Derm + ID/misc Flashcards
which layer does normal proliferation of skin occur in
basal layer
what are the layers of the epidermis
Come Lets Get Sun Burned stratum corneum stratum lucidum stratum granulosum stratum spinulosum stratum basale
what do melanocytes develop from, where are they found and what is their role
melanoblasts develop into melanocytes
melanocytes found in the basal layer of epidermis
produce melanin pigment responsible for skin colour + UV protection
what do sebaceous glands produce
sebaceous secretions = lubricate and waterproof hairs
what do eccrine glands secrete
thin/watery sweat everyone on the body
= regulate body temp
what do apocrine glands secrete
secrete sweat = armpits/groin especially
what is acne vulgaris and describe the pathology of it
long term skin disease
hair follicles become blocked
sebaceous glands produce too much sebum = mixes with dead skin cells = forms plug in follicle
localised inflammation occurs
what causes acne vulgaris
genetics hormones infections = propionibacterium acnes high glycaemic diet stress
how does acne present and how is it diagnosed
inflammatory acne = comedones inflammatory = papules/pustules and possible scarring - whiteheads - blackheads - papules - pimples - nodules diagnosed by presentation/age of onset/appearance
what is eczema and describe the 2 types
inflammation of skin ATOPIC = itchy rash in folds of elbow/knee = typically children = chronic dermatitis EXOGENOUS = itchy rash following contact with irritant = type 4 hypersensitivity
eczema and dermatitis are synonymous
how does eczema present
ATOPIC = itchy red rash = scaling and oozing EXOGENOUS = sharply demarcated skin inflamm = red, crusting, scaling, fissures, hyperpigmentation
how is eczema diagnosed
skin exam
skin biopsy/allergy test = make sure correct diagnosis
patch test for contact dermatitis
how is eczema treated
no cure ATOPIC = avoid irritants = regular emollients to hydrate = corticosteroids = calcineurin inhibitors = TACROLIMUS (immunosuppressive) EXOGENOUS = avoid irritants = steroid cream = antipruritic cream
what are the differentials for eczema
allergic contact dermatitis
seborrheic dermatitis
scabies
immunodeficiency
what is psoriasis and what are the different types
chronic AI disease = abnormal patches of red skin
chronic plaque = dependent on triggers
flexural psoriasis = heat/trauma/infection causes
guttate = genetic/HLA associated, strep triggered
erythrodermic and pustular = secondary to chronic plaque / infection/drugs/tar
how does psoriasis present
plaques = silvery centre surrounded by red = knees/elbow/scalp/back
red/scaly rash
pustules (pustular psoriasis)
nail pitting/yellowing (onycholysis)
guttate = explosive eruption teardrop plaque 2 weeks after strep infection
erythrodermic and pustular = systemic symptoms
how is psoriasis investigated and treated
skin exam and biopsy chronic plaque/flexural/guttate: = topical emolients = topical corticosteroids = vitamin D analogues = UV therapy erythrodermic and pustular: = bed rest = emollients = cool/wet dressings
what are skin ulcers
abnormal breaks in epithelial surface
what are the causes of skin ulcers
chronic wounds that dont heal due to poor circulation/CVS disease pressure sores bacterial/viral/fungal infection cancers venous = most common cause leg ulcers IBD = pyoderma gangrenosum
how do skin ulcers present
open craters often round with eroded skin inside
bleeding
pain in skin surrounding ulcer
swollen/red tissue
how to take a history for an ulcer
- number/pain/trauma
- comorbidities ?
- steroid use?
- self induced?
how are skin ulcers investigated
examination = site/number/SA/depth etc skin/ulcer biopsy fluid discharge = culture and Ab sensitivity radiograph = check for osteomyelitis CXR = possible TB manifestation
how are skin ulcers treated
treat cause and focus on prevention !!! treat infection with antibiotics remove discharge/surgical debridement charing cross bandages topical antibiotics for prophylaxis treat underlying IBD/CVD etc smoking cessation and increase exercise
what is cellulitis and what causes it
deep skin infection caused by S. pyogenes (and S.Aureus)
what are the RFs for cellulitis
immunosuppression diabetes poor peripheral circulation athletes foot IVDU
how does cellulitis present
erythematous rash with oedema
fever/malaise/fatigue
how is cellulitis diagnosed
history and exam no further test if: - limited area involved - minimal pain - no systemic signs - no RFs for serious illness further tests = USS + blood cultures
how is cellulitis managed
flucloxacillin
what is necrotising fasciitis and what is it caused by
infection of soft tissue that results in necrosis caused by: MRSA S.Aureus **S. Pyogenes** E.coli P.Aeruginosa
how does necrotising fasciitis present
intense pain of skin and underlying muscle red/purple skin pyrexia/nausea/vomiting/malaise/myalgia bleeding into skin loss of sensation SHOCK
how is necrotising fasciitis diagnosed
clinical
if in doubt make a cut and if finger can separate fascia = diagnosis
bloods = WCC + CRP high
how is necrotising fasciitis treated
rapid surgical debridement
IV antibiotics = benzylpenicillin, clindamycin, vancomycin, gentamycin
describe skin cancer
neoplastic lesions of skin
basal-cell carcinoma
squamous-cell carcinoma
malignant melanoma
what are the RFs/causes of skin cancer
HPV infection smoking UV sun exposure ionizing radiation BRAF/KIT gene mutations
how does a malignant melanoma present
ABCDE Asymmetry irregular Borders uneven Colour Diameter >6mm Evolving size/colour/shape glasgow 7 point checklist
how is malignant melanoma treated
urgent excision
chemo if metastatic
ipilimumab = biologic improves survival
how does a squamous cell carcinoma present
red/scaling skin plaques with keratinised crust
ulceration with hard raised edges in sun exposed sites
how is squamous cell carcinoma treated
excision and radiotherapy to treat recurrence/affected nodes
how does basal cell carcinoma present
ULTRAVIOLET LIGHT raised/smooth pearly papules or nodules on head/neck/shoulder skin crusting/bleeding at centre of tumour persistant scaly/red lesions = often mistaken for non healing sore
how is basal cell carcinoma treated
excision
cryotherapy/radiotherapy if need
superficial BCC = topical flourouracil or imiquimod
what dosage of paracetamol constitutes an overdose
12g or 150mg/kg patient
if malnourished than 75mg/kg
how does paracetamol overdose present
no symptoms/signs initially OR RUQ and vomiting
later = jaundice and encephalopathy
acute kidney injury
how is paracetamol overdose diagnosed and managed
diagnosis = mainly from history but pt may lie
GI decontamination if <4hr after OD = activated charcoal 1g/kg
N-acetylcysteine (NAC) IV = antidote
describe the physiology of paracetamol OD and the effect of NAC (4)
- paracetamol metabolised to reactive intermediate by CYP450
- reactive intermediate to stable metabolite by glutathione transferase GSH
- OD = overwhelms GSH, not enough to convert to safe metabolite
- NAC = precursor to glutathione, allows regeneration of GSH
describe the indicators for paracetamol-induced liver failure
late presentation = NAC less effective acidosis PTT >70secs serum Cr > or = 300 micromols/L = CONSIDER LIVER TRANSPLANT
what is amyloidosis
group of disorders characterised by extracellular deposits of protein in fibrillar form that is resistant to degradation and causes a buildup of amyloid in organs
can cause organ failure and death
how does primary amyloidosis present in the KIDNEYS and HEART
KIDNEYS:
glomerular lesions/proteinuria/nephROtic syndrome
= oedema
= tiredness/weak/loss of appetite
HEART:
restrictive cardiomyopathy/arrythmias/angina
= oedema/SOB
how does primary amyloidosis present in the NERVES, GUT and VASCULAR
NERVES: peripheral and autonomic neuropathy/carpal tunnel = numbness in hands and feet GUT: big tongue/weight loss/haemorrhage = nausea = diarrhoea = constipation VASCULAR: purpura especially periorbital = characteristic!!!!
what is the characteristic feature of primary amyloidosis
peri-orbital purpura = PURPLE BRUISED AROUND EYES
how is primary amyloidosis treated
optimise nutrition
melphalan = chemo
prednisolone
high dose IV melphalan with stem cell transplant may be better
what is secondary amyloidosis
amyloid is derived from serum amyloid A
= chronic inflammation in RA, Crohns, chronic infections
how does secondary amyloidosis present and how is it treated
KIDNEYS/LIVER/SPLEEN = proteinuria = nephrOtic syndrome = hepatosplenomegaly = NO big tongue TREAT UNDERLYING CAUSE
what is familial amyloidosis
autosomal dominant
usually sensory/autonomic neuropathy
renal/cardiac involvement
liver transplant can CURE
how is amyloidosis investigated
biopsy taken from infected area = look for amyloid deposits
what is lymphoedema
chronic non-pitting oedema due to lymphatic insufficiency
= most commonly legs
= chronic can cause secondary cobblestone thickness of skin
what are the 2 types of lymphoedema
primary = due to faulty genes e.g. miliary disease secondary = due to lymph damage e.g. filarial infection
what is miliary disease
autosomal dominant = VEGFR3
primary congenital lymphoedema
lower leg swelling from birth
Tx = compression stockings and exercise
what is filarial infection
transmitted by 5 genera of mosquito
acute = fever, lymphodenopathy, chyluria (white urine)
causes elaphantitis/massive hydrocele
what is a sarcoma
cancer arising from cells of mesenchymal origin
= malignant tumours of cancellous bone/cartilage/fat/muscle/vascular/haemopoeitc tissue
describe soft tissue sarcoma
e.g. liposarcoma rhabdomyosarcoma angiosarcoma neurofibromatosis 1/radiotherapy can cause present as painless enlarging mass malignant: = over 5cm = increasing size = deep fascia = painful MRI with biopsy to diagnose Tx = excision then radiotherapy
what is duct ectasia
inflammation and dilation of large breast ducts
menopausal women
causes nipple discharge(green), pain, mass
no Tx
what is a fibroadenoma
benign fibroepithelial tumour of breast = well circumscribed nodular mass
excision if large but mainly observe and reassure
no capacity for malignant behaviour
what is an intraductal papilloma
benign papillary tumour within duct system of breast
= nipple discharge (+/-blood stained) and possible outward growing pailloma
often no lump
YOUNGER patients
Tx = excision
what is fat necrosis in the breast
inflammatory reaction to damaged adipose tissue
= palpable mass
= clinically mimics carcinoma
no Tx once diagnosis confirmed = benign with no risk of cancer
what are breast cysts
common in over 35s
benign fluid filled rounded lump
occasionally painful
diagnosis confirmed on aspiration
what are the risk factors for breast carcinoma
early menarche/late menopause increased weight high alcohol consumption oral contraceptive use positive family history
describe the triple assessment for breast lumps
- clinical exam
- histology/cytology
- mammography/ultrasound
describe the staging of breast carcinoma
- confined to breast, mobile
- confined to breast, lymph nodes of ipsilateral
- tumour fixed to muscle, ipsilateral lymph nodes matted, skin involvement
- complete fixation of tumour to chest wall, distant mets
describe the treatment for stage 1 and 2 breast carcinoma
- wide surgical excision WSE/mastectomy
- radiotherapy for invasive after WSE
- chemo = adjuvant improves survival and reduce recurrence
- endocrine agents = lower oestrogen activity foe oestrogen receptor +ve cancer
describe the treatment for stage 3 or 4 breast carcinoma
- staging investigations (CXR, USS, MRI, PET for mets)
- radiotherapy for bony lesions
- tamoxifen for ER+ve
- CNS surgery for solitary mets
what chemotherapy is used for pre and post menopausal women
pre-menopausal = tamoxifen post-menopausal = anastrozole
what is a ductal carcinoma in situ
neoplastic proliferations arising from terminal duct with increased risk of progression to invasive breast carcinoma
genetic linked
lump/nipple discharge/nipple changes
Tx = excision
what is an invasive breast carcinoma
malignant invasive tumour of breast with capacity to SPREAD to distant sites
= breast lump
graded histologically
Tx = surgery/chemo/hormone tx/local radiotherapy
what is condylomata accuminata and what is it caused by
genital warts
caused by HPV 6+11 (+ others)
small fleshy protuberances slightly pigmented
may bleed or itch
how are genital warts treted
- topical podophyllum or cryotherapy
multiple = topical
solitary = cryotherapy - imiquimod cream
what are the 2 main types of contact dermatitis
- irritant contact = common
non-allergic reaction
due to weak acids/alkali
typical erythema + crusting (no vesicles) - allergic contact dermatitis
type 4 hypersensitivity
weeping eczema on margins of hair line (after hair dye)
what is pruritus ani
anal itching symptom
can be primary (no cause) = functional
secondary (underlying cause)
= skin conditions
= infections
= haemorrhoids/fissures
TREATMENT
1. soothing topical = zinc oxide
2. mildly potent topical steroid
3. antihistamine
what is pruritus vulvae
vaginal itching
usually has an underlying cause
irritant contact dermatitis most common cause
TREATMENT
- clean 1x day with emollient
- topical steroids
what are the most important non-skin causes to think about with itchy skin
liver disease
iron deficiency anaemia
polycythaemia (after warm bath)
chronic kidney disease
lymphoma
what is male androgenetic alopecia
male pattern hair loss
begins 20-25
50% white men affected by 50
what are the treatment options for male androgenetic alopecia
nothing
topical minoxidil or oral finasteride
wigs
hair transplant
what is alopecia areata
presumed autoimmune condition
localised well demarcated patches of hair loss
small exclamation mark hairs
hair regrows in 50% by 1 year and 80-90% eventually
what drugs commonly cause urticaria
aspirin
NSAIDs
penicillin
opiates
what is the most common type of drug erruption
morbilliform (measles-like)
exanthematous (systemic)
urticaria/angioedema
what is a fixed drug erruption
cutaneous allergic reaction
reoccurs at same site on re-exposure to medication
type 4 hypersensitivity reaction
single/small number of well defined round or oval patches
describe urticaria
pale pink raised skin
hives/wheals/nettle rash
pruritic
how is urticaria managed
- non-sedating antihistamines = loratidine/cetirizine
- sedating antihistamine if affecting sleep
- prednisolone for severe or resistant episodes
describe aquagenic urticaria
urticaria after contact with water/change in temp
no rash associated
responds poorly to antihistamines
treat with phototherapy
what skin condition can predate polycythaemia rubra vera and what are the consequences for management
aquagenic urticaria
predate by 5 years
annual FBC needed
what medications cause drug-induced photosensitivity
thiazide diuretics
tetracyclines/sulphonamides/ciprofloxacin
amiodarone
NSAIDs
psoralens
sulphonylureas
name 2 large vessel vasculitides
temporal arteritis
takayasu’s arteritis
name 2 medium vessel vasculitides
polyarteritis nodosa
kawasakis disease
describe small vessel vasculitides giving examples
ANCA associated:
- granulomatosis w polyangiitis
- churg-strauss syndrome
- microscopic polyangiitis
immune complex:
- Henoch-schonlein purpura
- goodpasture’s syndrome
- anti C1q vasculitis
palpable purpuric rash
abdominal pain
polyarthritis
haematuria
in a child following an infection
suggests what disease
henoch-schonlain purpura
excellent prognosis
monitor urine and renal function
- epistaxis
- sinusitis
- saddle nose
- dyspnoea
- vasculitis rash
- eye involvement
= indicated what disease and whats the management
granulomatosis with polyangiitis
cANCA +ve
CXR
renal biopsy
Tx:
steroids
cyclophosphamide
plasma exchange
8-9 year survival
- vasculitis
- sinusitis
- dyspnoea
- asthma
- eosinophilia >10%
indicates what disease
churg-strauss
pANCA +ve
45 year old man presenting:
- fever
- weight loss
- testicular pain
- hypertension
- haematuria
- +ve Hep B serology
what is it? and what is the treatment?
polyarteritis nodosa
pANCA in 20%
livedo reticularis = mottled net-like discolouration of skin
TREATMENT
non HBV:
immunosuppression with corticosteroids
cyclophophamide
HBV:
short course high dose corticosteroids
combination of antiviral therapy + plasma exchange
what is bullous pemphigoid
autoimmune condition
sub-epidermal blistering of skin
BP180 and BP230 antibodies
itchy tense blisters around flexures
NO mucosal involvement
Ix = immunofluorescence
Mx = oral corticosteorids + topical steroids + antibiotics
what is pemphigus vulgaris
autoimmune condition
desmoglein 3
more common ashkenazi jewish population
mucosal involvement most common (oral in 50-70%)
skin blistering bullae + lesions
Ix = biopsy = acantholysis
Tx = 1. steroids 2. immunosuppressants
how are pemphigus and pemphigoid different
pemphigus = mucosal involvement
pemphigoid = no mucosal involvement
what type of ulcer is this? what is the management?
- odoema
- brown pigmentation of skin
- eczema
- painless
venous ulcer
4 layer compression banding after excluding arterial disease
?skin graft
what type of ulcer is this? and why is it significant?
- at site of chronic inflammation (burn, old osteomyelitis)
- mainly in the lower limb
marjolin’s ulcer
= squamous cell carcinoma
what type of ulcer is this? what is the treatment?
- on the heel/toes
- painful
- deep/punched out
- cold
- no pulse
- low ABPI
arterial ulcer
- restoring bloodflow (surgery)
- prevent infection
- wound care
what type of ulcer is this? what is the treatment?
- over plantar surface of big toe/metatarsal head
- associated w diabetes
- due to pressure
neuropathic ulcer
cushioned shoes needed to reduce callous formation
what type of ulcer is this?
- rapidly enlargic
- painful !!!
- blue/purple borders
- associated with IBD and RA (can occur at stoma sites)
- erythematous nodules which ulcerate
pyoderma gangrenosum
treat by removing necrotic tissue
potent steroids
tacrolimus ointment
special dressings
what is seborrhoeic keratosis
benign skin disease
>50y/o
flat raised filiform pedunculated lesions over trunk/face
colour varies
leave alone or chop off
what is the fancy name for a mole
melanocytic naevi
what is congenital melanocytic naevi
appear soon or after birth
usually >1cm
increased risk of malignant transformation
which naevi would you commonly find on the palms and soles
junctional melanocytic naevi
which naevi are pinky red, appear in children and are often excised
spitz naevi
similar appearance to melanoma
what is atypical naevus syndrome
autosomal dominant
increased risk of melanoma
what is the difference between a an epidermoid cyst and a pilar cyst
epidermoid cyst lining is normal epidermis
pilar cyst lining is root of hair follicle
describe mild, moderate and severe acne
MILD
open/closed comedones +/- sparse inflammatory lesions
MODERATE
widespread non inflamm lesions + numerous papules + pustules
SEVERE
extensive inflamm lesions +/- nodules, pitting, scarring
describe the treatment for mild to moderate acne
12 week course topical combination therapy:
adapalene + benzyl peroxide
OR
tretinoin + clindamycin
OR
benzyl peroxide + clindamycin
(benz peroxide can be used as monotherapy if patient prefers)
what is important to remember when treating acne in pregnancy + children <12
tetracyclines cannot be used
switch doxycycline to erythromycin
describe the treatment for moderate to severe acne
12 week course:
topical adapalene + topical benzoyl peroxide
topical tretinoin + topical clindamycin
topical adapalene + topical benzoyl perozide + oral lymecycline/doxycycline
topical azaleic acid + oral doxycyline/lymecycline
how long can oral antibiotics be used for acne
up to 6 months
what is a potential side effect of long term antibiotic use
gram negative folliculitis
treat with trimethoprim
what is an alternative to oral antibiotics for acne for women
COCP
describe the superficial lymphatic vessels of the lower limb
MEDIAL
medial vessels originate from dorsum of foot
travel up ant + post medial lower leg with great saphenous vein
pass behind medial condyle of femure
end in groin draining into subinguinal inguinal lymph nodes
LATERAL
arise from lateral surface of foot
accompany small saphenous vein to enter popliteal nodes
OR cross below the knee and join medial vessels
describe the deep lymphatic vessels of the lower leg
anterior tibial
posterior tibial
peroneal
= each follow the artery
= enter popliteal lymph nodes
describe the venous drainage of the lower limb via the deep veins
dorsal venous arch
V
anterior tibial veins + fibular veins (+posterior tibial vein)
V
popliteal vein
V
femoral vein
V
external iliac vein
describe the venous drainage of the lower limb via the superficial veins
dorsal venous arch
V
long saphenous vein
V (anterior to medial malleoulus then post to medial condyle of knee)
femoral vein (immediately inferior to inguinal ligament)
OR
dorsal venous arch
V
small saphenous vein
V (post of leg then post to lateral malleolus up to knee)
empties into popliteal vein (between gastrocnemius muscle)
what is actinic keratosis
precancerous lesions on sun exposed regions
can lead to bowens disease which leads to SCC
scaly/crusty
yellowy/brown
rough to touch
commonly on nose
how is actinic keratosis treated
removal or cryotherapy
chemotherapy creams = flourouracil cream (effudix)
imiquimod cream
what can be used for prognosis with malignant melanoma
Breslow thickness
= greater thickness from ulcerated to to deepest area of involvement = greater chance of mets
describe the classification system for cellulitis
Eron classification
1 = no systemic + no comorbidities
2 = systemically unwell or well + comorbidity
3 = significant systemic upset OR unstable comorbidities that intefere with tratment
4 = sepsis/nec fasc
how is eron 1 cellulitis treated
oral fluclox
oral clarithromycin/erythromycin/doxycycline if pen allergic/pregnant
how is eron class 3-4 cellulitis treated
admit
oral/IV co-amoxiclav
oral/IV clindamycin
IV cefuroxime or IV ceftriaxone
name an RNA virus
HIV
which viruses cause immune suppression
MMR
EBV
HIV
CMV
how does HIV cause immune dysfunction
- CD4 cell death:
- direct cytotoxicity
- impaired homeostasis
- premature apoptosis
- reduce T cell production - CD8 CTL increased activation but decrease cytotoxic function
- B cells increased activation but non-specific antibodies
- decreased function of:
- natural killer cells
- macrophages
- neutrophils
describe the progression of an HIV infection
- acute primary infection
low then high CD4 count (mounted response) - asymptomatic phase
progressive loss of CD4
generalised lymphadenopathy - early symptomatic phase
= manifestation of clinical features
= approx 5-10 years - AIDS = CD4 <200
name 6 examples of AIDS defining illnesses
kaposis sarcoma (Herpes 8)
pneumocystitis jirovecii pneumonia (PCP)
cytomegalovirus
candidiasis (oesophageal or bronchial)
lymphomas (non-hodgkins or primary CNS lymphoma)
TB
what does the 4th generation lab test check (HIV testing) and when is it reliable
HIV antibodies
p24 antigen
= reliable after 45 days
what is a normal CD4 range
500-1200
fever + rash + non-specific symptoms = what do we worry about?
HIV
do test!!
describe antiretroviral treatment
2 nucleoside reverse transcriptase inhibitors (NRTI)
plus 3rd agent
name 2 NRTIs
tenofovir
emtricitabine
what is given to HIV patients with a CD4 <200 and why
prophylactic co-trimoxazole to protect against PCP
What additional screening is needed in those with HIV
cardiovascular
yearly cervical smears
vaccinations (but NOT live vaccines)
what is given when pregnant women have an unknown viral load or a viral load >1000
IV zidovudine during labour
describe the prophylaxis given to babies of HIV +ve mothers
low risk = zidovudine 2-4 weeks
high risk = zidovudine + lamivudine + nevirapine 4 weeks
can HIV +ve mothers breastfeed
no, they should avoid
what is PEP
emtricitabine/tenofovir (truvada) + raltegravir for 28 days
what is PrEP
emtricitabine/tenofovir (truvada)
what is typhoid and what causes it
enteric fever (typhoid/paratyphoid) caused by salmonella typhi / paratyphi
describe the presentation of typhoid
diarrhoea (para) constipation (typh)
headache
fever
arthralgia
abdo pain
ROSE SPOTS
what is the possible complication of enteric fever in a patient with sickle cell
osteomyelitis
what is the treatment for enteric fever
- azithromycin
- (severe) IV ceftriazone/cefotaxime
how is ebola spread and what are the symptoms
human to human via direct contact with blood/secretions/organs/bodily fluids + contaminated surfaces and materials
2-21 day incubation
sudden onset fever/muscle pain/headache/sore throat
+ D+V + rash + internal/external haemorrhage + kidney/liver damage
what countries pose a high risk of typhoid
india
pakistan
bangladesh
anywhere with unsafe water
what is the treatment for ebola
supportive
what countries pose a high risk of malaria
nigeria
DRC
uganda
mozambique
what countries the highest risk of lassa fever
guinea
liberia
nigeria
sierra leone
what countries are the highest risk for Ebola
central/west africa:
Uganda
Guinea
DRC
what countries pose the highest risk of MERS
around arabian penninsula
bahrain
iran
jordan
kuwait
lebanon
oman
qatar
UAE
saudi arabia
yemen
what is Q fever
coxiella burnetii
caught from abattoir/cattle/sheep
inhaled from infected dust
presents with fever/malaise/atypical pneumonia
raised liver transaminases
treat with doxycyline
what is bilharzia and how does it prevent and how is it diagnosed
schistosomiasis
caused by parasite
caught in infested waters
abdo pain/diarrhoea/blood in stool
bladder cancer is later complication
eggs detected in stool/urine
how is schistosomiases treated
short course praziquantel
may need to repeat dose
fever
flu-like sympts
subconjunctival redness
in a farmer
= what disease? how is it spread?
leptospirosis
rat urine
how is leptospirosis diagnosed and treated
PCR
urine culture in 2nd week of illness
high dose benpen or doxycyline
fever
flu-like illness
subconjunctival redness
abdominal discomfort
AKI
yellowing sclera
= what is it?
Weil’s disease = later stage of leptospirosis
what is borrelia burgdorferi and how does it present
lyme disease
w/n 30 days:
erythema migrans = bulls-eye rash at site of tick bite
painless
increase in size
systemic features
describe the late features of lyme disease
heart block
peri/myocarditis
facial nerve palsy
radiculopathies
meningitis
how is lyme disease diagnosed and treated
clinically if rash present
first line: ELISA shows antibodies to borrelia burgdorferi
repeat 4-6 weeks later if suspected
>12 weeks presentation: immunoblot
TREATMENT
early: doxycyline
disseminated: ceftriaxone
fever
rash
tachycardia
after first dose of doxycyline for lyme disease
= what is this??
jarisch-herxheimer reaction
name 3 common HAI
MRSA
C.diff
E.coli
name the causative organisms in hospital acquired pneumonia
pseudomonas aeruginosa
E.coli
klebsiella
acinetobacter
what is stemmer’s sign
assess for lymphoedema
pinch skin of 2nd toe/finger
if cannot tent skin = +ve
how is fluid volume in the limb measured
bioelectric impedance spectrometry
electrodes placed on skin and current measured
resistance = volume of fluid
what alternative treatments are there for lymphoedema
lymphaticovenular anastamosis = surgical procedure attaching lymphatics to veins
antibiotics for infection
CBT/antidepressants to manage psychological
what other type of sarcomas are there and how can they present
bone sarcoma:
osteosarcoma
chondrosarcoma
ewing’s sarcoma
BONE PAIN
swelling/mass
pathological fractures
how can sarcomas be investigated
XR
CT
MRI
PET
biopsy
how is gastrointestinal stromal tumour sarcoma treated
tyrosine kinase inhibitors added on (imatinib)
how is aspirin overdose treated
urinary alkalinization with IV bicarb
haemodialysis
how is benzodiazepine overdose treated
flumazenil
(risk of seizures so careful monitoring)
how is tricyclic antidepressant overdose managed
IV bicarb to reduce risk of seizures
arrhythmias - AVOID quinidine/flecainide/amiodarone
how is lithium overdose managed
mild-mod:
volume resus (saline)
severe:
haemodialysis
?sodium bicarb to promote lithium excretion
how is warfarin overdose treated
vitamin K
how is heparin overdose treated
protamine sulphate
how is beta blocker overdose treated
bradycardic = atropine
resistant = glucagon
how is ethylene glycol overdose treated (antifreeze)
- fomepizole
- ethanol = competes for enzyme
how is methanol poisoning managed
fomepizole or ethanol
haemodialysis
how is organophosphate poisoning managed
atropine
how is digoxin overdose treated
digoxin-specific antibody fragments
how is iron overdose treated
desferrioxamine (chelating agent)
how is lead poisoning treated
dimercaprol
calcium edetate
how is carbon monoxide poisoning treated
100% oxygen
hyperbaric oxygen
how is cyanide poisoning treated
hydroxocobalamin
how do live vaccines work and give 3 examples
weakened form of pathogen
full natural immune response
B+T cell
e.g. MMR, BCG, yellow fever
describe how inactivated vaccines work and give 3 examples
pathogens that have been killed to elicit immune response
may require boosters
e.g. rabies, hep A, flu
describe how toxoid vaccines work and give 3 examples
inactivated toxin
immune system response to non-toxic toxoid
require boosters
e.g. tetanus, diptheria, pertussis
describe subunit/conjugate vaccines and give 3 examples
part of pathogen used to generate response
e.g. pneumococcus, hep B, haemophilus
what is a monovalent, multivalent, polyvalent vaccine
monovalent = against single strain of virus
e.g. measles
multivalent/polyvalent = multiple antigenic components
e.g. influenza
