infections of the skin and soft tissue Flashcards

1
Q

what does the normal commensal flora of the skin help to do

A

helps to prevent the multiplication and invasion of pathogens

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2
Q

what may occur to the skin prior to infection (3)

A

trauma; surgery; burns

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3
Q

what is the most common micro-organism found in the normal skin flora that can become a pathogen

A

Staphylococcus Epidermidis

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4
Q

6 factors controlling the skin’s microbial load

A
  1. limited amount of moisture present;
  2. acid pH of normal skin;
  3. surface temperature < optimum for may pathogens (skin is at RT which is sub-optimal for many pathogens);
  4. salty sweat;
  5. excreted chemicals e.g. sebum, fatty acids, urea (prevent organism multiplication);
  6. competition between different species of the normal flora
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5
Q

4 signs of infection

A

rubor; calor; dolor; tumor

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6
Q

examples of viruses that can cause skin infection (5)

A
  1. herpes simplex 1/2
  2. HPV
  3. molluscum contagiosum
  4. orf (skin infection you can get from infected sheep or goats)
  5. varicella zoster virus
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7
Q

examples of fungi that can cause skin infection (5)

A
  1. epidermophyton;
  2. microsproum;
  3. trichophyton;
  4. candida;
  5. malassezia furfur
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8
Q

examples of bacteria that can cause skin infection (7)

A
  1. S.aureus;
  2. S.pyogenes;
  3. C. diphteriae;
  4. M. tuberculosis;
  5. M. marinum;
  6. M. ulcerans;
  7. pseudomonas aeruginosa
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9
Q

examples of toxin mediated bacteria that can cause skin infection (2)

A
  1. S.aureus - scalded skin, toxic shock;
  2. S.pyogenes - “flesh eating bacteria”, scarlet fever
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10
Q

what are the 3 layers of the skin and what does each contain

A
  1. epidermis - contains melanocytes, Langerhans’ cells, Merkel cells and sensory nerves and is made up of 5 layers: stratum corneum, The Stratum Granulosum & the Stratum Lucidum, The Squamous Cell Layer, The Basal Cell Layer (melanocytes);
  2. dermis - thickest of the layers and stores much of the body’s water supply, contains BVs, lymph vessels, sweat glands, hair follicules, sebacous glands, nerve endings, collagen & elastin;
  3. subcutis - network of fat and collagen cells, acts as an insulator, shock-absorber and fat reserve
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11
Q

function and structure of the squamous cell layer

A
  1. also known as the stratum spinosum or “spiny layer” due to the fact that the cells are held together with spiny projections;
  2. basal cells that have been pushed upward - now called squamous cells, or keratinocytes -> produce keratin;
  3. also contains Langerhans cells - attach themselves to antigens that invade damaged skin and alert the immune system to their presence
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12
Q

what occurs in the Stratum Granulosum & the Stratum Lucidum

A
  1. keratinocytes from the squamous layer are then pushed up through two thin epidermal layers called the stratum granulosum and the stratum lucidum;
  2. As these cells move further towards the surface of the skin, they get bigger and flatter and adhere together, and then eventually become dehydrated and die;
  3. This process results in the cells fusing together into layers of tough, durable material, which continue to migrate up to the surface of the skin
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13
Q

structure and function of The Stratum Corneum

A
  1. outermost layer of the epidermis - made up of 10 to 30 thin layers of continually shedding, dead keratinocytes;
  2. also known as the “horny layer,” because its cells are toughened like an animal’s horn;
  3. As the outermost cells age and wear down, they are replaced by new layers of strong, long-wearing cells;
  4. The stratum corneum is sloughed off continually as new cells take its place, but this shedding process slows down with age
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14
Q

if infection occurs in the epidermis or superficial dermis what syndromes can occur (6)

A
  1. erysipelas;
  2. impetigo;
  3. folliculitis;
  4. ecthyma (usually deep, invasion of the dermis);
  5. furunculosis;
  6. carbunculosis
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15
Q

if infection occurs in the dermis/ superficial subcutaneous tissue what syndrome can occur

A

cellulitis

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16
Q

if infection occurs in the subcutaneous tissue what syndrome can occur

A

necrotising faciitis

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17
Q

if infection occurs in the muscle what syndrome can occur

A

myonecrosis

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18
Q

macule vs papule vs vesicle vs ulcer vs papilloma

A

macule - flat, red, local inflammatory response;
papule - raised, red, marked inflammation involving neighboring tissues;
vesicle - small blister, microbe invades epithelium;
ulcer - rupture of epithelium, microbe discharged;
papilloma - raised surface with microbe growing directly int he epithelium (e.g. warts)

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19
Q

3 ways infection can be introduced to the skin

A
  1. arrival of microbe circulating in blood, exit vessel and invade dermal cells;
  2. arrival of circulating toxin/immune complex;
  3. direct introduction of microbe into epithelium
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20
Q

exotoxin vs endotoxin

A

exotoxin - toxins released into the surrounding medium, usually grown by gram +ve bacteria;
endotoxin - part of the outer potion of gram -ve bacteria’s cell wall, liberated when bacteria die

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21
Q

why are burns good ways of transmitting skin infections

A

break in the skin + lack of blood supply to deliver immune cells

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22
Q

5 risk factors for bacterial skin infections

A
  1. people with diabetes (poor blood flow and may have peripheral neuropathy);
  2. hopsitalised people/nursing homes (bed sores);
  3. older people;
  4. immune system disorders;
  5. patients recieving chemo
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23
Q

what paghogens cause impetigo

A

S. aureus; S. pyogenes

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24
Q

what layer of the skin does impetigo affect

A

epidermis

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25
Q

what causes the yellow crusting lesions in impetigo

A

the bead bacteria

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26
Q

what topical treatments can be given for impetigo (if severe and H2O2 cream is unsuitable e.g. eyes)

A

mupirocin, fusidic acid, retapamulin, and ozenoxacin

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27
Q

ecthyma vs impetigo healing

A

ecthyma heals with scarring

28
Q

what organism causes ecythma gangrenosum

A

pseudomonas aeruginosa

29
Q

investigations for ecthyma gangrenosum (5)

A
  1. gram staining from central haemorrhagic pustule;
  2. lift scab and take swab (if nor fluid resent);
  3. blood cultures (collection during temperature spike is optimum time);
  4. skin biopsy;
  5. tissue cultures
30
Q

Mgx for ecthyma gangrenosum

A
  1. antipseudomonal penicillin e.g. piperacillin;
  2. aminoglycosides;
  3. fluroquinolones;
  4. 3rd gen cephalosporin
31
Q

what are furuncles

A

boils - walled off collections of microorganisms associated with inflammaotry cells

32
Q

what is a carbuncle

A

development of a cluster of boils occuring on the neck, back or thigh often in conjunction with fever

33
Q

why is drainage important in treating staph infections

A

infection often results in a walled off collection with no blood supply and so it must be drained in order to allow Abx to reach the infection site

34
Q

what layers does cellulitis affect

A

all layers

35
Q

what is an abscess

A

a painful collection of pus, usually caused by a bacterial infection

36
Q

what should be tested for when presenting with a rash and how to test

A

blanching or non-blanching - roll a glass over the rash and if it fades w pressure applied then it is blanching

37
Q

what type of rash does meningococcal septicaemia present with

A

non-blanching

38
Q

what causes splinter haemorrhages in endocarditis

A

immune complexes

39
Q

what is toxic shock syndrome and what causes it

A

a rare but life-threatening condition caused by release of exotoxins from toxigenic strains of S.aureus

40
Q

what rash is seen in toxic shock syndrome

A

rash resembles sunburn followed by desquamation in large sheets - generalised and palmar

41
Q

symptoms of toxic shock syndrome

A

fever; chills; headache; fatigue; rash; shedding skin in large sheets; low BP. SOB, bleeding/bruising due to low platelets etc.

42
Q

investigations for TSS (4)

A
  1. bacterial swabs from infected site of origin;
  2. blood cultures;
  3. blood tests - FBC, renal/liver function test, creatine kinase;
  4. urinalysis
43
Q

Mgx for TSS

A
  1. remove source of infection;
  2. draining and cleaning site of wound;
  3. intravenous fluids to treat shock and prevent organ damage;
  4. treat symptoms e.g. dialysis for renal failure, meds for hypotension;
  5. administration of blood products;
  6. give flucloxacilling, linezolid, 1st gen cephalosporin
44
Q

what is staphyococcal scalded skin syndrome (ritter’s disease)

A

a rare, severe, superficial blistering skin disorder which is characterised by the detachment of the outermost skin layer

45
Q

what causes scalded skin syndrome

A

exotoxin release from specific strains of Staphylococcus aureus bacteria (ETA, ETB, ETD)

46
Q

scalded skin syndrome pathophys

A
  1. S. aureus releases two exotoxins (exfoliative toxins A and B);
  2. bind to a specific desmosome - desmoglein-1 in the epidermins;
  3. Desmoglein-1 is responsible for maintaining cell-to-cell adherence within the epidermis and preserving skin integrity -> break down leads to the skin cells becoming loose and “unstuck”;
  4. Loss of the epidermal layer and associated blistering occurs
47
Q

molluscum contagiosum Mgx

A

usually clears on its own in around 3 months; can give cryotherapy or cutteridge also

48
Q

what is hutchinson’s sign

A

painful vesicles or bumps at or near the tip of your nose - an early sign of opthalamic shingles

49
Q

how long must children avoid going to school for if they have impetigo

A

either 48hrs since starting treatment or if has crusted over

50
Q

what is used for carbuncle treatment

A

drainage then abx -> 1% clarythromycin, 2% erythromycin and a systemic anti-streptacoccal (beta-lactam)

51
Q

necrotising fasciitis vs. cellulitis

A

NF: skin appreas dusky + bullae may be present; deeper infection so appears darker, Hx of injurt/trauma;
cellulitis: Hx of infection, not relating to trauma

52
Q

gangrene vs necrotising fasciitis

A

gangrene - occurs due to lack of blood supply, then can get infected;
necrotising faciitis - bacteria infection of the dermis

53
Q

who is most commonly affected by scalding skin syndrome

A

children <5yro; elderly

54
Q

what might pts be infected with if they present with recurrent skin abscesses

A

S.aureus that carries panton-valetine leukocidin

55
Q

what abx is normally given for staph infection

A

flucloxacillin

56
Q

what should be done if MRSA is detected (if admitted to hospital)

A

nasal decontamination mupirocin; decontamination wash

57
Q

4 streptococcal toxins (and what they do)

A
  1. pyrogenic toxins (cause rash e.g. scarlet fever);
  2. streptolysins O/S (damage mammalian cells);
  3. streptokinase (plaminogen to plasmin, lysis of clots;
  4. hyluronidase (disrupts ground substance)
58
Q

what protein present in streptococci is a major virulence factor

A

M proteins

59
Q

what skin change is seen in meningococcal disease and why

A

petechiae due to endotoxin release causig endothelial damage and destruction of RBCs -> increased permeability and capillary leak (microhaemorrhages) -> activation of coagulation -> microvascular thrombosis

60
Q

what does NF initially present as

A

cellulitis -> progresses with inflammation, oedema, gangrene and anesthesia at local sight and systemic toxicity

61
Q

what organisms are usually responsible for NF (5)

A
  1. S.pyogenes;
  2. S.aureus;
  3. V.vulnificus;
  4. A.hydrophila
  5. anaerobic bacteria
62
Q

what is fournier’s gangrene associated with

A

diabetes;

63
Q

what is fournier’s gangrene

A

life threatening extensive necrotising infection of the genital, perineal, scrotum, groin regions

64
Q

what type of bacteria cause fournier’s gangrene (3)

A

grame -ve; group A strep; anaerobes

65
Q

what is clostridial gangrene

A

infection of traumatic/surgical wounds with clostridium species e.g. C.tetani

66
Q

4 ways of specimen collection

A
  1. scrapings;
  2. swabs;
  3. biopsies;
  4. swab for PCR