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Y2 Clinical Pathology > Clinical Infections - Orthopaedic, Skin & Soft Tissue > Flashcards

Clinical Infections - Orthopaedic, Skin & Soft Tissue Flashcards

1
Q

Label the components of the skin

A
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2
Q

What are the 3 layers of the skin and their functions?

A

epidermis:

  • outermost layer
  • provides a waterproof barrier & creates the skin tone

dermis:

  • contains tough connective tissue, hair follicles and sweat glands

subcutaenous adipose tissue:

  • (hypodermis)
  • made from fat and connective tissue
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3
Q

What cells and structures are found within the dermis?

A
  • fibroblasts
  • macrophages
  • monocytes
  • blood vessels & nerves
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4
Q

What are the 4 (or 5) layers of the epidermis?

A

from deep to superficial:

  • stratum basale
  • stratum spinosum
  • stratum granulosum
  • stratum corneum
  • stratum lucidum is between the stratum corneum and stratum granulosum
  • it is only found on the palms of the hands and soles of the feet
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5
Q

What is the difference between thin and thick skin?

A

“thin skin” has only four layers of the epidermis

“thick skin” is only found on the palms of the hands and soles of the feet

this has a fifth layer - stratum lucidum

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6
Q

What cells are found within the epidermis?

A
  • epidermis is composed of keratinised, stratified squamous epithelium
  • cells in all layers except the stratum basale are keratinocytes
  • the keratinocytes in the stratum corneum are dead and regularly slough away, being replaced by cells from the deeper layers
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7
Q

What are the 3 main functions of the skin?

A

physical barrier:

  • to chemicals, UV and micro-organisms

homeostasis:

  • thermoregulation
  • prevention of dessication and electrolyte loss

immunological function:

  • antigen presentation and phagocytosis
  • contains langerhans cells, lymphocytes & mononuclear phagocytic cells
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8
Q

What are Langerhans cells?

Where are they mainly found?

A

they are dendritic cells that are present in all layers of the epidermis, but are most prominent in the stratum spinosum

they are part of the skin immune system and specialise in antigen presentation

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9
Q

What is the microbiology of the skin like?

Which organisms are dominant?

A

the skin is heavily colonised

  • coagulase-negative staphylococci
  • Staphylococcus aureus
  • Propionibacterium
  • Corynebacterium spp.
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10
Q

What are the mechanisms behind localised infection of the skin?

A

Inoculation:

  • penetration of the skin with a contaminated object
  • contamination of pre-existing breach in the skin surface

other route of infection:

  • e.g. neuronal migration in herpes simplex
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11
Q

What is meant by inoculation in localised skin infections?

How might this happen?

A
  • penetration of the skin with a contaminated object
    • accidental - e.g. tooth, rusty nail, knife, etc.
    • deliberate - e.g. surgical procedure, therapeutic injection, injection drug use etc.
  • contamination of pre-existing breach in the skin surface
    • ​e.g. abrasion, athletes foot lesion etc.
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12
Q

What are examples of systemic / generalised skin infections?

A
  • chickenpox
  • meningococcal sepsis
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13
Q

What are viral warts?

What causes them and what is the pathogenesis?

A

small asymptomatic growths of skin (hands, genitals, feet, around nails, throat)

causative agent:

  • human papilloma virus (HPV)

pathogenesis:

  • cause proliferation and thickening of stratum corneum, granulosum and spinosum
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14
Q

What is the clinical presentation of viral warts?

A
  • often asymptomatic
  • mechanical
  • associated with cervical cancer
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15
Q

What is involved in the treatment and prevention of viral warts?

A

treatment:

  • topical - salicylic acid, silver nitrate
  • cryosurgery - the use of extreme cold to destroy abnormal tissues

prevention:

  • gardasil vaccination protects against diseases caused by HPV (types 16, 18, 6 and 11)
  • 16 and 18 cause 70% cancer
  • genital - barrier protection
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16
Q

What is a pilonadal cyst/abscess?

What are they caused by?

A

cysts or abscesses in the natal cleft (cleft at the top of the buttocks) which contain hair and debris

caused by ingrowing hair (??)

discharge to form pilonidal sinus (small hole/tunnel in the skin)

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17
Q

How does a pilonidal cyst present?

What is the treatment?

A

presents with pain, swelling and pus

they are often recurrent

treatment:

  • hot compress, analgesia, antibiotics
  • surgical excision
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18
Q

What is impetigo?

What causes it?

A

crusting (sores/blisters) around the nares of corners of the mouth

it affects the superficial skin

it is caused by Staphylococcus aureus and is transmissable

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19
Q

What is the treatment for impetigo?

A
  • topical antiseptics
  • oral antibiotics

it is a highly contagious disease but often gets better within a week with treatment

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20
Q

What is erysipelas?

What layers of the skin are affected?

A

a superficial form of cellulitis; a potentially serious bacterial infection affecting the skin

it involves a rash over the face which is raised and demarcated

it affects the upper dermis and can extend into the superficial cutaneous lymphatics (becoming systemic)

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21
Q

What causes erysipelas and how is it treated?

A

causative organism is Streptococcus pyogenes

it is transmissable and recurrent

it is treated with oral antibiotics

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22
Q

What is cellulitis?

Which layers of the skin are affected?

A

it is a common, potentially serious bacterial skin infection

it affects the inner layers of the skin

(dermis and subcutaneous fat, into lymphatics)

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23
Q

Which parts of the body are usually affected by cellulitis and how do they appear?

A

the affected skin appears swollen and red and is typically painful and warm to the touch

cellulitis usually affects the skin on the lower legs, but it can occur in the face, arms and other areas

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24
Q

What are the causative agents of cellulitis?

A
  • staphylococcus aureus
  • Group A streptococci (Strep. pyogenese)
  • other B-haemolytic streptococci
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25
Q

What is the pathogenesis involved in cellulitis?

A

the bacterium enters through breaks in the skin

  • wound, insect bite
  • pre-existing condition such as eczema, athletes foot, shingles (zoster) etc.
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26
Q

What is the clinical presentation of cellulitis?

A
  • rubor (red), calor (heat), dolor (pain), tumor (swelling)
  • loss of skin creases
  • blistering
  • pus / exudate
  • fever
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27
Q

What is involved in the diagnosis and treatment of cellulitis?

A

diagnosis:

  • clinical (unless septic, cultures rarely helpful)
  • exclude other causes of red hot swollen leg (e.g. DVT)

treatment:

  • elevation & rest
  • antibiotics
  • source control (drainage of pus)
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28
Q

What is orbital cellulitis?

What is the pathogenesis?

A

infection of the soft tissues around and behind the eye

it is most commonly caused by an acute spread of infection into the eye socket from the adjacent sinuses or through the blood

it can also occur after trauma

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29
Q

What is the clinical presentation of orbital cellulitis?

A
  • erythema
  • swelling with induration and pain on eye movement
  • bulging

(induration is the localised hardening of soft tissue - the area becomes firm, but not as hard as bone)

30
Q

What are the causative organisms for orbital cellulitis?

How is it treated?

A
  • S. aureus
  • S. pyogenes
  • S. pneumoniae
  • H. influenzae

it is treated with IV antibiotics

31
Q

What is necrotising fasciitis?

What happens in this disease and what is the end result?

A

a rare but serious bacterial infection that affects the tissue beneath the skin and surrounding organs/muscles (fascia)

it is sometimes called the “flesh-eating bug”

the bacteria release toxins that damage nearby tissue

there is tracking along the fascia and cutting off blood supply, leading to necrosis

32
Q

What is Type 1 necrotising fasciitis?

What are the risk factors?

A

synergistic / polymicrobial , host impairment

involves gram negative organisms, Streps & anaerobes

risk factors:

  • diabetes mellitus
  • obesity
  • immunosuppression
  • alcohol
  • older age group - e.g. Fournier gangrene
33
Q

What is Fournier’s gangrene?

A

a life-threatening form of necrotising fasciitis that affects the genital, perineal, or perianal regions of the body

34
Q

What is Type 2 necrotising fasciitis?

What is it associated with?

A

Type 2 is Group A Strep (S. pyogenese) mediated

it is associated with a younger age group

it is associated with a cut or injury

35
Q

What are Type 3 and Type 4 necrotising fasciitis associated with?

A
  • Type 3 is caused by Vibrio vulnificus, which is associated with sea water and coral
  • Type 4 is fungal
36
Q

What is the pathogenesis involved in type 1 and type 2 necrotising fasciitis?

A

Type 1:

  • ischaemic tissue, colonisation then infection resulting in further ischaemia and necrosis
  • e.g. diverticulitis , Fournier’s gangrene

Type 2:

  • infection, toxin release leading to disruption in blood supply and necrosis
37
Q

What is the clinical presentation and treatment for necrotising fasciitis?

A

clinical presentation:

  • swelling, erythema (non confluent), pain (out of context)
  • crepatus, sepsis/toxaemia, necrosis
  • “dish water” exudate

treatment:

  • it is a surgical emergency and is treated with debridement and antibiotics
38
Q

What is gangrene?

A

necrosis caused by inadequate blood supply

it typically starts in the toes, feet, fingers and hands

it can occur as a result of an injury, infection or a long-term condition that affects blood circulation

39
Q

What are the risk factors for gangrene?

A
  • atherosclerosis
  • smoking
  • diabetes mellitus
  • autoimmune conditions
40
Q

What are the 3 different types of gangrene?

A

dry gangrene:

  • occurs when the blood supply to a tissue is cut off
  • the area becomes dry, shrinks and turns black

wet gangrene:

  • occurs if bacteria invade the dry, shrunked tissue
  • this makes the area swell, drain fluid and smell bad

gas gangrene:

  • occurs when an infection develops deep inside the body and the bacteria responsible begin releasing gas
41
Q

What is involved in the pathogenesis of gangrene?

What are the causative agents?

A

Pathogenesis:

  • poor blood flow leads to tissue necrosis
  • colonisation leads to infection
  • synergistic infection leads to further necrosis

Causative agents:

  • skin - Staphs, Streps
  • enteric - GNB, anaerobes including Clostridium
42
Q

What is the clinical presentation of gangrene like?

A

Dry gangrene:

  • “mummified”
  • autoamputation - spontaneous detachment of an appendage from the body

wet gangrene:

  • boggy, swollen, “dactylitis”, exudate, surrounding erythema

gas gangrene:

  • the same presentation as wet gangrene
  • gas is present in the tissue, causing crepitus
43
Q

What is dactylitis?

A

severe inflammation of the finger and toe joints

the puffy nature of the inflammation can make the digits look like sausages

44
Q

What is the treatment for gangrene?

A

treatment is mostly surgical

  • source control
  • revascularisation
  • antibiotics
45
Q

What is a diabetic foot infection?

A

a spectrum of disease from superficial through to deep bone infection in patients with diabetes

46
Q

What is involved in the pathogenesis of diabetic foot infections?

A

damage to blood vessels:

  • ischaemia, impaired immunity and poor wound healing

damage to nerves:

  • neuropathy, trauma

high blood sugars:

  • prone to bacterial infection
47
Q

What are the causative organisms for a diabetic foot infection?

A

superficial:

  • skin flora
  • Staphylococcus aureus
  • Streptococci
  • Corynebacterium

deep:

  • skin and enteric flora
  • all as above and GNB + anaerobes
48
Q

What is involved in the treatment of diabetic foot infections?

A
  • surgical debridement
  • revascularisation
  • antibiotics
  • off-loading
  • diabetic contorl
49
Q

What is osteomyelitis?

A

an infection of the bone

this is a rare but serious condition

50
Q

What is involved in the mechanism behind osteomyelitis?

A

contiguous:

  • e.g. diabetic foot infection
  • spread from adjacent infected tissue or open wounds (e.g. open fracture, surgery)

haematogenous:

  • bugs in the bloodstream spread to the bone

penetrating:

  • peri-prosthetic, traumatic
  • e.g. infection around an artificial joint can spread to the bone
51
Q

What is the difference between acute and chronic osteomyelitis?

What does infection result from?

A

acute:

  • associated with inflammatory reaction, fulminant, sepsis

chronic:

  • present for > 1 month
  • smouldering with acute flares
  • infection results in bone death (sequestrum) and new bone formation (involucrum)
52
Q

What does fulminant mean?

A

a disease or symptom which is severe and sudden in onset

53
Q

What are the causative organisms in osteomyelitis?

A

haematogenous:

  • usually in children
  • S. aureus, Strep, Kingella, Haemophilus

contiguous:

  • skin - Staph, Streps
  • enteric - GNB, anaerobes

penetrating:

  • surgical - skin flora
  • open fracture - skin flora and from the environment

sickle cell:

  • salmonella spp.
54
Q

What is the clinical presentation of osteomyelitis?

How is it diagnosed?

A
  • acute pain
  • swelling
  • erythema
  • sinus
  • pathological fracture
  • diagnosed through imaging and microbiology (blood, tissue/bone)
55
Q

What is the treatment for osteomyelitis?

A
  • antibiotics alone for 4-6 weeks (haematogenous)
  • surgical debridement and stabilisation if dead bone is present
56
Q

What is septic (or pyogenic) arthritis?

What are the causative organisms?

A

it is an infection of the joint

it is usually bacterial but can also be caused by viruses, mycobacterium and fungi

causative organisms:

  • S. aureus
  • Streps
  • Haemophilius influenzae
  • N. gonnorrhoeae
  • E. coli
57
Q

What is the pathogenesis of septic arthritis like?

A
  • haematogenous - from bloodstream infection
  • local spread - from soft tissue, bone or bursitis
  • penetrating - from joint injections, surgery or trauma
58
Q

What is the clinical presentation of septic arthritis like?

A
  • pain
  • swelling
  • erythema
  • reduced range of movement (unable to weightbear)
  • sepsis
59
Q

What is involved in the diagnosis and treatment of septic arthritis?

A

diagnosis:

  • clinical, confirmed by joint aspiration (MCS)

treatment:

  • antibiotics (guided by cultures) for 4-6 weeks
  • surgical source control through joint washout
60
Q

What is a peri-prosthetic joint infection?

A

an infection of tissue and bone surrounding a prosthetic joint

61
Q

What is involved in the pathogenesis of a peri-prosthetic joint infection?

What is the difference between early and late?

A
  • bugs get onto the surface of the foreign body, which the immune system cannot reach
  • bugs establish a biofilm (slime)
  • early - implanted at the time of surgery or shortly after via a wound
  • late - haematogenous but can be a late presenting early infection
62
Q

What are the causative organisms for early and late peri-prosthetic joint infections?

A

early:

  • Staphylococcus aureus
  • Staphylococcus epidermidis
  • Propionibacterium

late:

  • as above
  • E. coli
  • B Haem Streps
  • Viridans Streps
63
Q

What is the clinical presentation of a prosthetic joint infection?

A
  • pain
  • instability
  • swelling & erythema
  • sinus formation with pus
64
Q

What are the treatment options for a prosthetic joint infection?

A
  • antibiotics alone
  • antibiotics with debridement
  • single-stage revision
  • two-stage revision
65
Q

What is the difference between single-stage and two-stage revision in treatment of a prosthetic joint infection?

A

single-stage revision:

  • remove infected joint and replace with a new one in the same operation

two-stage revision:

  • remove infected joint and give 6 weeks of antibiotics
  • insert new joint when sure that all infection has settled
66
Q

What causes syphilis?

What are the 3 stages to the disease?

A

it is congenital or sexually transmitted

it is caused by the spirochete, Treponema pallidum

the three stages to the disease are primary, secondary and tertiary

67
Q

What happens in primary syphilis?

A

a chancre develops - a painless, firm, non-itchy ulcer at the point of contact

it is usually solitary

it lasts 3-6 weeks

there may be lymphadenopathy

68
Q

When does secondary syphilis occur?

What is it characterised by?

A

occurs 4-10 weeks after chancre

  • symmetrical, red/pink, non-itchy rash develops
  • it is everywhere, including soles/palms/mucous membranes
  • it is maculopapular or pustular
  • rash contains Treponema
  • associated with other systemic symptoms
69
Q

When does tertiary (late) syphilis develop?

What are the 3 forms?

A
  • occurs 3 to 15 years after initial infection
  • 3 forms are gummatous, neurosyphilis and cardiovascular
70
Q

What are the 3 different forms of tertiary syphilis characterised by?

A

gummatous:

  • chronic gummas - large inflammatory swellings of skin, bone and liver

cardiovascular:

  • affects the heart and blood vessels

neurosyphilis:

  • affects the nervous system
71
Q
A

Y2 Clinical Pathology (76 decks)

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