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CLINICAL PATHOLOGY > Theme 10 - clinical infections in skin tissues > Flashcards

Theme 10 - clinical infections in skin tissues Flashcards

1
Q

What are the functions of the skin?

A

Physical barrier - chemicals, UV, microorganismsand chemical agents
Homeostasis - thermoregulation via sweating
Immunological function - Ag presentation and phagocytosis

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2
Q

Microbiology of the skin

A

Heavily colonised organ
Coagulase - negative staphylococci like Staph Aureus

other examples include:

  • propionbacterium
  • corynebacterium spp
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3
Q

Pathogenesis of the skin - localised infection

A

Penetration of skin with a contaminated object

Accidental, e.g. tooth, rusty nail, knife etc.

Deliberate, e.g. surgical procedure, therapeutic injection, injection drug use

This can cause contamination of pre-existing break in the skin surface e.g. abrasion, athlete’s foot

neuronal migration of herpes complex is another route of infection too

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4
Q

Pathogenesis of the skin - 2 examples of systemic/generalised infection

A

chickenpox

meningococcal sepsis

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5
Q

What are viral warts, what are they caused by and how do they cause symptoms?

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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6
Q

Clinical presentation of viral warts, how are they treated and how can they be prevented?

A

Clinical presentation:

asymptomatic, mechanical,
or cervical cancer sign (HPV cause)

Treatment:
Topical- salicylic acid,
silver nitrate, cryosurgery

Prevention:
Gardasil (types 16, 18, 6 and 11);
(16 and 18 cause 70% cancer)

Genital: Barrier protection e.g. condoms

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7
Q

What is a Pilonidal Cyst or Abscess?

A

cyst in natal cleft

caused by ingrown hair

contain hair and debris
discharge to form sinus
can present with pain, swelling and pus

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8
Q

how is a Pilonidal Cyst or Abscess treated?

A

Hot compress, analgesia and antibiotics

Surgical excision

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9
Q

What is impetigo, how does it present?

A

Crusting around the nares of the mouth in superficial skin

Caused by Staph aureus and is transmissible

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10
Q

How is impetigo treated?

A

Topical antiseptics

Oral antibiotics

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11
Q

What is Erysipelas?

A

Rash over face, raised, demarcated
Occurs in the upper dermis

Can involve lymphatics- systemic disease

Causative organism:
Strep pyogenes

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12
Q

Cellulitis - what is it and what causes it?

A

Infection affecting the inner layers of the skin

Infection spreads from dermis and subcutaneous fat, into lymphatics
Causative agent: Bacterial
Staph aureus, Group A Streptococci
(Strep pyogenese), other B-haemolytic
Streptococci
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13
Q

Pathogenesis of cellulitis

A

Bugs enter through breaks in skin
Wound, insect bite
Pre-existing condition eg. eczema,
Athletes foot, shingles (Zoster) etc.

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14
Q

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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15
Q

how is cellulitis diagnosed? how is it treated?

A

Clinical, unless septic cultures rarely helpful
Exclude other causes of red hot swollen leg (eg. DVT

treated by elevation, rest, antibiotics and drainage of pus

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16
Q

What is orbital cellulitis?

A

Infection of soft tissues around and behind eye

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17
Q

pathogenesis of orbital cellulitis…

A

from skin or sinuses or haematogenous or trauma

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18
Q

clinical presentation of orbital cellulitis

A

Erythema, swelling with induration

and pain on eye movement and bulging

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19
Q

causative organism of orbital cellulitis and treatement

A

S. aureus, S. pyogenes but also
S. pneumoniae and H. influenzae

IV antibiotics

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20
Q

What is necrotising fascitis?

A

“flesh eating bug”
There are 4 types:

Type 1: Synergistic/poly-microbial, host impairment- gram negatives,
Streps, anaerobes

Risk factors include:
Diabetes, 
obesity, 
immunosuppression, 
alcohol, 
older age group- eg. Fournier gangrene

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

Risk factors include:
younger age group, associated with cut or injury

Type 3:
Vibrio vulnificus-
sea water, coral

Type 4: fungal

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21
Q

what is the pathogenesis of necrotising fasciitis?

A

Type 1:
ischaemic tissue, colonisation then infection resulting in further ischaemia and necrosis

Eg. diverticulitis, Fournier

Type 2:

  • infection, toxin release
  • disruption in blood supply
  • necrosis
22
Q

clinical presentation of necrotising fasciitis?

A

Swelling, erythema (non confluent),
pain (out of context)

Crepatus, sepsis/toxaemia, necrosis, “dish water” exudate

Necrosis makes skin appear a very dark purple/red across the span of the limbs

23
Q

treatment for necrotising fasciitis

A

Surgical emergency, debridement and antibiotics

24
Q

What is gangrene?

What are the risk factors?

A

necrosis caused by inadequate blood supply

RISK FACTORS:

  • atherosclerosis
  • smoking
  • Diabetes
  • Autoimmune disease
25
Q

What are the different types of gangrene?

A

Dry” vs. “Wet” Gangrene vs. “Gas” Gangrene

26
Q

Pathogenesis of gangrene

A

Poor blood flow- tissue necrosis- colonisation- infection- synergistic infection- further necrosis

27
Q

Clinical presentation of gangrene (for each type - dry, wet and gas gangrene)

A

Dry- “mummified”, auto-amputate

Wet- boggy, swollen “dactylitis”, exudate, surrounding erythema

Gas- as above but with gas in tissue- crepitus

28
Q

What causes gangrene?

A

Skin (Staphs, Streps);

Enteric (GNB, Anaerobes inc. Clostridium)

29
Q

Treatment of gangrene

A

Surgical: source control (drainage of exudate) and
revascularisation

Antibiotics

30
Q

What is diabetic foot infection?

A

Spectrum of disease from superficial through to deep bone infection in patients with Diabetes

31
Q

Pathogenesis of diabetic foot infection

A

Damage to blood vessels -
Ischaemia, impaired immunity
and poor wound healing

Damage to nerves-
Neuropathy, trauma

High blood sugars-
prone to bacterial infection

32
Q

Causative organisms of DFI

A

Superficial- skin flora: Staph aureus, Streps, Corynebacterium

Deeper- skin and enteric flora: above + GNB, anerobes

33
Q

Treatment of DFI

A 
Surgical debridement
Revascularisation
Antibiotics
off-loading
Diabetic control
34
Q

Pathogenesis of osteomyelitis (the 3 routes of spread)

A

Contiguous: eg. Diabetic foot infection

Haematogenous: bugs in bloodstream

Penetrating: peri-prosthetic, traumatic

35
Q

Acute vs. Chronic osteomyelitis

A

acute:
inflammatory reaction e.g. sepsis

chronic:
more than a month
acute flares that smoulder
resulting in bone death and new bone formation

36
Q

new bone formation is called

A

involucrum

37
Q

bone death is called

A

sequestrum

38
Q

causative organisms of osteomyelitis relative to each route of pathogenesis

A

Haem- (children): S. aureus, Strep, Kingella, Haemophilus

Contiguous: Skin (Staph, Streps) enteric (GNB, anaerobes)

Penetrating: surgical- skin flora, open fracture- skin, environment

Sickle cell: Salmonella sp.

39
Q

Septic Arthritis - what is it?

A

Infection of the joint (usually bacterial but can also be cause by viruses, mycobacterium and fungi)

40
Q

pathogenesis of septic arthritis

A

Pathogenesis:
Haematogenous: blood stream infection
Local spread: soft tissue, bone, bursitis
Penetrating: joint injections, surgery, trauma

41
Q

causative organisms of septic arthritis

A 
Causative organisms:
S. aureus, 
Streps, 
Haemphilus, 
N. gonorrhoeae, 
E.coli
42
Q

clinical presentation of septic arthritis and diagnosis

A

Pain, swelling, erythema, reduced range of movement (unable to weightbear), Sepsis

diagnosis confirmed by joint aspiration

43
Q

septic arthritis is treated by

A

Antibiotics (guided by cultures)- 4 to 6 weeks

Surgical source control: Joint washout

44
Q

what is prosthetic joint infection?

A

infection of tissue and bone surrounding a prosthetic joint

45
Q

pathogenesis of prosthetic joint infection

A

Pathogenesis:

Bugs get onto surface of foreign body (prosthetics) immune system cannot reach- establishment of biofilm (slime) occurs

Early: Implanted at time of surgery or shortly after (via wound)

Late: Haematogenous but can be late presenting Early infections

46
Q

Causative organisms of prosthetic joint infections

A

Early:
Staph aureus, Staph epidermidis, Propionibacterium

Late: Above and E. coli, B Haem Streps, Viridans Streps

47
Q

Clinical presentation of PJI

A

pain
instability
swelling
sinus and pus formation

48
Q

treatment of PJI

A

Antibiotics alone
Antibiotics with debridement

Single-stage revision:

remove infected joint and
replace with new one at same operation

Two- Stage revision:

Remove old joint, given 6 weeks of antibiotics, insert new joint when sure all infection settled

49
Q

How is Syphilis transmitted and what is the causative agent?

A

Sexually transmitted infection

Caused by Treponema pallidum

50
Q

Primary syphilis presents as a chancre which is…

A

painless, firm non-itchy ulcer
at the point of contact e.g. penis tip

Usually solitary

Lasts 3-6 weeks

Lymphadenopathy

51
Q

Secondary syphilis presents as

A

4-10 weeks after primary

Symmetrical rash that is pink, itchy and is found everywhere (even mucous membranes and soles/palms of hands and feet)

  • Maculo-papular or pustular
  • Rash contains Treponema
52
Q

Tertiary syphilis presents as

A

3 to 15 years after initial infection in 3 forms:

Gummatous,
Neuro,
Cardiovascular

Gummatous is can be chronic causing large inflammatory swellings of skin, bone and liver.

CLINICAL PATHOLOGY (56 decks)

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