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Block 4 AR > Cells > Flashcards

Cells Flashcards

1
Q

What type of tissue is bone?

A

Specialised form of supporting tissue

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2
Q

Describe the structure of supporting tissues

A

Cells embedded in an extracellular matrix (ECM)
ECM consists of fibres, ground substance & structural glycoproteins
ECM composition determines the tissues physical properties

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3
Q

What is specialised about bone ECM?

A

Mineralised with Ca - hydroxyapatite

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4
Q

What 2 layers line the inside and outside of bone?

A

Periosteum is outside layer

Endosteum is inner layer

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5
Q

What type of fibres provide resilience in bone?

A

Type 1 collagen

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6
Q

What are functions of bone?

A 
Support 
Protection 
Movement 
Site of haematopoiesis 
Mineral homeostasis
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7
Q

Where is the physis (growth plate) in long bones?

A

Between epiphysis at end and metaphysis

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8
Q

What is cortical bone like? And where is it?

A

Compact and solid

Outer part of bone

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9
Q

What is trabecular bone like? And where is it?

A

Spongy or cancellous

Inner part of bone

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10
Q

Describe the structure of cortical bone

A

Cortical bone is composed of Haversian systems (osteons)
Osteon: concentric lamellae at 90 degrees to one another, bone laid down around central canal containing blood vessels
Periosteal blood vessel runs transversely across the bone in Volkmann’s canals to form the (Haversian) canals
Interstitial lamellae fill the space between osteons, result of bone remodelling and the formation of new Haversian systems
Extending around bone are outer circumferential lamellae

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11
Q

Describe the structure of trabecular bone

A

Beams and struts of lamellar bone oriented along lines of stress
Large surface area
Orderly layered arrangement of collagen fibres (lamellae) which makes it strong

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12
Q

What is woven bone and where will you find it?

A

Immature (woven) bone is found mainly in the foetus
Minimal in adults except fracture healing or sites of rapid bone remodelling
Produced quickly, but collagen fibres more haphazardly arranged and so is weaker than lamellar bone

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13
Q

Describe the clinical significance of the blood supply to the head of femur

A

Unidirectional flow and limited anastomoses, fractures may easily disrupt blood supply and lead to avascular necrosis
Medial circumflex artery is main supply which comes from neck of femur

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14
Q

Describe the blood supply of bones

A

Epiphyseal arteries supply epiphysis
Metaphyseal arteries supply metaphysis
Periosteal and nutrient arteries (volkman canals) supply diaphysis

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15
Q

What cell type are bone forming cells derived from?

A

Mesenchymal stem cell derived

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16
Q

What cell type are osteoclasts derived from?

A

Granulocyte / monocyte progenitor derived

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17
Q

Describe how bone forming cells go from stem cells to bone lining cells

A

Mesenchymal stem cells become osteoprogenitor cells
These become osteoblasts which release ECM to lay down new bone
Once embedded in the bone these become osteoclasts which maintain the ECM

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18
Q

What do osteoblasts do?

A

Bone formation - synthesise matrix (osteoid) & its subsequent mineralisation
Secrete type 1 collagen, proteoglycans & glycoproteins
Alkaline phosphatase & osteocalcin secreted to aid mineralisation of ECM
Surrounded by matrix to become osteocytes
Bone lining cells

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19
Q

What do osteocytes do?

A

Mature bone cell derived from osteoblast
Encased in bone matrix within lacunae interconnected by dendritic processes passing through canaliculi
No cell division
Roles in mechanotransduction and matrix maintenance / calcium
homeostasis

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20
Q

What do osteoclasts do?

A

Derived from monocyte-macrophage system
Multinucleated cells
Bone resorption - release enzymes & acid to resorb bone
Form resorption craters – Howship’s lacunae
Osteoclastic & osteoblastic activity linked in bone remodelling

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21
Q

Describe the bone remodelling cycle

A

Lining cells are quiescent
Mechanical stress or lack of causes change
Osteoclasts are recruited, differentiate and activated
Bone is resorbed
Osteoclasts apoptose and are removed
Reversal: osteoblasts are recruited, differentiate and activated
They synthesise matrix which is then mineralised

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22
Q

How many days are there per bone remodelling cycle?

A

Approx 160-200 days per cycle

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23
Q

What factors control bone resorption?

A

Osteoclast differentiation & activation controlled by RANK, which is activated by RANKL – produced by various cells, including osteoblasts OPG (osteoprotegerin) is a non-signalling decoy receptor for RANKL
Ratio of OPG to RANKL important in determining degree of resorption; system allows multilevel control

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24
Q

What effects do calcitriol, PTH and interleukins have on osteoblasts?

A

Signal osteoblasts to express RANKL which signals to osteoclast progenitor cells expressing RANK to differentiate and activate

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25
Q

At what time during development do bones begin to develop?

A

6th week of embryonic development

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26
Q

What signals initiate bone development?

A

Growth factors such as bone morphogenetic proteins (BMPs) and cytokines

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27
Q

What are the 2 types of bone development? And give examples

A

Intramembranous: mesenchyme to bone eg flat bones of skull, clavicle & mandible
Endochondral: mesenchyme to cartilage to bone eg weight bearing bones - long bones, vertebrae, pelvis

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28
Q

Describe the process of intramembranous ossification

A

Ossification centre forms with osteoblasts in centre which secrete osteoid which is calcified
Woven bone formed and Mesenchyme condenses to form periosteum
Bone collar forms and red marrow appears in cavity

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29
Q

Describe the process of endochondral ossification

A

Mesenchyme forms chondroblasts which form the cartilage model
Chondrocytes in centre hypertrophy, ECM calcifies so cell death
Bone collar develops at diaphysis and perichondrium becomes periosteum
Blood vessels invade dead cartilage bringing in bone forming cells Osteoblasts develop and secrete osteoid which becomes mineralised in primary ossification centre of diaphysis
Gradual replacement of cartilage by woven bone, bony trabeculae develop in the diaphysis
Secondary ossification centres form in epiphysis

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30
Q

By what time in development is there a medullary cavity in bone?

A

6th month of development due to resorption of central bone

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31
Q

When do secondary ossification centres form?

A

Develop in the cartilage at epiphyses
At birth secondary centre in femur; others appear in cartilaginous epiphyses at varying ages after birth
Appearance of ossification centres on X-rays can be used to determine the bone age

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32
Q

What form of growth occurs at the epiphyseal growth plate?

A

Allows growth in length of a long bone - longitudinal

Appositional growth allows the bone to grow in width (bone formed beneath the periosteum)

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33
Q

What are the distinct zones of the epiphyseal growth plate?

A

Resting quiescent zone
Growth proliferation zone - cartilage cells undergo mitosis
Hypertrophic zone - older cartilage cells enlarge
Calcification zone - matrix becomes calcified, cartilage cells die
Ossification zone - new bone formation occurring

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34
Q

What is the clinical significance of the epiphyseal growth plate in terms of fractures?

A

Fractures that involve a growth plate may cause significant deformities

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35
Q

What factors may influence growth plate closure?

A

Growth hormone, oestrogen

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36
Q

What is a fracture?

A

Breach in the integrity of part or the whole of a bone

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37
Q

What is a simple or closed fracture?

A

Clean break with intact overlying tissues

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38
Q

What is a compound or open fracture?

A

Direct communication between broken bone & skin surface

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39
Q

What is a transverse fracture?

A

Fracture line is perpendicular to the longitudinal axis

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40
Q

What is an oblique fracture?

A

Fracture line is usually angled ~30-45 ̊ to the longitudinal axis

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41
Q

What is a spiral fracture?

A

Fracture line is oblique & encircles a portion of the shaft

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42
Q

What is a comminuted fracture?

A

Multiple bone fragments

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43
Q

What is a compression or crush fracture?

A

Compression of (usually trabecular) bone e.g. vertebral bodies

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44
Q

What is a greenstick or incomplete fracture?

A

Bone incompletely fractured (portion of cortex & periosteum intact on compression side). Usually in children

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45
Q

What is a traumatic fracture?

A

Result of a single violent injury

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46
Q

What is a stress fracture?

A

Result of repeated stress (e.g. in athletes)

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47
Q

What is a pathological or secondary fracture?

A

Fracture occurring in bone weakened generally or locally by disease processes e.g. metabolic, neoplastic, hereditary

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48
Q

What are the stages of fracture healing?

A

Haematoma: Bleeding from ruptured vessels, Inflammatory reaction, phagocytes move into area
Granulation tissue: capillary loops in loose connective tissue replace
haematoma. Cell proliferation in response to growth factors/cytokines
Callus: irregular swelling bridges gap between bone ends, fibrocellular material and cartilage initially
Woven bone: Osteoprogenitor cells proliferate & move into area and form woven bone strengthening callus from ~3 weeks
Lamellar bone: woven bone callus replaced by mature lamellar bone
Remodelling: Osteoclasts and osteoblasts remodel lamellar bone into form related to function (in response to stresses). Excessive callus is resorbed & medullary cavity re-established

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49
Q

What factors aid fracture healing?

A

Stability of the fracture
Adequate blood supply
Apposition of bone ends
Age and general health of the patient /comorbitidies

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50
Q

What factors delay fracture healing?

A

Excessive movement of bone ends
Poor blood supply
Infection / foreign body

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51
Q

What is fracture Malunion?

A

Fracture heals in an unsatisfactory position

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52
Q

What is fracture delayed union?

A

Fracture healing takes longer than expected

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53
Q

What is fracture non union?

A

Fracture fails to unite

Resultant formation of fibrous union or pseudoarthrosis

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54
Q

What is supporting tissue?

A

Originates from embryonic mesoderm
Cells (5%): Fibroblasts, Adipocytes, Leukocytes
Extracellular Matrix (ECM, 95%): Fibres, collagen, elastin
Ground substance
Structural Glycoproteins

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55
Q

What function does bone have?

A

Protection and support

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56
Q

What function does cartilage have?

A

Semi rigid malleability
Support e.g. ‘shock absorbers’
Precursor for bone formation

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57
Q

What functions do ligaments have?

A

Flexible

Stability of joints

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58
Q

What varies the type of supporting structure found in tissue?

A

Variations in:
Proportion of ground substance
Proportion and type of fibrous elements

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59
Q

What are chondroblasts?

A

Precursors to cartilage that synthesise matrix

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60
Q

What are chondrocytes?

A

Mature cartilage cells that occupy lacunae & maintain matrix

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61
Q

What is the extracellular matrix of cartilage like?

A

Collagen +/- elastin fibres
Ground substance
Avascular

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62
Q

What is Perichondrium?

A 
Fibrocellular covering (absent from articular surfaces)
source of new chondroblasts
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63
Q

What are 3 types of cartilage?

A

Hyaline
Elastic
Fibrocartilage

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64
Q

What is hyaline cartilage? And where is it found?

A

Type 2 collagen
Articular surfaces, respiratory tract, & costal cartilages
Forms cartilage model during bone development
Abundant ECM
Allows friction free movement of joint

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65
Q

What is elastic cartilage? And where is it found?

A

Type 2 collagen & elastin

External ear, epiglottis

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66
Q

What is Fibrocartilage? And where is it found?

A

Type 1 collagen

Pubic symphysis; intervertebral discs; menisci of knee joint

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67
Q

Describe the formation of cartilage

A

Derived from mesoderm
Form chondroblasts
Mitotic division forms clusters of chondroblasts
Clusters synthesise ECM
ECM surrounds and segregates clusters
Blasts mature into chondrocytes which maintain integrity of ECM
Peripheral chondroblasts persist in perichondrium (capillaries here)

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68
Q

What is ground substance made from?

A

Proteoglycans aggregates
Protein core
Glycosaminoglycans attached: Negatively charged so cant form globules. Strands allow max volume for minimum weight
Hyaluronic acid (glycosaminoglycan backbone)
Water: volume, turgor, tense strength, storage of inactive enzymes, diffusion of metabolites

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69
Q

Describe hyaline cartilage of joints

A

Resist compression: elasticity and stiffness of proteoglycans
Tensile strength collagen and hydrogel ground substance
Maintained and turned over by chondrocytes
Limited repair and regeneration capacity - avascular: nutrition is by diffusion-limited thickness
Articular surfaces of joints - no perichondrium so no source of new chondroblasts

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70
Q

What are Common/ ImportantDiseases of Synovial Joints and Bones?

A

V- Vascular - Avascular necrosis following NOF
I- Infection, inflammation
T- Trauma - fracture, dislocation
A- Autoimmune - arthropathies, psoriatic
M- Metabolic - Osteoporosis, Pagets
I- Iatrogenic, idiopathic - Complications of drugs
N- Neoplasms and metastasis
C- Congenital - Achrondroplasia, Osteogenesis Imperfecta
D- Degenerative - Osteoarthritis
E- Endocrine - Hyperparathyroidism

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71
Q

What are the 5 cardinal signs of acute inflammation?

A 
Redness
Heat
Swelling
Loss of function
Pain
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72
Q

What can cause bursitis?

A

Repetitive use, trauma or systemic arthritis

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73
Q

What are common areas for bursitis?

A

Shoulder, olecranon (elbow) and knee

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74
Q

What are risk factors for osteoarthritis?

A

Age, trauma, inflammatory disease, joint defects, gender, race, bone mass and obesity

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75
Q

What are the cardinal signs of chronic inflammation?

A

Ongoing tissue damage
Ongoing tissue repair
Ongoing inflammation

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76
Q

What is osteoarthritis?

A

Destruction: Surface cracks in cartilage, bone exposed, burnished from wear: eburnation, bone and cartilage fragments in joint cavity
Repair: Osteophytes: bony outgrowths form, Reduced proteoglycans and collagen, increased water, chondrocyte hypertrophy, Alteration of mechanical properties, bone shock absorbing properties reduced

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77
Q

What progressive changes occur in osteoarthritis?

A

Cartilage splits and is eroded so joint space narrowed
Joint capsule inflamed and oedematous, synovium inflamed
Outgrowth of bone, Osteophytes
Bone articulates with bone, eburnation
Thickening of subchondral bone plate
Development of subarticular bone cysts

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78
Q

What are clinical features of osteoarthritis?

A

Presentation: Aching joint, enlarged, hard, limited movement, grinding
(crepitation), Other joints affected due to compensation
Diagnosis: History and examination, X-ray, Bloods- Normal, Synovial fluid- May show inflammation
Management: Rehabilitation, Drugs: pain, treatment of underlying predisposing factors, Surgery e.g. replacement of resurfacing

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79
Q

What is gout?

A

Crystal arthropathy
Hyperuricaemia
Presents with an acute red swollen joint and soft tissue lesions (tophi)
Multiple attacks lead to chronic damage

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80
Q

What is pseudogout?

A

Aging cartilage degeneration: age related OA - calcium pyrophosphate crystals into joint cavity. Common in the elderly

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81
Q

Describe how hyperuricaemia leads to gout

A

Precipitation of urate crystals in joints
Complement activation, neutrophils and phagocytosis by monocytes
Release of interleukins and TNF
Phagocytosis of crystals
Lysis of neutrophils
Release of lysosomal enzymes and proteases
Tissue injury and inflammation

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82
Q

What are Seronegative spondylo arthropathies?

A

Inflammatory systemic disease involving axial skeleton (spine and sacroilliac joints) but also peripheral joints. Negative to rheumatoid factor

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83
Q

What is Ankylosing spondylitis?

A

Erosion of sites where ligaments and tendons attach to bone
Eventual posterior fusion of spine and possible involvement of upper spine and large joints. 5x more common in men
90% have HLA-B27 antigen

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84
Q

What are Reactive arthropathies?

A

Inflammatory joint disorders with an infective cause but distant in time and place from the infection

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85
Q

What is Psoriatic arthritis?

A

Inflammation of the joints in 5-7% of psoriasis sufferers

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86
Q

What are the main 4 microbes that can cause osteomyelitis?

A

Staphylococcus aureus including MRSA
Streptococci (ß-haemolytic and S. pneumoniae)
Aerobic gram-negative rods eg. E. coli
Coagulase-negative staphylococci

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87
Q

Name some less common causes of osteomyelitis

A 
Neisseria gonorrhoeae 
Brucella spp. 
Mycobacterium tuberculosis 
Salmonella spp. 
Lyme disease (B. burgdorferi)
Fungi
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88
Q

What are the 5 stages of pathogenesis of bone infection?

A

Pathogens gain access to bone or joint
Pathogens adhere to target structures
Elaboration of virulence factors
Host responses, protective and destructive
Biofilm formation and establishment of chronicity

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89
Q

What are 3 phases of growth of a bacterial population?

A

Lag - adhesin genes on, toxin genes off, stick to surfaces
Log - quorum sensing, detect other bacteria around it
Post exponential - adhesin genes off, toxin genes on

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90
Q

What effect does foreign material have on infection?

A

Promotes it
Increases severity
Reduces the amount of innoculum required to establish an infection

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91
Q

What are the 2 methods of access that bacteria use to get to bones and joints?

A

Haematogenous: Primary or Secondary to obvious infective focus
Direct access: Trauma, Surgery, Arthrocentesis (joint fluid collection), Adjoining soft tissue infection, Chronic loss of soft tissue cover (ulcers and pressure sores)

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92
Q

What are the most common locations for Haematogenous spread of infection to bone? (Acute osteomyelitis)

A

Metaphyses of long bones and intervertebral discs due to end arteries
Most common joints: hip, knee, shoulder, elbow, ankle, wrist

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93
Q

What are common routes of infection spread for contiguous osteomyelitis? (Direct spread)

A

Focus of infection with direct spread: Otitis media/mastoiditis/
sinusitis, Infected fracture, Surgical wound e.g. mediastinitis
Chronic soft tissue loss: Pressure sores, Diabetic foot ulcers, Venous ulcers

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94
Q

How can a minor bone infection progress to lead to osteomyelitis?

A

Intramedullary spread of infection leads to more bone death

Dead bone permits infection to persist

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95
Q

Describe the pathophysiology of how diabetic foot ulcers can lead to osteomyelitis

A

Neuropathy leads to motor, sensory and autonomic changes
Abnormal foot biomechanics, unaware of damage and Reduced skin
compliance and lubrication can all lead to ulceration
This combined with vascular insufficiency complications can lead to infection

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96
Q

Describe the process of chronic bone infection

A

Dead bone acts as foreign material
Bacteria in hypoxic environment, on surface of dead bone, not killed
Unresolved infection causes chronic suppuration, tissue destruction and sinus formation which leads to further bone death
Formation of a sequestrum (dead) surrounded by an involucrum (alive) which is breached via one or more cloacae through which pus escapes

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97
Q

What are the clinical presentations of an acute osteomyelitis?

A

Pain
Loss of function
Fever and sepsis
Erythema, swelling, tenderness, drainage

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98
Q

What are the clinical presentations of a chronic osteomyelitis?

A

Pain
Loss of function
Chronically discharging wound
Chronic ill health

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99
Q

What are signs of osteomyelitis?

A

Tenderness
Irritable joint
Reduced range of movement
Inability to weight bear or use limb
Soft tissue abnormal: swelling, induration, erythema, sinus formation
May be indistinguishable from non-infective process

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100
Q

How do you diagnose acute osteomyelitis?

A

Pus on bone/prosthesis: Macroscopically or microscopic as ‘pus cells’ or neutrophils in tissue
Growth of bacteria in a normally sterile site - Arthrocentesis

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101
Q

What extra precaution is required to diagnose a chronic indolent osteomyelitis?

A

Multiple samples required to establish contaminant vs true pathogen

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102
Q

Which 2 joint affecting infective conditions cannot be cultured?

A

Lyme disease serology

Syphillis serology

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103
Q

What laboratory specimens should be taken for a prosthetic joint?

A

Difficult to distinguish contaminants from low-virulence organisms
Finding the same bacteria in multiple samples is predictive of infection
Neutrophils in bone histology is the gold standard

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104
Q

Alongside lab cultures, what supporting evidence can be used to test for osteomyelitis?

A

Inflammatory markers

Radiology: X-ray – bone destruction, Bone scan/white cell scan, MRI/CT

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105
Q

What surgical interventions can be used to treat osteomyelitis which is not treatable to antibiotics?

A

Debridement: removal of unhealthy tissue from wound
Revision (one or two stage): removal of existing prosthetic and replacement with new parts
Reconstruction

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106
Q

What supportive treatments can be given to aid in recovery from osteomyelitis?

A

Physiotherapy
Walking aids, prosthetics
Psychological

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107
Q

How can antibiotics be used against osteomyelitis?

A

Prolonged: Prosthetic joint infections following debridement surgery may need 6 months of antibiotic treatment
Shorter courses adequate if prosthetic material removed
Intravenous: Unproven benefit,mOften given in community as part of an OPAT service (outpatient parenteral antibiotic treatment)

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108
Q

How can infection be prevented before surgery?

A

Prophylactic antibiotics
Appropriate antibiotics administered within 60 minutes prior to surgery and only repeated if there is excessive blood loss, a prolonged operation or during prosthetic surgery

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109
Q

What is decolonisation?

A

Often recommended for MRSA colonised patients
Nasal ointment and antibacterial washes
May not result in long term clearance of MRSA but temporary measure immediately pre operatively

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110
Q

What factors of patient selection may be taken into account before proceeding with surgery?

A 
Higher risk if: 
Smoker
Poorly controlled diabetes 
Chronic disease 
Poor nutritional status, obesity
Malignancy 
Immunosuppression 
Infection elsewhere 
Ulcers 
Some medications
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111
Q

What preparation of the patient can be performed pre surgery to minimise risk of infection?

A 
MRSA screening and decolonisation
Pre-op shower/wash with soap: DoH: 2% chlorhexidine gluconate in 70% isopropyl alcohol solution, NICE: aqueous or alcohol-based, ensure that antiseptic skin preparations are dried by evaporation and pooling of alcohol-based preparations is avoided
Hair removal (clipping if required) 
Patient theatre wear: Drapes, NICE: If an incise drape is required, use an iodophor-impregnated drape unless the patient has an iodine allergy
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112
Q

What preparations should be surgeon take before a surgery to minimise infection risk?

A

NICE: wash hands prior to the first operation on the list using an aqueous antiseptic surgical solution, with a single-use brush or pick for the nails, and ensure that hands and nails are visibly clean
Before subsequent operations, hands should be washed using either an alcoholic hand rub or an antiseptic surgical solution. If hands are soiled then they should be washed again with an antiseptic surgical solution
PPE worn: Gowns, Gloves, Masks

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113
Q

What surgical skills should be used to minimise infection risk?

A 
Asepsis 
Haemostasis 
Management of deadspace 
Irrigation 
Drains 
Wound closure
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114
Q

What aspects of theatre environment should be controlled to minimise infection spread?

A 
Theatre discipline (e.g staff traffic, closed doors, scrub areas) 
Theatre air: A/C per hour, Ventilation systems
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115
Q

How should a wound be dressed?

A

Wound covered at the end of technique and surgery
Undisturbed for a minimum of 48 hours unless there is leakage
ASEPSIS (non touch technique) when the wound is being redressed

116
Q

What is an antigen?

A

Substance capable of generating an immune response

Usually a biological substance & not just an inflammatory response

117
Q

What is immunological tolerance?

A

Unresponsiveness of the immune system to an antigen

Not only self antigens, but also fetus, gut flora, plant pollens etc.

118
Q

What is autoimmunity?

A

An immune response to self-antigens
Due to a failure of immunological tolerance
Usually due to a combination of genetic & environmental factors
Leads to immune-mediated damage of specific tissues

119
Q

What mechanisms can underly auto immunity?

A

Immune system can respond to an infinite number of antigens by genetic recombination in T & B cells so variety of receptors on surface
If a specific T or B cell is stimulated by an antigen, it will replicate to provide a specific response (clonal selection - T & B Lymphocytes with Best Fit → Multiply → Evolve → Repeat)
We also have pre-programmed T & B cells that recognise our own (self) antigens, which need to be controlled (immunological tolerance)

120
Q

How does immunological tolerance work?

A

Central tolerance develops in thymus & bone marrow to prevent immune responses to self antigens
Most active in fetus & declines after birth
Immature lymphocytes that recognise self antigens undergo clonal deletion by apoptosis or clonal anergy by regulatory T lymphocytes Peripheral tolerance develops in other lymphoid tissues
Also prevents immune responses to fetus, gut flora, plant pollens etc. Active throughout life
Mature lymphocytes that recognise self or benign antigens undergo clonal suppression by regulatory T lymphocytes

121
Q

What disorders and diseases are linked to altered immunological tolerance?

A 
Autoimmune diseases 
Recurrent miscarriages 
Hypersensitivity disorders 
Chronic infections that evade clearance 
Malignancies that seem to induce tolerance
122
Q

Which cells seem to mediate loss of immunological tolerance?

A

B cells

123
Q

Name some autoimmune conditions that affect the CNS

A

Multiple sclerosis
Myasthenia gravis
Guillain–Barré syndrome
Autoimmune encephalitis

124
Q

Name some autoimmune conditions that affect the CV system

A

Dressler’s syndrome
Rheumatic fever
Temporalarteritis

125
Q

Name some autoimmune conditions that affect the endocrine system

A 
Graves’ disease
Hashimoto’s thyroiditis
Riedel’s thyroiditis
Addison’s disease
Diabetes mellitus (type 1)
126
Q

What GI conditions can be caused by autoimmune problems?

A 
Pernicious  anaemia
Coeliac  disease
Crohn’s disease
Ulcerative  colitis
Primary  biliary  cirrhosis
Chronic autoimmune hepatitis
127
Q

What dermatological conditions can be caused by auto immune problems?

A 
Psoriasis
Vitiligo
Alopecia
Systemic sclerosis
Scleroderma
Dermatomyositis
Sjögren’s syndrome
128
Q

What rheumatological conditions can be caused by autoimmune problems?

A

Rheumatoid arthritis
Lupus
Ankylosing spondylitis

129
Q

What genetic links can underly autoimmunity?

A

MHC (HLA) genes seem to be the most important overall :
HLA-B27 (MHC-1) : ankylosing spondylitis, reactive arthritis
HLA-DR2 (MHC-2) : systemic lupus erythematosus (SLE)
HLA-DR3 (MHC-2) : autoimmune hepatitis, Sjögren’s syndrome, T1DM, SLE
HLA-DR4 (MHC-2) : rheumatoid arthritis, Type 1 diabetes mellitus

130
Q

What environmental links exist with autoimmunity?

A

Possibly due to molecular mimicry of self antigens by:
Infections : Streptococcal infection → rheumatic fever
urethritis or gastroenteritis → reactive arthritis
Campylobacter gastroenteritis → Guillain–Barré syndrome
Chemicals : anti-convulsants or antibiotics → drug-induced lupus
halothane (general anaesthetic) → liver necrosis
Neoplasms : teratoma → autoimmune encephalitis)
Trauma: exposure of self antigens in protected sites (eg. eye, testes)

131
Q

What autoantibodies can be detected to aid a diagnosis?

A

Grave’s disease = TSH receptor
Hashimoto’s thyroiditis = thyroid peroxidase
Rheumatoid arthritis = RhF
SLE (systemic lupus erythematosus) = ANA (95% sensitivity) & dsDNA
Sjögren’s syndrome = ANA
Coeliac disease = anti-gliadin & anti-endomysial
Primary biliary cirrhosis = ANA & AMA

132
Q

What are principles of treatment of autoimmune conditions?

A

Treatments depend on organs affected +/- immunosuppression
Steroids: anti-inflammatory & immunosuppressive
Disease modifying drugs: anti-inflammatory & immunosuppressive
methotrexate, azathioprine, sulphasalazine
Monoclonal antibodies: specific actions, infliximab = anti-TNF cytokine
used in RA, Crohn’s, ank spond, rituximab = anti-CD20 on B lymphocytes used in leukaemia, rejection, RA, SLE

133
Q

Describe the epidemiology of autoimmune disorders

A

Overall prevalence 1-3% in developed countries
Top prevalences : Graves’ disease = 1152 per 100 000
Rheumatoid arthritis = 860 per 100 000
Overall : 1 in 31 currently affected by an autoimmune disease, 75% = female (x2.7 greater risk). A top ten cause of death for women

134
Q

What is Graves’ disease?

A

Thyrotoxicosis, Most common autoimmune disease & cause of hyperthyroidism
Often familial, 85% = female (2% of all women develop Grave’s)
Auto-antibodies against TSH receptor (TSHR-Ab) persistent stimulation of thyroid gland,↑thyroid hormones = tri-iodothyronine (T3) + thyroxine (T4)→ ↑basal metabolic rate +↑sensitivity to catecholamines
40% also have auto-antibodies against ophthalmic muscles, Grave’s ophthalmopathy = exophthalmos

135
Q

What are treatments for Graves’ disease?

A

Beta-blocker (eg. propanolol)
Anti-thyroid drugs (eg. carbimazole, propylthiouracil)
Radio-active iodine treatment (131I)
Thyroidectomy (partial)

136
Q

What is systemic lupus erythematosus? SLE

A

Rare autoimmune disorder affecting many tissues
Systemic : malaise, fever, weight loss
Skin : rash, photosensitivity, vasculitis, hair loss
CNS : cerebral lupus, transverse myelitis
Heart : pericarditis, Libman-Sacks endocarditis
Lungs : pleural effusions, pulmonary fibrosis
Kidneys : glomerulonephritis (lupus nephropathy)
Blood : anaemia, leukopenia, thrombocytopenia, 2° APLS
Other : 2° Sjögren’s syndrome, arthralgia, non-deforming arthritis
Anti-phospholipid syndrome (APLS) → thrombophilia, recurrent miscarriages

137
Q

How can you diagnose SLE?

A

FBC =↓Hb (chronic/haemolytic),↓WCC,↓Plts
ESR : raised
CRP : moderately raised
ANA : 95% sensitivity
dsDNA : 50% sensitivity & 99% specificity
anti-cardiolipin (phospholipid) antibodies

138
Q

What are treatments for SLE?

A

Sun-avoidance / sun screens
Steroids: as for other autoimmune rheumatological disorders
NSAIDs : as for other autoimmune rheumatological disorders
DMDs : hydroxychloroquine, azathioprine (anti-proliferative), cyclophosphamide (anti-proliferative)
mAbs : rituximab (anti-CD20 on B lymphocytes)

139
Q

What is Sjögren’s Syndrome (Sicca Syndrome)?

A

Rare autoimmune disorder affecting some mucus-secreting tissues
Primary = idiopathic autoimmune disease (90%=female), associated with ANA especially anti-Ro (SS-A) & anti-La (SS-B), possibly RhF
Secondary (2°) = secondary to another autoimmune disease, direct associations include RA, SLE, SD, SS, PBC
Possible rashes, vasculitis, pulmonary fibrosis & 5% risk of lymphoma
Shows the spectrum & overlapping nature of autoimmune diseases

140
Q

What tests can be done to test for Sjogrens syndrome?

A

Schirmer’s test / slit lamp examination / saliva flow test
autoantibodies (anti-La = most specific)
USS of salivary glands = hypoechoic lesions & loss of tissue biopsy of lip or salivary gland = lymphocytic infiltration tissue damage & loss

141
Q

What treatments can be used for Sjögren’s syndrome?

A

Artificial tears, punctal plugs into lacrimal ducts, mouth care, regular sips of fluid, artificial saliva, topical cyclosporine or other DMDs
awareness of lymphoma risk

142
Q

What are significant regional variations in skin?

A

Presence of appendages: hair, nails, glands, receptors
Thickness
Colour

143
Q

What protection does the skin offer?

A

Barrier: Water impermeable, bacteria (Langerhans cells) chemicals
Mechanical: against friction due to SA of dermal/epidermal junction
Melanin against UV radiation damage

144
Q

What types of sensation does the skin have receptors for?

A 
Touch
Pressure
Pain
Temperature 
No of receptors proportional to contact with solid objects and high in specialised sexual organs
145
Q

How does skin help with thermoregulation?

A

Blood circulation to extremities can be modulated: Glomus bodies
Sweat from eccrine glands
Body hair
Subcutaneous tissue: fat

146
Q

What is a Glomus body?

A

Arterial venous shunt in skin that allows blood flow to extremities to be modulated

147
Q

What the key components of sweat?

A

Water

Na Cl

148
Q

What is the principle metabolic function of the skin?

A

Produces 7 dehydro cholesterol which is precursor of active vitamin D
Darker skin means greater UV exposure is needed to ensure adequate Vitamin D

149
Q

What is the purpose of hair in humans?

A

Sign of sexual maturation
Sexual differentiation: eg beard, chest and back
Thermoregulation

150
Q

What do nails do?

A

Provide physical support for finger tips and toes

151
Q

What are the layers of the skin?

A

Epidermis
Dermis: papillary and reticular
Subcutis

152
Q

What type of epithelium is in the epidermis?

A

Keratinised stratified squamous epithelium

153
Q

What is the proliferative potential of the epithelium?

A

Labile - basal cells can proliferate to replace lost cells

154
Q

What is normal transit time for epidermal maturation?

A

Up to 50-60 days

155
Q

What is the transit time for epidermal maturation in psoriasis?

A

7 days - cells at surface are less mature as they have had less time

156
Q

What is collective name for cells making up epidermis?

A

Keratinocytes

157
Q

What are the additional cells of the epidermis? And which are dendritic?

A

Merkel cells - touch receptors
Melanocytes - dendritic (transport melanin to keratinocytes)
Langerhans cells - dendritic (antigen presenting function)

158
Q

What organelle is damaged by lose dose UV radiation? And why is melanin therefore important?

A

Nucleus so DNA damage

Melanin produces cap over nucleus for protection

159
Q

Which cells produce cytokeratin in the skin?

A

Basal cells - anchors it to underlying tissue to hemidesmasome

160
Q

What are anchoring filaments?

A

Anchor hemidesmasomes to basement membrane

161
Q

Which types of collagen help to anchor the basement membrane to the dermis?

A

Type I, III, VII

162
Q

What are Langerhans cells?

A

Intra epithelial and dermal antigen presenting cells - MHC II
Predominantly in the prickle cell layer

163
Q

Describe how Langerhans cells activate an immune response

A 
Antigen detected
LC moves to dermis
Travels in lymphatics
Moves in lymph node
Cell mediated immune response generated
164
Q

When might Langerhan cell numbers be reduced?

A

UV exposure - less able to generate immune response to neoplastic cells and so higher risk of skin cancer

165
Q

What are melanocytes? And what do they do?

A

Determines skin and hair colour
Dendritic cells at base of epidermis
UV exposure means more production of melanin

166
Q

What is vitiligo?

A

Autoimmune destruction of melanocytes

167
Q

What type of tissue is the dermis?

A

Supporting tissue

168
Q

What tissue types are in dermis?

A

Fibrous
Elastic
Fibroadipose

169
Q

What is the function of the dermis?

A

Physical and metabolic support for the epidermis - blood vessels nerves etc

170
Q

What are types of hair?

A

Terminal - thick hair

Vellus - fine thin hair

171
Q

What are the phases of hair growth?

A

Anagen: long active growth
Catagen: short phase involution (regressing back)
Telogen: short phase inactivation

172
Q

What causes vellus hair to become terminal hair in groin and axilla?

A

Testosterone

173
Q

What is a pilosebaceous unit?

A

Sebaceous glands secrete sebum onto hair shaft

174
Q

What is the nature of the subcutis?

A

Adipose tissue - supporting tissue

175
Q

How is the subcutis arranged?

A

Lobules of fat separated by fibrous septae

176
Q

What is panniculitis?

A

Inflammation of the subcutis

177
Q

What are the layers of the epidermis?

A

Stratum basale
Prickle cell layer (stratum spinosum) (start to produce keratin, larger cytoplasm)
Granular layer (kerratohyaline granules)
Straum corneum (anucleate cells, keratin plaques)

178
Q

What do eccrine glands produce?

A

Sweat

179
Q

What do apocrine glands do?

A

Don’t know!

Breast tissue is modified apocrine tissue

180
Q

What are options for sampling skin lesions?

A

Punch biopsy
Shave biopsy
Excision biopsy

181
Q

What are the functions of the skin?

A

Protection: External insults, Impermeable (Prevents dehydration, Prevents entry of micro-organisms)
Sensation
Thermoregulation
Metabolic Function

182
Q

What are Epidermal appendages?

A

Hair, nails, sweat glands, sebaceous glands

183
Q

What do basal cells look like?

A

Cuboidal so can sit tightly together
Large nucleus for reproducing
Little cytoplasm

184
Q

What do keratinocytes in epidermis have lots of that basal cells have less of?

A

Rough ER and ribosomes for production of keratin

185
Q

Where are melanocytes found?

A

In basal cell layer of epidermis

186
Q

What determines tanning ability of the skin?

A

Amount and type of melanin

187
Q

Which area of skin on the body is likely to have deep Rete pegs?

A

Feet as lots of friction here

188
Q

What is a pustule?

A

Vesicle containing pus: packed with polymorphonuclear leucocytes and serum
May be non-infective, as in acne vulgaris or pustular psoriasis
May arise on ordinary skin or maybe follicular in origin

189
Q

What is erythema?

A

Redness of skin caused by vascular dilation
May be transient or chronic
Can be blanched

190
Q

What is purpura?

A

Extravasation of blood into skin
Does not blanch
Blood in tissue is degraded within phagocytes to haemosiderin which is a brown pigment

191
Q

What is ecchymosis?

A

Subcutaneous purpura larger than 1cm in diameter

192
Q

What is a haematoma?

A

Bruise: palpable and detectable by touch alone

193
Q

What are weals?

A

Elevations of skin caused by oedema of dermis
Sometimes linear in shape and usually erythematous
Caused by increased permeability of the walls of blood capillaries

194
Q

What are scales?

A

Abnormality of process of keratinisation of epidermal cells
Found when imperfectly keratinized cells of the horny layer (which maybe nucleated), adhere together
They may be small, as in dandruff, or large, as in psoriasis

195
Q

What are burrows?

A

Irregular, short, linear elevations of horny layer, usually dark or speckled black
Characteristic lesions of scabies

196
Q

What are blackheads?

A

Small plugs of laminated horny cells and sebum blocking the pilo-sebaceous orifices
Primary lesions of acne vulgaris

197
Q

What are fissures?

A

Small cracks extending through epidermis so that dermis is exposed

198
Q

What are ulcers?

A

Lesions formed by destruction of whole skin, e.g. by ischaemia, infection or neoplasia
Base of an ulcer may be granulation tissue, tendon, etc. but cannot be any layer of the skin

199
Q

What is erosion?

A

Superficial loss of tissue whose base is in the skin

200
Q

What is atrophy of skin?

A

Shrinkage of skin
Epidermis may be atrophic, ischaemic skin, or dermis may become atrophic due to loss of collagen, e.g. from life-long exposure to sunlight

201
Q

Define the common descriptors used to describe skin lesions

A

Flat or raised

Size and consistency

202
Q

What terms are given to flat lesions?

A

Macule if under 5mm

Patch if over

203
Q

What terms are given to raised solid lesions?

A

Papule if under 5mm
Plaque if over
Exophytic nodule if over 5mm and deep to the skin

204
Q

What terms are given to raised fluid filled lesions that are clear?

A

Vesicles if under 5mm
Bulla if over
Filled with serous fluid

205
Q

What terms are given to raised fluid filled lesions that are cloudy?

A

Pustules

206
Q

What are common types of skin cancer?

A

Basal Cell Carcinoma
Squamous Cell Carcinoma
Melanoma

207
Q

Which is the most common skin cancer?

A

Basal cell carcinoma

208
Q

What are risk factors for basal cell carcinomas?

A

Sun exposure
Immunosuppression
Inherited defects of DNA repair e.g. Gorlin’s Syndrome

209
Q

Describe how a basal cell carcinoma develops

A

Slowly growing and essentially does not metastasise but can be locally destructive (rodent Ulcer)
Can be superficial or nodular

210
Q

What are risk factors for squamous cell carcinoma?

A 
Sun Exposure 
Male sex 
Occupational exposure e.g. tars, oils and ionising radiation 
Chronic healing: Ulcers, Burns
Immunosuppression esp HPV
211
Q

What determines the risk of metastasis with squamous cell carcinoma?

A

Thickness of the lesion

212
Q

What patterns of squamous cell carcinoma are there?

A

SCC in situ: no chance of metastasis

SCC with kerotic crust

213
Q

What types of melanocytic lesions are there?

A

Composed of cells differentiating towards melanocytes
Benign: Naevi
Boderline/Unsure: dysplastic or MelUMP (uncertain melanocytic potential)
Malignant: In Situ or Invasive

214
Q

What should be evaluated with a macroscopic assessment of a melanocytic lesion?

A 
A - asymmetry
B - border
C - colour
D - diameter
E - evolution
215
Q

What are risk factors for melanocytic lesions?

A

Sun exposure

Presence of dysplastic or abundant naevi

216
Q

Describe the Morphology of melanocytic lesions

A

In situ: epidermal nest of melanocytes

Invasive: Epidermal and Dermal nests of atypical melanocytes

217
Q

Describe the Prognosis and Prediction of melanocytic lesions

A

Staged using TMN and AJCC

Molecular testing to see if suitable for molecular therapy e.g. Tyrosine Kinase Inhibitors

218
Q

What are the major 2 tissue types in the body?

A

Parenchyma - functional or doing cells

Stroma - supporting framework

219
Q

What are the different types of proliferative capacity of cells?

A

Labile cells: Continuously dividing
Stable Cells: Infrequent divisions but rapid division if needed
Permanent Cells: Never divide in adult life

220
Q

What are labile cells?

A

Continuously dividing, Cells proliferate throughout life, from stem cells
Epithelia: skin, gastrointestinal tract, cervix, endometrium, urinary tract

221
Q

What are stable cells?

A

Low level of replication under normal circumstances (considered G0)
Undergo rapid division in response to certain stimuli
e.g. liver, kidney, endothelial cells, fibroblasts, smooth muscle cells, chondrocytes, osteocytes

222
Q

What are permanent cells?

A

Left the cell cycle & cannot divide in postnatal life

e.g. Cardiac muscle, nerve cells, skeletal muscle

223
Q

What is inflammation?

A

Protective mechanism designed to rid body of initial cause of injury
Remove debris and tissues damaged secondary to this injury
Not a disease, but a response

224
Q

What can go wrong with inflammation?

A

Excessive inflammation: Inappropriately triggered e.g. Arthritis
Poorly controlled e.g. leakage of enzymes out of cells in Gout
Inadequate inflammation e.g. AIDS and HIV

225
Q

What are the patterns of healing after tissue injury?

A

Regeneration: resolution, compensatory. Normal function restored
Scarring: chronic inflammation, excessive stromal damage

226
Q

What can regeneration of tissue lead to?

A

Complete resolution and restoration of tissue architecture

Compensatory regeneration

227
Q

What is the difference between scar and fibrosis?

A

Scar: single insult that has repaired
Fibrosis: collagen deposition in internal organs in chronic disease

228
Q

What is resolution in wound healing?

A

Restoration of normal structure and function
Requires minimal damage to tissue architecture / support structures,
Proliferation of parenchymal cells from residual tissue stem cells
e.g. Resolution of acute inflammatory exudate in lobar pneumonia

229
Q

What is compensatory growth in wound healing?

A

Compensatory growth of cells to restore normal tissue function
Growth of cells (stable) & tissues to replace lost structures
Requires source of architecture / support structures and ability to reproduce them
e.g. (compensatory) growth of liver following partial hepatectomy or of kidney following unilateral nephrectomy

230
Q

What is fibrous repair?

A

Healing by deposition of connective tissue
In response to: Damage to parenchyma AND stroma in labile or stable tissues, Wound e.g. skin (Scar), Inflammatory process in internal organ (Fibrosis), Cell necrosis in organs unable to regenerate (permanent)
Associated with loss of function of tissue, plugging a deficit in tissue

231
Q

What are the key features of chronic inflammation?

A

Ongoing attempts at repair
Ongoing inflammation
Ongoing tissue destruction

232
Q

What does fibrous repair involve?

A

Inflammation
Granulation tissue/ Proliferation: Angiogenesis, Migration, proliferation of fibroblasts
Scar formation/ maturation: Connective Tissue Remodelling, Recovery of tensile strength

233
Q

What is the pink cobblestone appearance seen in ulcers or deep tissue injury?

A

Granulation tissue

234
Q

What are the stages of the healing of fractures?

A 
Haematoma 
Granulation tissue
Callus 
Woven bone 
Lamellar bone 
Remodelling
235
Q

What are the steps of cutaneous wound healing?

A

Formation of a blood clot
Formation of granulation tissue: Cell proliferation, collagen deposition
Scar formation: Wound contraction, Connective tissue remodelling, Recovery of tensile strength

236
Q

What is the role of angiogenesis in wound healing?

A

Pre-existing capillaries bud / sprout into damaged area - VEGF
Endothelial precursor cells from bone marrow (Vascular granulation tissue)

237
Q

What are the hallmarks of granulation tissue?

A

Angiogenesis

Fibroblast proliferation

238
Q

What are variable features of granulation tissue?

A

Inflammatory cells

Oedema

239
Q

What is the role of Cell proliferation and collagen deposition in wound healing?

A

Fibroblasts migrate to site & proliferate – TGF-beta
Active collagen synthesis
(Fibrovascular granulation tissue)

240
Q

How is collagen formed?

A

Pro collagen 1 cleaved by proteinases to give mature triple helix collagen

241
Q

How do fibroblasts form a scar?

A

Fibroblasts produce collagen
Fibroblasts align, so collagen uniform, increasing tensile strength
(Fibrous granulation tissue = scar)

242
Q

What controls Remodelling in wound healing?

A

MMPs = matrix metalloproteinases
From fibroblasts, macrophages
Stimulated by PDGF
Cleave collagen and remodel it along stress lines

243
Q

Describe the timeline of a wound healing

A

Day 1: Acute inflammatory response, Epithelial cells divide & migrate
Day 2: Macrophages infiltrate, Epithelial cells continue proliferating
Day 3-5: Vascular granulation tissue, Collagen progressively deposited, Epithelial layer thickens
Day 7: Wound10% tensile strength of normal skin
Day 10: Further fibroblast proliferation & collagen deposition increases
wound strength
Day 15: Collagen deposition follows stress lines, Granulation tissue loses vascularity
Day 30: Wound 50% tensile strength normal skin
3 months: Wound 80% tensile strength normal skin

244
Q

What is healing by primary intention?

A

Clean incision
Edges of wound in opposition
Dermis has a scar but epidermis will look virtually normal
No dermal appendages in the region
Epidermis regenerates
Scar matures over next 2 years- 80% max strength

245
Q

What is healing by secondary intention?

A 
Unable to oppose the wound edges eg burn, ulcer
Depression of epithelium due to wound contraction
Initial contraction - myofibroblasts
Eschar forms 
Epidermis regenerates at base 
Granulation tissue bed 
Takes longer 
More scarring 
More contraction
246
Q

What local factors affect wound healing?

A

Infection: prolongs chronic inflammation
Mechanical factors: eg bending of knee
Foreign bodies
Size of wound: more granulation tissue and fibroblasts
Location of wound
Type of wound: clean incision

247
Q

What systemic factors can affect wound healing?

A

Nutritional status: vitamin c, zinc
Metabolic status: diabetes
Circulatory status: peripheral vascular disease
Hormones: Glucocorticoids

248
Q

What can be Pathological aspects of repair?

A

Inadequate formation
Excessive formation
Formation of contracture

249
Q

What inadequate repair can occur with wound healing?

A

Dehiscence or rupture: wound reopens

Ulceration: inadequate blood supply

250
Q

What can be problems with excessive formation in wound healing?

A

Scar: Keloid, Hypertrophic

Granulation tissue: Proud flesh

251
Q

Describe staph aureus structure

A

Gram positive
Cocci clumps (grapes)
Coagulase positive

252
Q

What is infection?

A

Bugs causing disease and inciting host response

253
Q

What is colonisation?

A

Bugs present without causing harm to host

254
Q

Which sites of the body are sterile?

A 
Blood
Bone marrow
CSF
Middle ear
Lower respiratory tract
Muscle
Bone 
Joints
Liver 
Gallbladder
Pleura
Peritoneum
Bladder 
Kidneys
255
Q

What bugs are normal in the mouth and upper respiratory tract?

A

Staph aureus
Strep pneumoniae
Haemophilus influenzae
Neisseira meningitides

256
Q

What bugs are normal on the skin?

A

Coagulase negative staphylococci

257
Q

What bugs are normal in the GI tract?

A

E. coli
Klebsiella
Enterococci
Anaerobes

258
Q

What bugs are normal in female GU tract?

A

Anaerobes

Lactobacillus

259
Q

What bugs are normal in the urethra?

A

Coagulase negative staph
E. coli
Lactobacilli
Anaerobes

260
Q

Which groups may be at increased risk of infection?

A

Immunocompromised, elderly, neonates, pregnancy, people with prosthetic joints

261
Q

Give examples of frequent pathogens

A

St. Aureus (coagulase positive)
Streptococcus
Gram negative rod

262
Q

Describe the normal skin defence against infection

A

Normal cutaneous flora (competitive)
Mechanical barrier
Low pH of normal skin (acids produced by commensal flora)
Immune system

263
Q

What do we find in our cutaneous flora?

A

Gram positive: Staphylococcus epidermidis (coag-neg staph), Staphylococcus aureus (skin folds and nose of <25% healthy)
Gram negatives: Moist areas, Ulcers
Fungi: Malassezia species (needs fat. Found on scalp, face, upper body) Trichophyton species (cause of athletes foot)

264
Q

How do bacteria cause disease?

A

Opportunistic – defect in immunity or foreign body allow infection
Primary pathogens – establish infection in healthy people
Virulence determinants – proteins/toxins enable bacteria to cause infection/disease
Variety of different effects – E coli disease varies, Bacteria controls their expression as situation requires, Some on plasmids and can be transferred between strains

265
Q

What do Virulence determinants do?

A

Aid colonisation: Adhesion proteins, Invasion (e.g. Neisseria)
Aid survival: Immune avoidance eg. Strep M protein, Staph aureus catalase, Immunosuppression
Damage host: Toxins damage directly or by stimulating cytokines, Obtain nutrition from host

266
Q

What are Obligatory steps for infection?

A 
Exposure to pathogen
Adherence to skin or mucosa
Invasion through epithelium 
Colonisation and growth 
Production of virulent factors
Toxicity and/or invasiveness 
Tissue damage and disease
267
Q

How would you assess a patient with a skin lesion for potential infection?

A

Is it infection?
Is there a route of entry? E.g. bite, athletes foot
Are there impaired host defences? E.g. steroids
Any environmental factors? E.g. bite, trauma, water
Site and appearance
Are there signs or symptoms? E.g. systemic toxicity
What are the likely pathogens? E.g. risk of MRSA or other resistant or unusual organism not covered by normal therapy?

268
Q

What is impetigo? What can cause it? And what is the therapy?

A

Very superficial, usually facial with crusting
Staph aureus or Group A streptococci
INFECTIOUS (direct contact) so hygiene important (e.g. schools)
Topical therapy

269
Q

What is Erysipelas? What causes it? And what is the therapy?

A

Superficial dermis, usually facial or leg, clearly demarcated
Extremes of age
Streptococci mostly, usually group A
Usually treated like cellulitis with systemic antibiotics

270
Q

What is cellulitis? What causes it? And what is the therapy?

A

Non contagious spread along full thickness subcutaneous tissues
May be clear entry point, e.g. athletes foot
Staph aureus or Group A Strep
Not cultured and systemic treatment given empirically covering above organisms E.g. flucloxacillin and benzylpenicillin. Oral usually fine but may need to start IV
Elevation important
Beware: MRSA, animal/human bites, necrotising infection, unusual environmental exposures (sea, fresh water)

271
Q

What can be done to prevent cellulitis?

A

Check for fungal foot infections, nail problems, foot problems
Consider diabetes especially if recurrent
Manage heart failure

272
Q

What is necrotising fasciitis? What causes it? And what is the therapy?

A

Deep infection involving subcutaneous and fascial layers
Affect any body area (limbs, pelvis, trunk)
Predisposed by abdominal surgery or trauma
Fourniers gangrene (necrotising perineal infection)
Rapid onset, well demarcated, with or without necrosis
Usually Gp A streptococci or polymicrobial (Gram-negs and anaerobes)
Causes extensive tissue destruction and sepsis
Patients usually SEPTIC, unlike (most) cellulitis

273
Q

Describe How to recognise nec fasc

A

Think of it if…
Failure to respond to antibiotics
Marked pain out of proportion to appearance
Development of gangrene or anaesthesia
Marked systemic toxicity “out of proportion” to appearance
Late findings include crepitus and deep purple/black appearance
Only diagnosis (and treatment) is surgical exploration and debridement

274
Q

How do you manage necrotising fasciitis?

A

ABC – and management of sepsis
Broad-acting antibiotic choice: IV meropenem & IV clindamycin
Patient will not recover until source of sepsis is removed
Young patients may tolerate severe sepsis → sudden decompensation
Surgical debridement must be done by first surgeons to see patient
Subsequent management will require plastic surgery input
Good prognosis if diagnosed & treated early

275
Q

What is Clostridial myonecrosis (gas gangrene)?

A

Necrotising gas-forming process of muscle associated with shock and often haemolysis
Often abrupt onset with shock and hypotension
Muscle and soft tissue destruction

276
Q

How do you diagnose and manage clostridial myonecrosis?

A

Diagnosis: Clinical, Typical features at surgery, Gram stain of tissue Management: Surgery and antibiotics (including metronidazole)
Antibiotics alone will not work

277
Q

Describe the pathology of clostridial myonecrosis

A

Clostridium enters skin through breakages
Common in combat injuries due to non-sterile field surgery and nature of projectile injuries
Organisms produce “exo-toxins” as they proliferate in wound
Toxins destroy nearby tissue, bacterial metabolism and cell death generate gas which destroys muscle and fascia/skin
Discharge watery rather than thick pus due to neutrophil lysis by toxins

278
Q

What is Staph toxic shock syndrome?

A

Temperature > 38.9
Systolic BP < 90mmHg
Diffuse macular rash, subsequent desquamation, palms and soles
Disorder of three or more systems (GI, muscle, renal, liver, plts, CNS)

279
Q

How do you diagnose and manage staph toxic shock syndrome?

A

Diagnosis: Clinical features, Blood cultures, Swabs, pus
Management: Supportive (ITU, fluids, vasopressors), Antibiotics

280
Q

What is Tetanus?

A

Infection of dirty wounds by Clostridium tetani
Produces neurotoxin, blocks release of inhibitory neurotransmitters at skeletal muscle producing spasms
Generalised – start with mild jaw spasms then whole body
Can be severe enough to tear muscles and cause fractures
Local – uncommon, Affects only muscles in same area as injury
Neonatal – is born to unvaccinated mother. Usually due to infection of umbilical stump. 14% of neonatal deaths in developing settings

281
Q

What is treatment for tetanus?

A

Supportive, muscle relaxants, wound debridement
Tetanus immunoglobulin and antibiotics
Prevention by vaccination

282
Q

What is a surgical wound infection and what can cause it?

A

Common cause of nosocomial infection
Related to operation occurring within 30 days, or 90 days if prosthetic material implanted
SSI superficial (skin only) or deep and organisms vary with nature of op
Most wound infections after clean procedures (no viscus entered) are caused by skin flora
Clean-contaminated procedures (e.g. viscus entered under controlled conditions) also have Gram negs, enterococci
Contaminated procedures may lead to infection by any/several
organisms from that viscus

283
Q

What can be done to prevent surgical wound infection?

A

Sterile technique, air flow systems
Antibiotic prophylaxis: Reduce burden of micro-organisms at site during procedure, most clean-contaminated procedures upwards
Given 1-2 hours before incision (infection rate higher if earlier or later)
Agent should be active against the likely pathogens
Usually single dose sufficient, may rarely give 24 hours worth
Think about MRSA, allergies

284
Q

What happens after the mechanical injury in osteoarthritis?

A 
Chondrocyte response
Release of cytokines TNF IL1
Production of enzymes -> destruction of joint structure
Loss of smooth cartilage surface
Development of surface cracks
Destruction of subchondral bone
Osteophyte formation
285
Q

What are the 5 main tissue types?

A 
Epithelia
Muscle
Nervous tissue
Blood
Supporting tissue

Block 4 AR (8 decks)

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