicity during movement.
Rapid movement- not viscous, highly elastic
Slow movement- viscous, not very elastic.

56

Describe synovial fluid in inflammatory conditions

Viscosity would be low
May be straw to yellow coloured.
Will be translucent
Contains 2000-75000 white cells.

57

Describe synovial fluid in sepsis

Viscosity would be variable as would colour. However it would be opaque and often have greater than 100,000 white cells.

58

Describe normal synovial fluid

Viscosity is high. Colour of synovial fluid is colourless and transparent. Very few white cells (<200)

59

Describe the nuclei of skeletal muscle cells

Multinucleated and are near the edge of the fibre.

60

Describe the mitochondria distribution, force and stamina of each type of muscle fibre

Slow oxidative fibres- lots of mitochondria. Resistant to fatigue and produce relatively little force.
Fast oxidative fibres- relatively fast contracting and reasonably resistant to fatigue.
Fast glycolytic fibres- very few mitochondria, fatigue quickly and produce great force.

61

What are muscle fibres grouped into?

Fasicles.

62

What is the connective tissue that surrounds several fascicles called?

Epimysium

63

What is the connective tissue that surrounds a single fascicle called?

Perimysium

64

What is the connective tissue that surrounds a single muscle fibre called?

Endomysium

65

Differences between cartilage and bone

Cartilage- semi rigid, permeable, avascular, cells nourished by diffusion through the ECM.
Bone- rigid, not permeable, has its own vascular network

66

Where do chondrocytes live and what is there function?

They live in a space in the ECM called the lacuna. They are active cells that secrete and maintain the ECM.

67

What is the function of bone (other than structure ofc)?

Calcium store (95% of the bodies calcium)
Haemopoesis- blood cell production in the bone marrow.

68

What types of bone are there?

Cortical bone- dense lamellar structure
Trabecular (cancellous) bone- has marrow cavities that run adjacent to the trabecular bone.

69

What are Haversion canals?

Carry blood vessels parallel to the axis of the bone

70

What are Volksmann canals?

They carry blood vessels across the bone.

71

What are canniculi?

Small canals spreading outwards from osteocytes that allow the dendritic processes of the osteocytes to connect together with neighbouring osteoblasts.

72

What are cement lines?

Lines that are often visible surrounding the osteon. Only found in osteons made during remodelling.

73

What is different about osteocytes in trabecular bone to cortical bone?

They haven't got haversion canals because osteocytes can obtain their nutrients from the bone marrow.

74

Describe osteoblasts

Bone forming cells found on the surface of developing bone. Plentiful RER and prominent mitochondria.

75

Describe osteoprogenitor cells

They are the reserve pool of osteoblasts. They are located under the periosteum.

76

Describe osteocytes

Bone absorbing cells. Found on the surface of bone.

77

Describe osteocytes

A bone cell trapped in a bone matrix.

78

Describe the process of bone remodelling

Number of osteoclasts congregate and begin to drill into the bone forming a tunnel. Blood vessels then grow in here and begin to lay down lamellar bone. This continues until all that is left is a Haversion canal.

79

What is woven bone?

After a fracture woven bone is layed down. It is haphazard in fashion and becomes remodelled into lamellar bone by being broken down by osteoclasts and reformed by osteoblasts.

80

Describe the process of bone mineralization

Osteoblasts secrete proteoglycans and other organic components of the bone matrix- becomes collectively termed the osteoid. Over time this undergoes mineralisation.

81

What is vasculitis?

Inflammation of the blood vessels.

82

Causes of vasculitis

Infection
Inflammation close to the vessel
Autoimmune

83

What specific antibodies are associated with vasculitis?

Anti-nuetrophil cytoplasmic antibody -ANCA
Anti-endothelial antibody

84

Anti-endothelial antibody is associated with what disease?

Kawasaki's disease.

85

What does cANCA react with?

Proteinase 3

86

What does pANCA react with?

myeloperoxidase

87

Name some large vessel vasculitis's

Granulomatos disease e.g.
Giant cell arteritis
Takayasu arteritis

88

Which artery is affected by giant cell arteritis? Why may a biopsy of this artery be negative?

Temporal artery
It has skip lesions therefore negative biopsy doesn't rule it out.

89

Cause of GCA

Unknown cause however presumably autoimmune basis.

90

Symptoms of GCA

Specific temporal headache, jaw claudication, sensitivity when combing the hair.

91

If GCA is untreated, what may happen?

Patient may go blind.

92

Treatment of GCA

Steroids.

93

Name some medium cell vasculitis

Immune complex mediated e.g. polyarteritis nodes
Anti-endothelial antibodies e.g. Kawasaki's.

94

Polyarteritis nodosa is due to

Circulating immune complexes. ANCA negative.

95

Polyarteritis nodosa is highly related to

Hep B virus.

96

What does PA cause?

Fibrin depositation in vessel walls. Transmural necrotising inflammation. Different vessels will be involved to varying degrees.
GI complications and renal involvement.
However it spares the lungs.

97

Name some small vessel vasculitis

Microscopic polyangitis
Granulomatosis with polyangitis
Eosinophillic granulomatosis.

98

Describe microscopic polyangitis

Vasculitis without asthma or granulomas.

99

Describe granulomatosis with polyangitis

Vasculitis with granulomas
Also known as wegners

100

Describe eosinophillic granulomatosis

Vasculitis with granulomas and asthma.
Also known as Churg-Strauss.

101

Why is there a build up or uric acid in the body (e.g. in gout)

Adenine and guanine are purine bases and therefore when they undergo DNA replication they leave behind the waste product urate. We lack uricase to break down this so uric acid crystals build up.

102

Gout is ..... birefringent

Negatively

103

Why do patients get gout?

Could be making too much uric acid e.g.
-idiopathic enzyme defect
-Lysch Nyhan syndrome
-Increased cell turnover e.g. cancer

Getting rid of too little
Under-excretion
Drugs e.g. thiazide diuretics which stop excretion.

104

What shape are gout crystals?

Needle shaped.

105

What shape are calcium pyrophosphate crystals?

Rhomboid shaped

106

What is calcium pyrophosphate build up in the joints also called?

Psuedogout

107

Pseudogout is .... birefringent

weakly postiive

108

What causes psuedogout?

Usually idiopathic
Occasionally there is a cause e.g. hypercalcaemia, haemachromotosis, hypomagnesaemia, hypothyroidism.

109

What is pagets disease?

Abnormality of bone turnover meaning you get increased osteoclast (and subsequently osteoblast) activity making thick excess bone.

110

Where does pagets effect?

Can affect all bones but usually axial.

111

Symptoms of pagets disease?

Pain- could be due to nerve compression or micro fractures.
Increase in metabolism- heat, warm skin, AV shunt, high output cardiac failure.

112

What is osteomalacia?

Abnormal vitamin D metabolism

113

What is osteomalacia called in the young?

Rickets

114

Signs of osteomalacia

Bowed legs, square head, pigeon chest.

115

At neuromuscular junctions- describe the process of synthesis of the neurotransmitter

Choline is transported into the terminal bouton by the choline transporter (symport with Na+)
Acetylcholine is synthesised by choline and acetyl CoA in the presence of choline-acetyl-transferase (CAT)
AcH becomes concentrated in vesicles

116

Where does the acetyl CoA come from to form the neurotransmitter at neuromuscular junctions?

From the mitochondria in the cell.

117

What type of receptors are present at the neuromuscular end plate?

Nicotinic

118

What is a quantum of neurotransmitter?

A quantum of neurotransmitter brings about a miniature end plate potential. These summate to produce the end plate potential.

119

What is pain?

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

120

What are the three classifications of pain?

Nociceptive pain
Inflammatory pain
Pathological pain

121

Describe nociceptive pain

Normally activated by intense stimuli. Serves as an early warning system to detect and minimise contact with damaging stimuli.
Over-rides most other ongoing activity.

122

Describe inflammatory pain

Assists in healing of the damaged part- discourages physical contact (pain hypersensitivity), discourages movement.
Allodynia- innocuous stimuli now elicit pain.

123

Describe pathological pain

Maladaptive
Can be neuropathic or dysfunctional
Neuropathic pain can result from damage to the axon or neurological disaster e.g. stroke
Dysfunctional is when nerve fibres that normally respond to non-noxious stimuli become activated.

124

What mutation causes the absence of pain?

SCN9A gene that encodes for a particular voltage gated Na+ channel found in nociceptors.

125

What injuries are people with absence of pain prone too?

Lip and tongue injury
Bruises and cuts
Multiple scars
Bone fractures
Joint deformity
Premature mortality

126

How are action potentials initiated from pain?

A noxious stimulus arrives activating a (mechanical/thermal/chemical) selective channel which allows positive charge to move into the axon. This allows an AP to be initiated. It then propagates along the axon.

127

Describe the process of neurogenic inflammation

Nociceptors release substance P and CGRP due to tissue damage or inflammatory mediators.
Substance P acts on mast cells to get them to release histamine- causing vasodilation and extravasation of plasma proteins. Also sensitises surrounding nociceptors.
CGRP also induces vasodilation
Primary and secondary hyperalgesia (abnormally high sensitivity to pain) and allodynia ensue.

128

Name the different subtypes of nociceptors

Alpha delta fibres- mechanical/thermal
C fibres-respond to all noxious stimuli

129

What are alpha delta fibres responsible for?

Mechanical/thermal stimuli.
Mediate first/fast pain

130

What are C fibres responsible for?

Respond to all noxious stimuli
Mediate slow or second pain.

131

How are chemical stimuli detected?

H+ activates acid sensing ion channels (ASIC's)

132

How are thermal stimulus detected?

heat/cold sensitive receptors- members of transient receptor potential (TRP) family- especially TRPV1 activated by noxious heat.

133

What is osteomyelitis?

Inflammation of the bone and medullary cavity (usually in long bones) due to INFECTION.

134

How is osteomyelitis classified?

Acute or chronic.

135

In adults, osteomyelitis is caused by?

Staph aureus

136

In children, osteomyelitis is caused by?

strep.

137

Presentation of osteomyelitis

Fever
Severe bone pain
Swelling, redness and warmth in the affected area.

138

Who is at risk of developing osteomyelitis?

IV drug users, circulation disorders e.g. (poorly controlled diabetics, sickle cell disease, peripheral vascular disease), recent fracture or op, immunocompromised.

139

What is a clue that osteomyelitis is developing after an open fracture?

Non union and poor wound healing.

140

What organisms cause osteomyelitis after an open fracture?

Staph aureas
Aerobic gram negative bacteria.

141

Treatment of an open fracture osteomyelitis

Agressive debridement
Fixation
Soft tissue cover.

142

What organisms are likely to cause osteomyelitis in a diabetic?

Often polymicrobial.

143

Presentation of diabetics with osteomyelitis? and treatment?

Diabetics tend to lose their nociceptive reflex- and therefore don't feel pain. Can often put a probe straight to the bone.
Treatment- debridement and antibiotics.

144

Who is likely to get haematogenous osteomyelitis?

Pre pubertal children, people who inject drugs, central lines, dialysis and the elderly.

145

Organisms likely to cause haematogenous osteomyelitis?

staphylococcus, streptococcus
Unusual pathogens- pseudomonas, candida, eikenella corrodens (needle lickers), mycobacterium tb.

146

Patients on dialysis are most likely to have which organisms causing the osteomyelitis?

staph aureus in the most common.

147

How would someone with vertebral osteomyelitis present clinically?

Only have a fever.
Insidious pain and tenderness (they will jump if you touch their vertebrae)
sometimes neurological symptoms
Sometimes increased inflammatory markers.

148

Treatment of vertebral osteomyelitis?

Drainage of any epidural/paravertebral abscesses.
Antimicrobials for 6 weeks
Expect greater than 50% decrease in ESR

149

What organisms release Panton valentine leucocidin?

MSSA and MRSA.

150

Will the lab tell you if your staph aureus releases PVL?

nope- have to ask for it.

151

What does PVL release from staph aureus cause?

Very sick patient.
Severe skin infections, necrotising pneumonias, invasive.

152

What would you treat PVL releasing staph aureus with?

Flucloxicillin and an antitoxin.

153

When is PVL producing staph aureus likely to cause osteomyelitis?

In patients with prosthetic joint infections.

154

Treatment of prosthetic joint osteomyelitis?

Ideally removal of prosthesis for 6 weeks. Reimplant with antibiotic therapy.

155

What organisms are likely to cause sickle cell osteomyelitis?

salmonella
staph aureus.

156

What is gauchers disease? If it becomes infected what is the likely organism?

Lysosomal storage disorder. May mimic bone crisis and often affects the tibia.
Sterile- if bone crisis
Staph aureus if infected.

157

What are the common bacterial causes of septic arthritis??

-staph aureus
-steptococci
-coagulase neg staph
-neisseria gonorrhoea
-haemophilus influenza.

158

What is tetanus?

Bacteria that produces neurotoxin cause spastic paralysis.

159

What organisms cause tetanus?

Gram positive and strictly anaerobic.

160

Treatment of tetanus

surgical debridement
antitoxins
supportive measures
antibiotics- penicillin/metronidazole.