skin + musculoskeletal Flashcards
what type of cancers are the majority oral cavity cancers
squamous cell carcinomas
oral squamous cell carcinoma risk factors:
- main two?
- others? 4
main risk:
- smoking (incl chewing tobacco)
- alcohol
nb these are strongly synergistic (if have together, more than double risk)
other risks:
- male
- FH
- HPV virus
- diet low in fruit + veg + high in red meat
which strains of HPV increase risk of oral squamous cell carcinomas?
16 + 18
‘high risk’ ones
ie same that cause cervical cancer
what are the 4 histological changes/stages which lead to invasive carcinomas?
hyperplasia -> dysplasia -> carcinoma in situ -> invasive carcinoma
name 5 pre-cancerous lesions of the oral cavity
- submucous fibrosis
- actinic keratosis
- lichen planus
- leukoplakia + erythroplakia
- chronic hyperplastic candidosis
cancer of the larynx:
- most common type?
squamous cell carcinoma
risk factors for cancer of the larynx? 9
main 2:
- tobacco
- alcohol
- HPV virus
- diets low in fruit + veg + high in meat
- metal/plastic workers
- exposure to paint, diesel + gas fumes, asbestos
- exposure to radiation
- laryngopharyngeal reflux
- genetic susceptibility/FH
infection with which strains of HPV increase your risk of laryngeal cancer?
6 + 11
ie the OPPOSITE to ones which cause cancer of oral cavity + cervical cancer
lichen planus:
- what is it? inc cause
- clinical presentation?
- who is most likely to get it?
muco-cutaneous condition (ie affects mucous membranes + skin)
pathogenesis unknown but thought to be autoimmune mediated
cutaneous lesions:
- itchy
- purple
- lumpy
oral lesions:
- red + white patches on inner cheak + tongue
- burning + discomfort when eating/drinking
nb can also affect genitals
- middle/old-aged people
- affects men + women equally
small change of malignant transformation
nb histoligaclly you see a lot of lymphocytic infiltrate
vocal cord nodules:
- what are they?
- causes? 2
- where located?
- symptoms?
- age/gender affected?
reactive lesions to damage
- heavy smokers
- people who use their voice a lot (eg singers)
usually located on TRUE vocal cords
most commonly associated with a voice change:
- hoarseness
- change in voice quality
- increased effort in producing voice
- adults
- predominantly men
nasal polyps:
- cause?
- appearance histologically?
- possible sequalae?
features point to an allergic aetiology, but most patients with nasal polyps are not atopic
- however can follow recurrent attacks of rhinitis (eg in hayfever)
oedematous glands with lots of inflammatory infiltrate, especially eosinophils
when large +/or multiple can encroach on the airway, impeding on sinus drainage -> sinusitis
acute sinusitis:
- causes? 3
- when does it normally progress to chronic?
- causative organisms?
- possible rare complications? 3
- acute rhinitis
- chronic rhinitis
- tooth/gum infection (-> maxillary sinusitis)
normally becomes chronic is there is an impairment of sinus drainage
normally mixed microbial flora
- the normal inhabitants of the oral cavity
- cranial osteomyelitis
- meningitis
- cerebral abscess
rare but very serious
sialadenitis:
- what is it?
- common causes? 2
inflammation of salivary glands
duct obstruction
- stones (bacterial infection)
- tumours (malignant or benign)
“think of muesli on the stray bus”
what is the most common type of tumour of the salivary glands?
- risk factors/causes? 3
- malignant or benign?
- cell of origin?
- most common gland affected
pleomorphic adenoma (2/3rds)
- heavy smoking
- blockage of salivary ducts
- radiation
almost always benign but can become malignant
mixed origin, lots of different cell lines (hence pleomorphic)
80% are in the parotid gland
what are the signs/symptoms of acute arthritis of a joint? 5
- pain
- heat
- redness
- swelling
- loss of function
osteoarthritis:
- aka?
- pathogenesis?
degenerative joint disease
deterioration or loss of cartilage that acts as a protective cushion in between bones
as the cartilage is worn away, bone forms spurs
fluid filled cysts in the marrow (subchondral cysts)
-> pain + limitation of movement
what main things can predispose a person to getting OA?
- obesity
- genes
- injury
- overuse/repetitive motion
what types of conditions can lead to secondary OA?
- repetitive strain/injury (eg knee in basketball players)
- meningeal tears
- congenital skeletal abnormalities
- obesity
- diabetes
- gout
- RA
what is the cell that is most involved in the pathogenesis of OA?
how?
chondrocytes
produce interleukin-1 (this initiates matrix breakdown)
prostaglandin derivatives induce the release of lytic enzymes - prevents matrix synthesis
what two types of nodes are present in the fingers of someone with OA?
which joints do they affect?
bouchard’s nodes
- proximal IP joint
- “nearer the Base of the finger”
herberden’s nodes
- distal IP joint
- “the HEBRides islands are very remote and far out”
which joints are more commonly affected in OA of:
- women? 2
- men?
women
- hands
- knees
men
- hips
what is ‘swan neck deformity’ a reference to?
abnormality seen in people with severe RA’s hands
RA:
- change induced in joints?
change induced in joints:
- non-suppurative proliferative synovitis
- destruction of articular cartilage + ankylosis of joints
what does ankylosis mean?
abnormal stiffening and immobility of a joint due to fusion of the bones
symptoms of RA:
- joints?
- systemic?
joints: - swollen - warm - painful - stiff in morning + after inactivity
systemic:
- malaise
- fatigue
- generalised MSK pain
- weight loss
- fever
- poor appetite
which joints does RA tend to affect first?
small joints of hands and feet
nb normally affected symmetrically (unlike OA, which is often asymmetric distribution)
what things can lead to the initiation of the inflammation that occurs in RA?
which is the most common one?
- genetic susceptibility (HLA, DR1 + DR4 type)
- – most commonly!
- primary exogenous arthritogen (eg EBV, other viruses, borrelia)
- autoimmune reaction within the synovial membranes (CD4 positive T cells)
- over production of mediators of joint damage (cytokines, IL-1-6 + TNF alpha + beta)
what are the two typical radiographic changes seen in people with RA?
- narrowing of joint space
- loss of articular cartilage
what two blood tests can be used to support the diagnosis of RA?
- which is better?
what other fluid can be analysed? for what?
- anti-CCP (anti-cyclic citrulinated peptide) - BETTER
- rheumatoid factor (RF)
synovial fluid
- presence of a lot of neutrophils -> inflammatory picture
other organs taht can be affected in RA, apart from joints?
what happens to them?
skin (about 50%)
- rhematoid nodules
lungs
- fibrosis of lungs (can also be caused by drugs given to treat RA)
- also methotrexate can caue lung damage (methotrexate lung)
heart + blood vessels
- a lot more prone to atherosclerosis + subsequent MIs/strokes
bones
- osteomalacia can develop due to the RA, but also due to steroids to treat it
eyes
- sjogrens syndrome can occur
- can get scleritis (inflammation of the sclera)
nb can also get liver and kidney problems as side effects of drugs for RA
nb can rarely attack other systems as well
- most common symptoms are in the joints and treating them means less likely to affect other systems but still likely to have some affect on other organs, even if this is sub-clinical
where do rheumatoid nodules occur?
areas of pressure
eg on fingers or elbow etc
gout:
- what is it?
- caused by end product of what nucleic acid metabolism?
end point of a group of disorders producing hyperuricemia
uric acid is the end product of PURINE metabolism
“if your diet is not PURE then you will get gout”
what are tophi?
a deposit of uric acid crystals in people with longstanding hyperuricemia (pathognomic for gout)
Tophi form in the joints, cartilage, bones, and other places throughout the body. Sometimes, tophi break through the skin and appear as white or yellowish-white, chalky nodules
The development of gouty tophi can also limit joint function and cause bone destruction, leading to noticeable disabilities, especially when gout cannot successfully be treated
what are the 4 main clinical features of gout?
- acute arthritis
- chronic arthritis
- tophi in various sites
- gouty nephropathy
get transient attacks of acute arthritis - crystallisation of urates within and about joints, leading to chronic gouty arthritis + deposition of masses of urates in joints and other sites = tophi
definition of a soft tissue tumour?
embryological tissue type origin?
soft tissue-nonepithelial extraskeletal structures exclusive of supportive tissue of organs and lyphoid/haematopoietic tissue
eg:
- fibrous tissue
- adipose tissue
- skeletal muscle
- blood
- lymphatic vasculature
- PNS
mesodermal in origin
name benign soft tissue tumours arising from these tissues:
- fat tissue
- fibrous tissue
- smooth muscle
- striated muscle
- blood vessels
- lymphatic vessels
- peripheral nerves
fat = lipoma
fibrous tissue = fibroma
smooth muscle = leimyoma
striated muscle = rhabdomyoma
blood vessel = haemangioma
lymphatic vessel = lymphangioma
peripheral nerves = neuroma
which type of cancer typically spreads via blood and which typically via lymph:
- sarcomas?
- carcinomas?
sarcomas
- mainly by blood
carcinomas
- mainly by lymph
“people are always worrying about lymph node involvement of most tumours and most common tumours that you see are carcinomas”
name 4 syndrome which are associated with soft-tissue tumours
which tumours are they associated with?
neurofibromatosis type 1
- neurofibroma
gardener syndrome
- fibromatosis
carney syndrome
- myoxoma
- melanotic schwannoma
turner syndrome
- cystic hygroma (a type of lymphangioma)
what is gardeners syndrome?
a subtype of FAP (familial adenomatous polyposis) in which you also commonly get fibromas as well as the typical presentation of FAP
what is the proper names for:
- benign cartilage tumours?
- mixed bone + cartilage bone tumours?
chondromas
osteochondromas
ossteosarcoma:
- age group most affected?
- site of body most commonly affected?
young age group (kids + teenagers)
- “that’swhen your bones are growing the most normally”
around the knee (60%)
chondrosarcoma
- age group affected?
- treatment?
any age group
huge variation in grade and speed of progression
surgical resection +/or amputation
nb very chemo and radio resistant
ewings sarcoma:
- what is it?
- age group most commonly affected?
malignant small, round, blue cell tumour
a rare disease in which cancer cells are found in both bone and soft tissue
- can have characteristics of both mesodermal and ectodermal origin
teenagers/young adults
which tumours most commonly metastasise to bone?
which type of bone lesions do they cause?
prostate
- sclerotic (build new bone)
breast
- mixed
kidney
- lytic (breaks down bone -> high blood Ca)
thyroid
- lytic
lung
- lytic
“lead KeTtLe”
- Pb is the chemical symbol for lead
“cancers only found in men or women are either sclerotic or mixed, ones in both genders are lytic”
what are the 5 layers of the epidermis in thick skin?
from deep to superficial:
- stratum basale (basal cell layer)
- stratum spinosum (prickle cell layer)
- stratum granulosum (granule cell layer)
- stratum lucidum (not in thin skin!)
- stratum corneum (fully keratinised)
what are the 3 clinical stages of dermatitis?
incl features of each stage?
acute dermatitis:
- skin red
- weeping serious exudate
+/- small vesicles
subacute dermatitis:
- skin is red
- less exudate
- very itchy
- crusting
chronic dermatitis:
- skin thick + leathery secondary to scratching
what does dermatitis look like microscopically/histologically?
‘spongiosis’
- intracellular oedema within epidermis
chronic inflammation
- predominantly superficial dermis
epidermal hyperplasia + hyperkeratosis
- mild in acute dermatitis, marked in chronic dermatitis
what are the three most common type of dermtitis?
type of hypersensitivity reaction? (if relevant)
what tends to be the allergen/trigger
atopic dermatitis (ezcema) - type 1 hypersensitivity
allergic contact dermatitis
- type 4 hypersensitivity
- nickel, dyes, rubber
contact irritant dermatitis
- direct injury to skin by irritant
- acid, alkali, strong detergent etc
- anyone could have this
psoriasis:
- what the skin lesions look like?
- two other body parts possibly affected?
well defined, red oval plaques on extensor surfaces (ezcema is on flexor surfaces)
- fine silvery scale on top
- removal of scale causes small bleeding points
+/- pitting nails
+/- sero-negative arthritis (don’t get rhematoid factor)
nb psoritic arthritis typically affects small joints
what is auspitz sign?
Auspitz’s sign is the appearance of punctate bleeding spots when psoriasis scales are scraped off
a clinical test for psoriasis
describe the pathogenesis of psoriasis + what is looks like histologically
thickening of the dermis (especially the dermal pupillae)
and parakeratotic scale (the silvery scale)
collections of neutrophils in scale
basically it’s an overproduction of epidermis
- the scale is due to the relative immaturity of the top cells because they’re being turned over tooquickly
clinical + microscopic features reflect massive cell turnover
aetiology of psoriasis?
it’s an autoimmune condition
- often due to genetics (lots of genetic loci, often a FH of this or other autoimmune conditions)
- can be triggered by environmental triggers (much rarer though) - eg drugs, infection, trauma
what causes symptoms of psoriasis to worsen? 4
- stress
- winter (ie low vit D)
- some drugs (eg nsaids + beta blockers)
- infections
apart from arthropathy, what other co-morbidities can occur alongside psoriasis?
psychosocial effects (eg depression/anxiety), due to appearance
cardiovascular disease
- mechanism unknown
increased skin cancer risk
what are the two different types of lupus?
what’s the difference?
discoid lupus erythematosus (DLE)
- skin only
systemic lupus erythematosus (SLE)
- visceral disease +/- skin involvement
how does lupus affect the skin?
red scaly patches on sun-exposed skin
+/- scarring
scalp involvement causes alopecia
‘butterfly rash’ on cheeks and nose (where the sun hits your face)
what are the two immunological tests for lupus?
- ANA (anti-nuclear antibodies)
- anti-dsDNA (anti double-stranded DNA antibodies)
histology of skin in lupus?
microscopically, if antibodies in lupus are tagged, where are they found, under immunoflurescense?
thin atrophic epidermis
- inflammation + destruction of adnexal structures
IgG deposited in basement membrane
what organs are most commonly affected in systemic lupus? 8
- arthralgia/arthritis (90%)
- fever/fatigue (80%)
- vasculitis/skin involvement (70%)
- butterfly erythema (50%)
- renal involvement/nephrotic syndrome (50%)
- pleuropericarditis (50%)
- CNS involvement (30%)
- discoid skin involvement (20%)
dermatomyositis:
- main signs/symptoms?
- cause?
- peri-ocular oedema + erythema
- heliotropic rash (purple)
- erythema in photsensitive distribution
- myositis, proximal muscle weakness
- most is idiopathic
- in adults, 25% associated with underlying visceral cancer
nb can affect any age
nb when remove tumour, rash and muscle inflammation dissapear!
what blood test can be done to look for any sort of myositis
createnine kinase
released from muscle cells
however also elevated in heart muscle breakdown so not very specific
what does bullous mean?
characterised by blisters or bullae on the skin
what are the three main groups of bullous diseases?
how do they differ by:
- where bullae are?
- pathogenesis?
- image seen on immunoflurescence?
bullous pemphiguS
- bulla (blisters) within the epidermis (intra-epidermal)
- autoantibodies, directed against intercellular material within epidermis
- immunoflurescense shines up whole of epidermis
- “pemphiguS is Superficial”
bullous pemphigoiD
- bulla (blisters) are sub-epidermal
- autoantibodies to glycoprotein in basement membrane
- immunoflurescence shines up basement membrane (between epidermis + dermis)
- pemphigoiD is Deep”
dermatitis herpetiformis
- small itchy blisters
- IgA deposition in dermal papillae
- immunoflurescence shines up dermal papillae (bits of dermis that protrude out into epidermis)
nb these are all autoimmune, the antibodies are just directed against different things in the skin
difference in blisters/bullae in the three main different types of bullous diseases?
bullous pemphiguS
- all types cause FRAGILE blisters/bullae which rupture easily
- nb often see more burst blisters than intect ones o/e
- can be extnsive + /- involve mucous membranes (eg mouth, oesophagus)
bullous pemphigoiD
- large TENSE bullae which don’trupture easily
- can be localised (tend to mainly affect lower legs) or extensive
dermatitis herpetiformis
- SMALL, intensely ITCHY blisters
- tend to be on extensor surfaces
who does each type of bullous disease tend to affect?
bullous pemphiguS
- between 30 + 60
bullous pemphigoiD
- normally elderly
- “elderly people have been through more and so have thicker skin”
dermatitis herpetiformis
- often young patients
- associated with COELIAC disease
what systemic disease can these skin lesions be a sign of:
- dermatomyositis?
- dermatitis herpetiformis?
dermatomyositis
- visceral cancer (eg breast, lung etc)
dermatitis herpetiformis
- coeliac disease
what systemic disease can these skin lesions be a sign of, + what do they look like:
- acanthosis nigricans?
- necrobiosis lipoidica?
- erythema nodosum?
acanthosis nigricans
- brown to black, poorly defined, velvety hyperpigmentation of the skin, normally in skin folds (eg arm pit, groin, neck)
- internal malignancy (norm GI or genitourinary)
necrobiosis lipoidica
- large yellow laques with red edges on legs
- diabetes mellitus
- nb this is rare though
erythema nodosum
- red tender patches on skin
- associated with infections elsewhere (esp lung, drug reactions + others)
basal cell carcinoma (BCC)
- prognosis?
- where on body?
- who is at risk? 3
can be fairly invasive but almost never metastasises
- so if resected early, absolutely fine
nb most common malignant tumour
sun exposed site (esp face)
- also can be secondary to radiation
- pale skin that burns easily
- immunosuppressed people
- rarely: gorlin’s syndrome (get lots)
basal cell carcinoma, what does it look like:
- clinically?
- microscopically?
clinically:
- early: nodule
- late: ulcer
- morphoeic BCC: ill defined and infiltrative
microscopically:
- tumour composed of islands of basaloid cells with peripheral palisade
what type of ulcer do you see in late basal cell carcinoma?
describe it
‘rodent ulcer’
has a rolled edge
“looks like a rodent has burrowed into skin”
squamous cell carcinoma causes?
- UV radiation (esp sun exposed sites)
- radiotherapy
- drugs (some drugs used to treat melanomas)
- hydrocarbon exposure (tars, mineral oils, soot)
- chronic scars/ulcers (SCC arises within these)
- immunosuppression (renal transplant patients at increased risk)
squamous cell carcinoma, what does it look like:
- clinically?
- microscopically?
clinically:
- nodule with ulcerated, crusted surface
microscopically:
- invasive islands and trabeculae of squampous cells showing cytological atypia
squamous cell carcinoma:
- do they often metastasise?
- what increases likelihood of metastasis? 4
95% don’t metastasise
- certain areas (lip, ear, genital area - “next to an entrance into the body”)
- more than 2cm in diameter
- more than 4mm thick
- high grade
what is the function of melanocytes?
where do they derive from embryologically?
to form melanin which is transferred to the epidermal cells where it protects the nucleus from mutation, due to UV radiation
“effectively act like a sunhat over the nucleus of the epidermal cells”
neural crest cells
what is a benign tumour of melanocytes called?
naevi
aka moles
what is atypical mole syndrome?
multiple clinically atypical moles
- histologically atypical/dysplastic naevi
increased risk of developing melanoma
have to be watched carefully!
genetic, so runs in families
how do you tell the difference between a mole which is likely to be benign (naevus) + one that’s likely to be malignant? 4
ABCD
moles which are likely to be melanomas are:
- A - Asymmetrical
- B - Borders unevem
- C - Colour variation
- D - Diameter >6mm
naevi are:
- symmetrical
- even borders
- colour is uniform
- diameter <6mm
what are the 4 main risk factors for getting melanoma?
sun exposure
- especially short intermittent severe exposure
race
- fair skin (rarely in darker people)
family history
- atypical mole syndrome
giant congenital naevi
- small risk of turning malignant
if an afro-carribean person does get melanoma, where is it likely to be?
basically where their skin is lighter
- under nails
- on palms/soles of hands/feet
what mutation is often found in melanomas?
BRAF mutations
so use BRAF inhibitors to treat
- but nb these increase risk of squamous cell carcinomas
what is the most important feature of melanomas which predicts priognosis?
breslow tumour thickness
- measure on microscope from granular layer of epidermis to base of tumour
basically the thicker it is, the lower the 5 year survival rate
- if <1mm - 91-95% survival
- if >4mm - 45-60% survival
apart from tumour thickness, what other features of melanoma affect prognosis? 4
site
- BANS (back, arms, neck, scalp) have poorer prognosis
ulceration
presence of satellites/in-transits
sentinel node positive
what are satellites and in-transits?
cutaneous deposits that occur before first lymph node
satellites are within 2cm of tumour
in-transits are further than 2cm from tumour
what is the name of the cell which is the macrophage in the skin?
langerhans cells
what type of fungi causes infections of the skin?
what do they feed off?
what layer of the skin are they normally restricted to? why?
dermatophytosis
keratin
stratum corneum (outermost layer of the epidermis) - as that's where the keratin is
rarely penetrate the living cells of the epidermis
name for fungal infection of:
- torso?
- foot?
- groin?
- nails? 2
torso = tinea corporis (ring worm)
foot = tinea pedis (athletes foot)
groin = tinea cruris (groin)
nails = onychomycosis aka tinea unguium
what is kerion?
the result of the host’s response to a fungal ringworm infection of the hair follicles of the scalp (occasionally the beard) that can be accompanied by secondary bacterial infection(s). It usually appears as raised, spongy lesions, and typically occurs in children
basically a complicated of scalp ringworm (aka tinea capitis)
fungal infections of the skin:
- diagnosis?
- management?
skin scrapings
- microscopy + culture
- to rule out other conditions (eg psoriasis)
topical or systemic antifungal agents
- nb normally topically!!
name a common topical antifungal
clotrimazole
viral warts:
- causative virus?
- clinical appearance?
- pathogenesis?
human papilloma virus
small asymptomatic growths of skin (hands, genitals, feet, around nails, throat)
virus causes proliferation and thickening of stratum corneum, granulosum + spinosum
nb if on feet, often called verrucas
what is the treatment for viral warts?
what prevention can be used to prevent contraction of the virus?
topical:
- salicylic acid
- silver nitrate
- cryosurgery (freezing)
gardasil vaccine (HPV 6, 11, 16, 18)
barrier protection for genital contraction
pilonidal cyst (or abscess):
- what/where are they found?
- cause?
- clinical presentation?
- treatment?
cysts/abscess in natal cleft (ie bum crack)
caused by ingrowing hair which then gets superimposed bacterial infection
- contains hair + debris
present with:
- pain
- swelling
- pus
treatment:
- hot compress
- analgesia
- antibiotics
- surgical drainage/excision
nb can often be recurrent
nb more common in men (as they have harier but cracks?)
impetigo:
- clinical presentation?
- normal causative organism?
- treatment?
crusting around nares or corners of mouth
staph aureus
nb this is easily transmissable
treatment:
- topical antiseptics
- (occasionally oral antibiotics)
cellulitis:
- what is it?
- most common causative organisms? 2
- pathogenesis?
bacterial infection affecting the inner layers of the skin
- dermis + subcutaneous fat (can even get into lymphatics)
- staph aureus
- group A strep (strep pyogenes)
bugs enter through breaks in the skin
- eg due to wound, insect bite, eczema, athletes foot, shingles etc
cellulitis:
- clinical presentation?
- diagnosis?
- differential diagnosis?
- treatment?
- red
- hot
- pain
- swelling (loss of skin creases)
- blistering
- pus/exudate
(- fever, if severe)
clinical (cultures are only really helpful is get septic)
DVT!
- must exclude this!
- elevation
- rest
- antibiotics
- source control (drainage of pus)
orbital cellulitis:
- what is it?
- pathogenesis?
- signs/symptoms? 4
- common causative organisms? 2
- treatment?
infection of soft tissue around AND behind eye
from broken skin, sinuses, haematogenous or trauma
- erythema
- swelling
- pain on eye movement
- bulging eyeball (due to swelling behind eye)
- staph aureus
- strep pyogenes
(also strep pneumoniae + h influenzae)
IV antibiotics
ecthyma gangranosum:
- what is it?
- causative organism?
- who does it affect?
- pathogenesis?
- clinical appearance?
- treatment?
skin infection caused by PSEUDOMONAS AERUGINOSA, secondary to blood stream infection
very rare, almost always in immunosuppressed
blood stream infection -> blocking of blood supply -> small visible patches of erythema -> necrosis -> ulceration -> scar
treatment is to treat underlying blood stream infection
pyoderma gangrenosum:
- what is it?
- cause?
- clinical appearance?
- often mistaken for?
- treatment?
progressive necrosis of skin -> ulceration
autoimmune/inflammatory (NOT infectious - though can get superimposed bacterial infection)
associated with IBD, RA and other autoimmune conditions
often mistaken for an infected ulcer (eg due to diabetes or ischaemia)
steroids = treatment
nb if superinfection then use Abx as well
necrotising fasciitis:
- pathogenesis?
- two main types?
- difference in people affected in each type?
- difference in causative organism(s) in each type?
‘flesh-eating bug’
bugs track along fascia, cutting off blood supply -> necrosis -> other organisms infecting/feeding off necrotic tissue -> repeat
type 1:
- ischaemic tissue -> colonisation then infection -> further ischaemia + necrosis
- host norm has underlying condition (eg DM, obesity, immunosuppression, alcohol, elderly etc)
- poly-microbial (gram negs, streps, anaerobes)
type 2:
- infection of wound -> toxin release -> distruption in blood supply -> necrosis -> further infection + necrosis
- younger age group, associated with cut or injury
- strep pyogenes
nb type 2 is the one often referenced in the ‘flesh-eating bug’ headlines
what is fournier gangrene?
a sub-type of type 1 necrotising fasciitis found in the groin of older people
clinical presentation of all types of necrotising fasciitis?
- swelling
- erythema
- pain (excruciating/out of context)
later stages:
- crepatus
- sepsis/toxaemia
- necrosis
- ‘dish water exudate’
treatment of necrotising fasciitis? 2
surgical emergency!!
- debridement
- antibiotics
what is gangrene?
norm causative organisms? 2
difference between wet and dry?
necrosis due to inadequate blood supply (ischaemia)
staph + strep (skin organisms)
dry = not infected wet = superimposed infection of necrotic tissue (exudate, surrounding erythema)
what is gas gangrene?
causative organism?
wet gangrene PLUS gas in tissue (crepitus)
clostridium perfingens
treatment of gangrene? 3
- source control
- revascularisation
- antibiotics
diabetic foot infection:
- defintion?
- 3 reasons why they occur?
huge spectrum of disease fromn superficial through to deep bone infection in patients with diabetes mellitus
damage to blood vessels (glycation)
- > ischaemia
- > impaired immunity + poor wound healing
damage to nerves
- > neuropathy
- > unrecognised trauma
high blood sugars
-> prone to bacterial infections
diabetis foot infection:
- causative organisms?
- clinical presentation?
- treatment?
superficial: skin flora: staph aureus, streps, corynebacterium
deeper: skin + enteric flora: above + GNB, anaerobes
infected ulcers/skin etc
- surgical debridement
- revascularisation
- antibiotics
- off-loading
- diabetic control
nb need weight off feet so they can heal properly and the pressurfe doesn’t disrupt new tissue growth
osteomyelitis:
- 3 mechanisms of pathogenesis?
- what happens to the bone?
- contiguous (eg diabetic foot infection)
- haematogenous (bugs in bloodstream)
- penetrating (peri-prosthetic, traumatic)
infection results in bone death (sequestrum) + new bone formation (involcrum)
osteomyelitis, common causative organism in:
- haematogenous spread? 4
- contiguous spread? 4
- penetrating? 2
haematogenous:
- staph aureus
- strep
- kingella
- haemophillus
contiguous:
- skin (staph, streps)
- enteric (GNB, anaerobes)
penetrating:
- surgical: skin flora
- open fracture: skin or environmental flora
what organism can cause osteomyelitis in people with sickle cell disease (+ other haemoglobinopathies)?
via which route of spread?
salmonella sp.
haematogenous spread
nb reason for this is unknown
osteomyelitis:
- clinical presentation?
- diagnosis?
- treatment?
- acute pain
- swelling
- erythema
- sinus (between bone + skin)
- pathological fracture
- imaging
- microbiology (blood, tissue/bone)
- antibiotics (4-6 weeks)
- surgical debridement + stabilisation (if dead bone present)
septic arthritis:
- aka?
- what is it?
- pathogenesis?
- causative organisms?
pyogenic arthritis
infection of the joint
(usually bacterial but can be viral, fungal or mycobacterial but rare)
- haematogenous (blood stream infection)
- local spread (soft tissue, bone, bursitis)
- penetrating (joint injections, surgery, trauma)
- staph aureus
- streps
- haemophillus
- N. gonorrhoea (from PID)
- e. coli
septic arthritis:
- symptoms?
- diagnosis?
- treatment?
- pain
- swelling
- erythema
- reduced range of movement (incl inability to weight bear)
- (sepsis)
- clinical diagnosis
- – confirmed by joint aspiration of synovial fluid + culture
- antibiotics 4-6 wks (guided by what grown from synovial fluid)
- surgical joint wash out (if patient very unwell)
prosthetic joint infection:
- what is it?
- pathogenesis?
- ‘early’ causative organisms?
- ‘late’ causative organisms?
actually a PERI-prosthetic joint infection
- infection of tissue + bone surrounding a prosthetic joint
bugs get onto surface of foreign body, immune system cannot reach
- bugs establish biofilm (slime)
- > loosening of joints + inability for immune system to attack bugs
early:
- implanted at time of surgery (or shortly after, via wound)
- staph aureus
- staph epidermidis
- propionibacterium
late:
- haematogenous spread (but can be late presenting ‘early; infection)
- above (from early)
- e. coli
- B haemolytic strep
- viridans strep
prosthetic joint infection:
- clinical presentation?
- treatment? 4
- pain
- instability of joint
- swelling
- erythema
- sinus formation (pus)
4 stages of treatment:
antibiotics alone
- rarely works
antibiotics with debridement
- also pretty shite
single-stage revision
- remove infected joint + replace with new one at SAME operation
two-stage revision
- remove old joint
- give 6 weeks of Abx
- insert new joint when sure all infection gone
- BY FAR THE MOST EFFECTIVE
syphillis:
- 2 methods of spread?
- causative organism?
- treatment?
- STI
- congenital (mother to child)
treponema pallidum
“neurosyphillis makes you go TRYPPY and it was contracted in PALACES in the middle ages”
penicillin
3 stages of syphillis?
describe clinical presentation of each and time period
primary syphillis:
- get a (usually solitary) CHANCRE at point of contact
- this is a firm, painless, non-itchy ulcer
- lasts 3-6 weeks
- lymphadenopathy
secondary syphillis:
- occurs 4-10 weeks after chancre disappeared
- mac-pap (or pustular) rash
- can be found anywhere but mainly all over trunk
tertiary (late) syphillis:
- 3-15 years after initial infection
- 3 forms:
- – gummatous
- – neuro
- – cardiovascular
what is gummatous syphillis?
a component of tertiary syphillis
large inflammatory soft tissue swellings of skin, bone + liver
