Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Musculoskeletal > MSK week 1 > Flashcards

MSK week 1 Flashcards

1
Q

Three types of muscles and their description

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What makes up a motor unit?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the differences between skeletal and cardiac muscle?

A

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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is contained within a sarcomere?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the process of an action potential causing muscle contraction.

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is contraction ended?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are myofibrils?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a sarcomere?

A

The functional unit of the muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where are sarcomeres found?

A

Between two Z lines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the M line?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the H zone?

A

Space where only thick filaments are.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the I band?

A

Space where only thin filaments are.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the A band?

A

The area of overlapping thick and thin filaments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gradation of skeletal muscle tension depends on two factors?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is motor unit recruitment?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe tetanus

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When can maximal tetanus occur?

A

When a muscle is at its optimal length before contracting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Two types of skeletal muscle contractions

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the differences between skeletal muscles?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the metabolic pathways that supply ATP in a muscle fibre

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Three types of skeletal muscle fibres

A 
Slow oxidative (type 1) fibres
Fast oxidative (type 2a) fibres
Fast glycolytic (type 2b) fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe slow oxidative fibres

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe fast oxidative fibres

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe fast glycolytic fibres

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is a reflex action?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a stretch reflex?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the sensory receptor involved in a stretch reflex?

A

Muscle spindle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the stretch reflex

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe muscle spindles

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is special at muscle spindles nerve supply?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Three types of joints

A

Fibrous, cartilaginous and synovial.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe fibrous joints

A

Bones united by fibrous tissue

Hard, not-moveable joints e.g. in the skull.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe cartilaginous joints

A

Bones united by cartilage.

Allow limited movement. e.g. chostochondrol joints, intervertebral discs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe synovial joints

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the purpose of a synovial membrane

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the articular surfaces of synovial joints covered in?

A

Hyaline cartilage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the function of articular cartilage?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the extracellular matrix of cartilage

A 
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What happens to cartilage with age?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How is water distributed within the cartilage?

A

Unevenly- 80% is near the articular surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the function of water within the cartilage?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Where is the highest concentration of proteoglycans in cartilage?

A

highest in middle and deep zones of the cartilage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the role of proteoglycans in cartilage?

A

Compressive properties and load bearing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the role of collagen in cartilage?

A

Maintains cartilage architecture and provides tensile strength and stiffness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Catabolic and anabolic factors of cartilage matrix turnover

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

A

Metallo-proteinase enzymes e.g. collagenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Markers of cartilage degradation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the functions of synovial fluid?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

General characteristics of synovial fluid

A 
Continuously replenished and absorbed by the synovial membrane. 
Highly viscous (mainly due to presence of hyaluronic acid)
Viscosity varies with joint movement.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How are constituents of synovial fluid derived?

A

Uric acid- dialysis of blood plasma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Does synovial fluid contain cells?

A

Normally very few mononuclear leukocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What changes in synovial fluid can occur?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Describe synovial fluid in inflammatory conditions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe synovial fluid in sepsis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Describe normal synovial fluid

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe the nuclei of skeletal muscle cells

A

Multinucleated and are near the edge of the fibre.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are muscle fibres grouped into?

A

Fasicles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the connective tissue that surrounds several fascicles called?

A

Epimysium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

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

A

Perimysium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

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

A

Endomysium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Differences between cartilage and bone

A

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

66
Q

Where do chondrocytes live and what is there function?

A

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

67
Q

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

A 
Calcium store (95% of the bodies calcium)
Haemopoesis- blood cell production in the bone marrow.
68
Q

What types of bone are there?

A

Cortical bone- dense lamellar structure

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

69
Q

What are Haversion canals?

A

Carry blood vessels parallel to the axis of the bone

70
Q

What are Volksmann canals?

A

They carry blood vessels across the bone.

71
Q

What are canniculi?

A

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

72
Q

What are cement lines?

A

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

73
Q

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

A

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

74
Q

Describe osteoblasts

A

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

75
Q

Describe osteoprogenitor cells

A

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

76
Q

Describe osteocytes

A

Bone absorbing cells. Found on the surface of bone.

77
Q

Describe osteocytes

A

A bone cell trapped in a bone matrix.

78
Q

Describe the process of bone remodelling

A

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
Q

What is woven bone?

A

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
Q

Describe the process of bone mineralization

A

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

81
Q

What is vasculitis?

A

Inflammation of the blood vessels.

82
Q

Causes of vasculitis

A

Infection
Inflammation close to the vessel
Autoimmune

83
Q

What specific antibodies are associated with vasculitis?

A

Anti-nuetrophil cytoplasmic antibody -ANCA

Anti-endothelial antibody

84
Q

Anti-endothelial antibody is associated with what disease?

A

Kawasaki’s disease.

85
Q

What does cANCA react with?

A

Proteinase 3

86
Q

What does pANCA react with?

A

myeloperoxidase

87
Q

Name some large vessel vasculitis’s

A

Granulomatos disease e.g.
Giant cell arteritis
Takayasu arteritis

88
Q

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

A

Temporal artery

It has skip lesions therefore negative biopsy doesn’t rule it out.

89
Q

Cause of GCA

A

Unknown cause however presumably autoimmune basis.

90
Q

Symptoms of GCA

A

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

91
Q

If GCA is untreated, what may happen?

A

Patient may go blind.

92
Q

Treatment of GCA

A

Steroids.

93
Q

Name some medium cell vasculitis

A

Immune complex mediated e.g. polyarteritis nodes

Anti-endothelial antibodies e.g. Kawasaki’s.

94
Q

Polyarteritis nodosa is due to

A

Circulating immune complexes. ANCA negative.

95
Q

Polyarteritis nodosa is highly related to

A

Hep B virus.

96
Q

What does PA cause?

A

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
Q

Name some small vessel vasculitis

A

Microscopic polyangitis
Granulomatosis with polyangitis
Eosinophillic granulomatosis.

98
Q

Describe microscopic polyangitis

A

Vasculitis without asthma or granulomas.

99
Q

Describe granulomatosis with polyangitis

A

Vasculitis with granulomas

Also known as wegners

100
Q

Describe eosinophillic granulomatosis

A

Vasculitis with granulomas and asthma.

Also known as Churg-Strauss.

101
Q

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

A

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
Q

Gout is ….. birefringent

A

Negatively

103
Q

Why do patients get gout?

A

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
Q

What shape are gout crystals?

A

Needle shaped.

105
Q

What shape are calcium pyrophosphate crystals?

A

Rhomboid shaped

106
Q

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

A

Psuedogout

107
Q

Pseudogout is …. birefringent

A

weakly postiive

108
Q

What causes psuedogout?

A

Usually idiopathic

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

109
Q

What is pagets disease?

A

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

110
Q

Where does pagets effect?

A

Can affect all bones but usually axial.

111
Q

Symptoms of pagets disease?

A

Pain- could be due to nerve compression or micro fractures.

Increase in metabolism- heat, warm skin, AV shunt, high output cardiac failure.

112
Q

What is osteomalacia?

A

Abnormal vitamin D metabolism

113
Q

What is osteomalacia called in the young?

A

Rickets

114
Q

Signs of osteomalacia

A

Bowed legs, square head, pigeon chest.

115
Q

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

A

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
Q

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

A

From the mitochondria in the cell.

117
Q

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

A

Nicotinic

118
Q

What is a quantum of neurotransmitter?

A

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

119
Q

What is pain?

A

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

120
Q

What are the three classifications of pain?

A

Nociceptive pain
Inflammatory pain
Pathological pain

121
Q

Describe nociceptive pain

A

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
Q

Describe inflammatory pain

A

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

123
Q

Describe pathological pain

A

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
Q

What mutation causes the absence of pain?

A

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

125
Q

What injuries are people with absence of pain prone too?

A 
Lip and tongue injury
Bruises and cuts
Multiple scars
Bone fractures
Joint deformity
Premature mortality
126
Q

How are action potentials initiated from pain?

A

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
Q

Describe the process of neurogenic inflammation

A

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
Q

Name the different subtypes of nociceptors

A

Alpha delta fibres- mechanical/thermal

C fibres-respond to all noxious stimuli

129
Q

What are alpha delta fibres responsible for?

A

Mechanical/thermal stimuli.

Mediate first/fast pain

130
Q

What are C fibres responsible for?

A

Respond to all noxious stimuli

Mediate slow or second pain.

131
Q

How are chemical stimuli detected?

A

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

132
Q

How are thermal stimulus detected?

A

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

133
Q

What is osteomyelitis?

A

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

134
Q

How is osteomyelitis classified?

A

Acute or chronic.

135
Q

In adults, osteomyelitis is caused by?

A

Staph aureus

136
Q

In children, osteomyelitis is caused by?

A

strep.

137
Q

Presentation of osteomyelitis

A

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

138
Q

Who is at risk of developing osteomyelitis?

A

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

139
Q

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

A

Non union and poor wound healing.

140
Q

What organisms cause osteomyelitis after an open fracture?

A

Staph aureas

Aerobic gram negative bacteria.

141
Q

Treatment of an open fracture osteomyelitis

A

Agressive debridement
Fixation
Soft tissue cover.

142
Q

What organisms are likely to cause osteomyelitis in a diabetic?

A

Often polymicrobial.

143
Q

Presentation of diabetics with osteomyelitis? and treatment?

A

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
Q

Who is likely to get haematogenous osteomyelitis?

A

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

145
Q

Organisms likely to cause haematogenous osteomyelitis?

A

staphylococcus, streptococcus

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

146
Q

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

A

staph aureus in the most common.

147
Q

How would someone with vertebral osteomyelitis present clinically?

A

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

148
Q

Treatment of vertebral osteomyelitis?

A

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

149
Q

What organisms release Panton valentine leucocidin?

A

MSSA and MRSA.

150
Q

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

A

nope- have to ask for it.

151
Q

What does PVL release from staph aureus cause?

A

Very sick patient.

Severe skin infections, necrotising pneumonias, invasive.

152
Q

What would you treat PVL releasing staph aureus with?

A

Flucloxicillin and an antitoxin.

153
Q

When is PVL producing staph aureus likely to cause osteomyelitis?

A

In patients with prosthetic joint infections.

154
Q

Treatment of prosthetic joint osteomyelitis?

A

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

155
Q

What organisms are likely to cause sickle cell osteomyelitis?

A

salmonella

staph aureus.

156
Q

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

A

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

157
Q

What are the common bacterial causes of septic arthritis??

A
  • staph aureus
  • steptococci
  • coagulase neg staph
  • neisseria gonorrhoea
  • haemophilus influenza.
158
Q

What is tetanus?

A

Bacteria that produces neurotoxin cause spastic paralysis.

159
Q

What organisms cause tetanus?

A

Gram positive and strictly anaerobic.

160
Q

Treatment of tetanus

A

surgical debridement
antitoxins
supportive measures
antibiotics- penicillin/metronidazole.

Musculoskeletal (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions