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Phase 2a > Derm + ID/misc > Flashcards

Derm + ID/misc Flashcards

1
Q

which layer does normal proliferation of skin occur in

A

basal layer

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2
Q

what are the layers of the epidermis

A 
Come Lets Get Sun Burned
stratum corneum
stratum lucidum
stratum granulosum
stratum spinulosum
stratum basale
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3
Q

what do melanocytes develop from, where are they found and what is their role

A

melanoblasts develop into melanocytes
melanocytes found in the basal layer of epidermis
produce melanin pigment responsible for skin colour + UV protection

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4
Q

what do sebaceous glands produce

A

sebaceous secretions = lubricate and waterproof hairs

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5
Q

what do eccrine glands secrete

A

thin/watery sweat everyone on the body

= regulate body temp

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6
Q

what do apocrine glands secrete

A

secrete sweat = armpits/groin especially

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7
Q

what is acne vulgaris and describe the pathology of it

A

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

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8
Q

what causes acne vulgaris

A 
genetics
hormones
infections = propionibacterium acnes
high glycaemic diet
stress
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9
Q

how does acne present and how is it diagnosed

A 
inflammatory acne = comedones
inflammatory = papules/pustules and possible scarring
- whiteheads
- blackheads
- papules
- pimples
- nodules
diagnosed by presentation/age of onset/appearance
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10
Q

what is eczema and describe the 2 types

A 
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

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11
Q

how does eczema present

A 
ATOPIC 
= itchy red rash
= scaling and oozing
EXOGENOUS 
= sharply demarcated skin inflamm
= red, crusting, scaling, fissures, hyperpigmentation
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12
Q

how is eczema diagnosed

A

skin exam
skin biopsy/allergy test = make sure correct diagnosis
patch test for contact dermatitis

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13
Q

how is eczema treated

A 
no cure
ATOPIC
= avoid irritants
= regular emollients to hydrate
= corticosteroids
= calcineurin inhibitors = TACROLIMUS (immunosuppressive)
EXOGENOUS
= avoid irritants
= steroid cream
= antipruritic cream
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14
Q

what are the differentials for eczema

A

allergic contact dermatitis
seborrheic dermatitis
scabies
immunodeficiency

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15
Q

what is psoriasis and what are the different types

A

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

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16
Q

how does psoriasis present

A

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

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17
Q

how is psoriasis investigated and treated

A 
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
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18
Q

what are skin ulcers

A

abnormal breaks in epithelial surface

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19
Q

what are the causes of skin ulcers

A 
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
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20
Q

how do skin ulcers present

A

open craters often round with eroded skin inside
bleeding
pain in skin surrounding ulcer
swollen/red tissue

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21
Q

how to take a history for an ulcer

A
  1. number/pain/trauma
  2. comorbidities ?
  3. steroid use?
  4. self induced?
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22
Q

how are skin ulcers investigated

A 
examination = site/number/SA/depth etc
skin/ulcer biopsy
fluid discharge = culture and Ab sensitivity 
radiograph = check for osteomyelitis
CXR = possible TB manifestation
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23
Q

how are skin ulcers treated

A 
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
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24
Q

what is cellulitis and what causes it

A

deep skin infection caused by S. pyogenes (and S.Aureus)

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25
Q

what are the RFs for cellulitis

A 
immunosuppression
diabetes
poor peripheral circulation
athletes foot
IVDU
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26
Q

how does cellulitis present

A

erythematous rash with oedema

fever/malaise/fatigue

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27
Q

how is cellulitis diagnosed

A 
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
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28
Q

how is cellulitis managed

A

flucloxacillin

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29
Q

what is necrotising fasciitis and what is it caused by

A 
infection of soft tissue that results in necrosis caused by:
MRSA
S.Aureus
**S. Pyogenes**
E.coli
P.Aeruginosa
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30
Q

how does necrotising fasciitis present

A 
intense pain of skin and underlying muscle
red/purple skin
pyrexia/nausea/vomiting/malaise/myalgia
bleeding into skin
loss of sensation
SHOCK
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31
Q

how is necrotising fasciitis diagnosed

A

clinical
if in doubt make a cut and if finger can separate fascia = diagnosis
bloods = WCC + CRP high

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32
Q

how is necrotising fasciitis treated

A

rapid surgical debridement

IV antibiotics = benzylpenicillin, clindamycin, vancomycin, gentamycin

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33
Q

describe skin cancer

A

neoplastic lesions of skin
basal-cell carcinoma
squamous-cell carcinoma
malignant melanoma

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34
Q

what are the RFs/causes of skin cancer

A 
HPV infection
smoking
UV sun exposure
ionizing radiation
BRAF/KIT gene mutations
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35
Q

how does a malignant melanoma present

A 
ABCDE
Asymmetry
irregular Borders
uneven Colour
Diameter >6mm
Evolving size/colour/shape
glasgow 7 point checklist
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36
Q

how is malignant melanoma treated

A

urgent excision
chemo if metastatic
ipilimumab = biologic improves survival

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37
Q

how does a squamous cell carcinoma present

A

red/scaling skin plaques with keratinised crust

ulceration with hard raised edges in sun exposed sites

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38
Q

how is squamous cell carcinoma treated

A

excision and radiotherapy to treat recurrence/affected nodes

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39
Q

how does basal cell carcinoma present

A 
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
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40
Q

how is basal cell carcinoma treated

A

excision
cryotherapy/radiotherapy if need
superficial BCC = topical flourouracil or imiquimod

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41
Q

what dosage of paracetamol constitutes an overdose

A

12g or 150mg/kg patient

if malnourished than 75mg/kg

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42
Q

how does paracetamol overdose present

A

no symptoms/signs initially OR RUQ and vomiting
later = jaundice and encephalopathy
acute kidney injury

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43
Q

how is paracetamol overdose diagnosed and managed

A

diagnosis = mainly from history but pt may lie
GI decontamination if <4hr after OD = activated charcoal 1g/kg
N-acetylcysteine (NAC) IV = antidote

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44
Q

describe the physiology of paracetamol OD and the effect of NAC (4)

A
  1. paracetamol metabolised to reactive intermediate by CYP450
  2. reactive intermediate to stable metabolite by glutathione transferase GSH
  3. OD = overwhelms GSH, not enough to convert to safe metabolite
  4. NAC = precursor to glutathione, allows regeneration of GSH
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45
Q

describe the indicators for paracetamol-induced liver failure

A 
late presentation = NAC less effective 
acidosis
PTT >70secs
serum Cr > or = 300 micromols/L
= CONSIDER LIVER TRANSPLANT
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46
Q

what is amyloidosis

A

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

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47
Q

how does primary amyloidosis present in the KIDNEYS and HEART

A

KIDNEYS:
glomerular lesions/proteinuria/nephROtic syndrome
= oedema
= tiredness/weak/loss of appetite
HEART:
restrictive cardiomyopathy/arrythmias/angina
= oedema/SOB

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48
Q

how does primary amyloidosis present in the NERVES, GUT and VASCULAR

A 
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!!!!
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49
Q

what is the characteristic feature of primary amyloidosis

A

peri-orbital purpura = PURPLE BRUISED AROUND EYES

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50
Q

how is primary amyloidosis treated

A

optimise nutrition
melphalan = chemo
prednisolone
high dose IV melphalan with stem cell transplant may be better

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51
Q

what is secondary amyloidosis

A

amyloid is derived from serum amyloid A

= chronic inflammation in RA, Crohns, chronic infections

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52
Q

how does secondary amyloidosis present and how is it treated

A 
KIDNEYS/LIVER/SPLEEN
= proteinuria
= nephrOtic syndrome
= hepatosplenomegaly
= NO big tongue
TREAT UNDERLYING CAUSE
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53
Q

what is familial amyloidosis

A

autosomal dominant
usually sensory/autonomic neuropathy
renal/cardiac involvement
liver transplant can CURE

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54
Q

how is amyloidosis investigated

A

biopsy taken from infected area = look for amyloid deposits

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55
Q

what is lymphoedema

A

chronic non-pitting oedema due to lymphatic insufficiency
= most commonly legs
= chronic can cause secondary cobblestone thickness of skin

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56
Q

what are the 2 types of lymphoedema

A 
primary = due to faulty genes e.g. miliary disease
secondary = due to lymph damage e.g. filarial infection
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57
Q

what is miliary disease

A

autosomal dominant = VEGFR3
primary congenital lymphoedema
lower leg swelling from birth
Tx = compression stockings and exercise

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58
Q

what is filarial infection

A

transmitted by 5 genera of mosquito
acute = fever, lymphodenopathy, chyluria (white urine)
causes elaphantitis/massive hydrocele

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59
Q

what is a sarcoma

A

cancer arising from cells of mesenchymal origin

= malignant tumours of cancellous bone/cartilage/fat/muscle/vascular/haemopoeitc tissue

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60
Q

describe soft tissue sarcoma

A 
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
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61
Q

what is duct ectasia

A

inflammation and dilation of large breast ducts
menopausal women
causes nipple discharge(green), pain, mass
no Tx

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62
Q

what is a fibroadenoma

A

benign fibroepithelial tumour of breast = well circumscribed nodular mass
excision if large but mainly observe and reassure
no capacity for malignant behaviour

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63
Q

what is an intraductal papilloma

A

benign papillary tumour within duct system of breast
= nipple discharge (+/-blood stained) and possible outward growing pailloma
often no lump
YOUNGER patients
Tx = excision

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64
Q

what is fat necrosis in the breast

A

inflammatory reaction to damaged adipose tissue
= palpable mass
= clinically mimics carcinoma
no Tx once diagnosis confirmed = benign with no risk of cancer

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65
Q

what are breast cysts

A

common in over 35s
benign fluid filled rounded lump
occasionally painful
diagnosis confirmed on aspiration

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66
Q

what are the risk factors for breast carcinoma

A 
early menarche/late menopause
increased weight
high alcohol consumption
oral contraceptive use
positive family history
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67
Q

describe the triple assessment for breast lumps

A
  1. clinical exam
  2. histology/cytology
  3. mammography/ultrasound
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68
Q

describe the staging of breast carcinoma

A
  1. confined to breast, mobile
  2. confined to breast, lymph nodes of ipsilateral
  3. tumour fixed to muscle, ipsilateral lymph nodes matted, skin involvement
  4. complete fixation of tumour to chest wall, distant mets
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69
Q

describe the treatment for stage 1 and 2 breast carcinoma

A
  1. wide surgical excision WSE/mastectomy
  2. radiotherapy for invasive after WSE
  3. chemo = adjuvant improves survival and reduce recurrence
  4. endocrine agents = lower oestrogen activity foe oestrogen receptor +ve cancer
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70
Q

describe the treatment for stage 3 or 4 breast carcinoma

A
  1. staging investigations (CXR, USS, MRI, PET for mets)
  2. radiotherapy for bony lesions
  3. tamoxifen for ER+ve
  4. CNS surgery for solitary mets
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71
Q

what chemotherapy is used for pre and post menopausal women

A 
pre-menopausal = tamoxifen
post-menopausal = anastrozole
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72
Q

what is a ductal carcinoma in situ

A

neoplastic proliferations arising from terminal duct with increased risk of progression to invasive breast carcinoma
genetic linked
lump/nipple discharge/nipple changes
Tx = excision

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73
Q

what is an invasive breast carcinoma

A

malignant invasive tumour of breast with capacity to SPREAD to distant sites
= breast lump
graded histologically
Tx = surgery/chemo/hormone tx/local radiotherapy

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74
Q

what is condylomata accuminata and what is it caused by

A

genital warts
caused by HPV 6+11 (+ others)
small fleshy protuberances slightly pigmented
may bleed or itch

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75
Q

how are genital warts treted

A
  1. topical podophyllum or cryotherapy
    multiple = topical
    solitary = cryotherapy
  2. imiquimod cream
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76
Q

what are the 2 main types of contact dermatitis

A
  1. irritant contact = common
    non-allergic reaction
    due to weak acids/alkali
    typical erythema + crusting (no vesicles)
  2. allergic contact dermatitis
    type 4 hypersensitivity
    weeping eczema on margins of hair line (after hair dye)
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77
Q

what is pruritus ani

A

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

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78
Q

what is pruritus vulvae

A

vaginal itching
usually has an underlying cause
irritant contact dermatitis most common cause
TREATMENT
- clean 1x day with emollient
- topical steroids

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79
Q

what are the most important non-skin causes to think about with itchy skin

A

liver disease
iron deficiency anaemia
polycythaemia (after warm bath)
chronic kidney disease
lymphoma

80
Q

what is male androgenetic alopecia

A

male pattern hair loss
begins 20-25
50% white men affected by 50

81
Q

what are the treatment options for male androgenetic alopecia

A

nothing
topical minoxidil or oral finasteride
wigs
hair transplant

82
Q

what is alopecia areata

A

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

83
Q

what drugs commonly cause urticaria

A

aspirin
NSAIDs
penicillin
opiates

84
Q

what is the most common type of drug erruption

A

morbilliform (measles-like)
exanthematous (systemic)
urticaria/angioedema

85
Q

what is a fixed drug erruption

A

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

86
Q

describe urticaria

A

pale pink raised skin
hives/wheals/nettle rash
pruritic

87
Q

how is urticaria managed

A
  1. non-sedating antihistamines = loratidine/cetirizine
  2. sedating antihistamine if affecting sleep
  3. prednisolone for severe or resistant episodes
88
Q

describe aquagenic urticaria

A

urticaria after contact with water/change in temp
no rash associated
responds poorly to antihistamines
treat with phototherapy

89
Q

what skin condition can predate polycythaemia rubra vera and what are the consequences for management

A

aquagenic urticaria
predate by 5 years
annual FBC needed

90
Q

what medications cause drug-induced photosensitivity

A

thiazide diuretics
tetracyclines/sulphonamides/ciprofloxacin
amiodarone
NSAIDs
psoralens
sulphonylureas

91
Q

name 2 large vessel vasculitides

A

temporal arteritis
takayasu’s arteritis

92
Q

name 2 medium vessel vasculitides

A

polyarteritis nodosa
kawasakis disease

93
Q

describe small vessel vasculitides giving examples

A

ANCA associated:
- granulomatosis w polyangiitis
- churg-strauss syndrome
- microscopic polyangiitis
immune complex:
- Henoch-schonlein purpura
- goodpasture’s syndrome
- anti C1q vasculitis

94
Q

palpable purpuric rash
abdominal pain
polyarthritis
haematuria
in a child following an infection
suggests what disease

A

henoch-schonlain purpura
excellent prognosis
monitor urine and renal function

95
Q
  • epistaxis
  • sinusitis
  • saddle nose
  • dyspnoea
  • vasculitis rash
  • eye involvement
    = indicated what disease and whats the management
A

granulomatosis with polyangiitis
cANCA +ve
CXR
renal biopsy
Tx:
steroids
cyclophosphamide
plasma exchange
8-9 year survival

96
Q
  • vasculitis
  • sinusitis
  • dyspnoea
  • asthma
  • eosinophilia >10%
    indicates what disease
A

churg-strauss
pANCA +ve

97
Q

45 year old man presenting:
- fever
- weight loss
- testicular pain
- hypertension
- haematuria
- +ve Hep B serology
what is it? and what is the treatment?

A

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

98
Q

what is bullous pemphigoid

A

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

99
Q

what is pemphigus vulgaris

A

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

100
Q

how are pemphigus and pemphigoid different

A

pemphigus = mucosal involvement
pemphigoid = no mucosal involvement

101
Q

what type of ulcer is this? what is the management?
- odoema
- brown pigmentation of skin
- eczema
- painless

A

venous ulcer
4 layer compression banding after excluding arterial disease
?skin graft

102
Q

what type of ulcer is this? and why is it significant?
- at site of chronic inflammation (burn, old osteomyelitis)
- mainly in the lower limb

A

marjolin’s ulcer
= squamous cell carcinoma

103
Q

what type of ulcer is this? what is the treatment?
- on the heel/toes
- painful
- deep/punched out
- cold
- no pulse
- low ABPI

A

arterial ulcer
- restoring bloodflow (surgery)
- prevent infection
- wound care

104
Q

what type of ulcer is this? what is the treatment?
- over plantar surface of big toe/metatarsal head
- associated w diabetes
- due to pressure

A

neuropathic ulcer
cushioned shoes needed to reduce callous formation

105
Q

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

A

pyoderma gangrenosum
treat by removing necrotic tissue
potent steroids
tacrolimus ointment
special dressings

106
Q

what is seborrhoeic keratosis

A

benign skin disease
>50y/o
flat raised filiform pedunculated lesions over trunk/face
colour varies
leave alone or chop off

107
Q

what is the fancy name for a mole

A

melanocytic naevi

108
Q

what is congenital melanocytic naevi

A

appear soon or after birth
usually >1cm
increased risk of malignant transformation

109
Q

which naevi would you commonly find on the palms and soles

A

junctional melanocytic naevi

110
Q

which naevi are pinky red, appear in children and are often excised

A

spitz naevi
similar appearance to melanoma

111
Q

what is atypical naevus syndrome

A

autosomal dominant
increased risk of melanoma

112
Q

what is the difference between a an epidermoid cyst and a pilar cyst

A

epidermoid cyst lining is normal epidermis
pilar cyst lining is root of hair follicle

113
Q

describe mild, moderate and severe acne

A

MILD
open/closed comedones +/- sparse inflammatory lesions
MODERATE
widespread non inflamm lesions + numerous papules + pustules
SEVERE
extensive inflamm lesions +/- nodules, pitting, scarring

114
Q

describe the treatment for mild to moderate acne

A

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)

114
Q

what is important to remember when treating acne in pregnancy + children <12

A

tetracyclines cannot be used
switch doxycycline to erythromycin

114
Q

describe the treatment for moderate to severe acne

A

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

115
Q

how long can oral antibiotics be used for acne

A

up to 6 months

116
Q

what is a potential side effect of long term antibiotic use

A

gram negative folliculitis
treat with trimethoprim

117
Q

what is an alternative to oral antibiotics for acne for women

A

COCP

118
Q

describe the superficial lymphatic vessels of the lower limb

A

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

119
Q

describe the deep lymphatic vessels of the lower leg

A

anterior tibial
posterior tibial
peroneal
= each follow the artery
= enter popliteal lymph nodes

120
Q

describe the venous drainage of the lower limb via the deep veins

A

dorsal venous arch
V
anterior tibial veins + fibular veins (+posterior tibial vein)
V
popliteal vein
V
femoral vein
V
external iliac vein

121
Q

describe the venous drainage of the lower limb via the superficial veins

A

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)

122
Q

what is actinic keratosis

A

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

123
Q

how is actinic keratosis treated

A

removal or cryotherapy
chemotherapy creams = flourouracil cream (effudix)
imiquimod cream

124
Q

what can be used for prognosis with malignant melanoma

A

Breslow thickness
= greater thickness from ulcerated to to deepest area of involvement = greater chance of mets

125
Q

describe the classification system for cellulitis

A

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

126
Q

how is eron 1 cellulitis treated

A

oral fluclox
oral clarithromycin/erythromycin/doxycycline if pen allergic/pregnant

127
Q

how is eron class 3-4 cellulitis treated

A

admit
oral/IV co-amoxiclav
oral/IV clindamycin
IV cefuroxime or IV ceftriaxone

128
Q

name an RNA virus

A

HIV

129
Q

which viruses cause immune suppression

A

MMR
EBV
HIV
CMV

130
Q

how does HIV cause immune dysfunction

A
  1. CD4 cell death:
    - direct cytotoxicity
    - impaired homeostasis
    - premature apoptosis
    - reduce T cell production
  2. CD8 CTL increased activation but decrease cytotoxic function
  3. B cells increased activation but non-specific antibodies
  4. decreased function of:
    - natural killer cells
    - macrophages
    - neutrophils
131
Q

describe the progression of an HIV infection

A
  1. acute primary infection
    low then high CD4 count (mounted response)
  2. asymptomatic phase
    progressive loss of CD4
    generalised lymphadenopathy
  3. early symptomatic phase
    = manifestation of clinical features
    = approx 5-10 years
  4. AIDS = CD4 <200
132
Q

name 6 examples of AIDS defining illnesses

A

kaposis sarcoma (Herpes 8)
pneumocystitis jirovecii pneumonia (PCP)
cytomegalovirus
candidiasis (oesophageal or bronchial)
lymphomas (non-hodgkins or primary CNS lymphoma)
TB

133
Q

what does the 4th generation lab test check (HIV testing) and when is it reliable

A

HIV antibodies
p24 antigen
= reliable after 45 days

134
Q

what is a normal CD4 range

A

500-1200

135
Q

fever + rash + non-specific symptoms = what do we worry about?

A

HIV
do test!!

136
Q

describe antiretroviral treatment

A

2 nucleoside reverse transcriptase inhibitors (NRTI)
plus 3rd agent

137
Q

name 2 NRTIs

A

tenofovir
emtricitabine

138
Q

what is given to HIV patients with a CD4 <200 and why

A

prophylactic co-trimoxazole to protect against PCP

139
Q

What additional screening is needed in those with HIV

A

cardiovascular
yearly cervical smears
vaccinations (but NOT live vaccines)

140
Q

what is given when pregnant women have an unknown viral load or a viral load >1000

A

IV zidovudine during labour

141
Q

describe the prophylaxis given to babies of HIV +ve mothers

A

low risk = zidovudine 2-4 weeks
high risk = zidovudine + lamivudine + nevirapine 4 weeks

142
Q

can HIV +ve mothers breastfeed

A

no, they should avoid

143
Q

what is PEP

A

emtricitabine/tenofovir (truvada) + raltegravir for 28 days

144
Q

what is PrEP

A

emtricitabine/tenofovir (truvada)

145
Q

what is typhoid and what causes it

A

enteric fever (typhoid/paratyphoid) caused by salmonella typhi / paratyphi

146
Q

describe the presentation of typhoid

A

diarrhoea (para) constipation (typh)
headache
fever
arthralgia
abdo pain
ROSE SPOTS

147
Q

what is the possible complication of enteric fever in a patient with sickle cell

A

osteomyelitis

148
Q

what is the treatment for enteric fever

A
  1. azithromycin
  2. (severe) IV ceftriazone/cefotaxime
149
Q

how is ebola spread and what are the symptoms

A

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

150
Q

what countries pose a high risk of typhoid

A

india
pakistan
bangladesh
anywhere with unsafe water

150
Q

what is the treatment for ebola

A

supportive

150
Q

what countries pose a high risk of malaria

A

nigeria
DRC
uganda
mozambique

151
Q

what countries the highest risk of lassa fever

A

guinea
liberia
nigeria
sierra leone

152
Q

what countries are the highest risk for Ebola

A

central/west africa:
Uganda
Guinea
DRC

153
Q

what countries pose the highest risk of MERS

A

around arabian penninsula
bahrain
iran
jordan
kuwait
lebanon
oman
qatar
UAE
saudi arabia
yemen

154
Q

what is Q fever

A

coxiella burnetii
caught from abattoir/cattle/sheep
inhaled from infected dust
presents with fever/malaise/atypical pneumonia
raised liver transaminases
treat with doxycyline

155
Q

what is bilharzia and how does it prevent and how is it diagnosed

A

schistosomiasis
caused by parasite
caught in infested waters
abdo pain/diarrhoea/blood in stool
bladder cancer is later complication
eggs detected in stool/urine

156
Q

how is schistosomiases treated

A

short course praziquantel
may need to repeat dose

157
Q

fever
flu-like sympts
subconjunctival redness
in a farmer
= what disease? how is it spread?

A

leptospirosis
rat urine

158
Q

how is leptospirosis diagnosed and treated

A

PCR
urine culture in 2nd week of illness
high dose benpen or doxycyline

159
Q

fever
flu-like illness
subconjunctival redness
abdominal discomfort
AKI
yellowing sclera
= what is it?

A

Weil’s disease = later stage of leptospirosis

160
Q

what is borrelia burgdorferi and how does it present

A

lyme disease
w/n 30 days:
erythema migrans = bulls-eye rash at site of tick bite
painless
increase in size
systemic features

161
Q

describe the late features of lyme disease

A

heart block
peri/myocarditis
facial nerve palsy
radiculopathies
meningitis

162
Q

how is lyme disease diagnosed and treated

A

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

163
Q

fever
rash
tachycardia
after first dose of doxycyline for lyme disease
= what is this??

A

jarisch-herxheimer reaction

164
Q

name 3 common HAI

A

MRSA
C.diff
E.coli

165
Q

name the causative organisms in hospital acquired pneumonia

A

pseudomonas aeruginosa
E.coli
klebsiella
acinetobacter

166
Q

what is stemmer’s sign

A

assess for lymphoedema
pinch skin of 2nd toe/finger
if cannot tent skin = +ve

167
Q

how is fluid volume in the limb measured

A

bioelectric impedance spectrometry
electrodes placed on skin and current measured
resistance = volume of fluid

168
Q

what alternative treatments are there for lymphoedema

A

lymphaticovenular anastamosis = surgical procedure attaching lymphatics to veins
antibiotics for infection
CBT/antidepressants to manage psychological

169
Q

what other type of sarcomas are there and how can they present

A

bone sarcoma:
osteosarcoma
chondrosarcoma
ewing’s sarcoma
BONE PAIN
swelling/mass
pathological fractures

170
Q

how can sarcomas be investigated

A

XR
CT
MRI
PET
biopsy

171
Q

how is gastrointestinal stromal tumour sarcoma treated

A

tyrosine kinase inhibitors added on (imatinib)

172
Q

how is aspirin overdose treated

A

urinary alkalinization with IV bicarb
haemodialysis

173
Q

how is benzodiazepine overdose treated

A

flumazenil
(risk of seizures so careful monitoring)

174
Q

how is tricyclic antidepressant overdose managed

A

IV bicarb to reduce risk of seizures
arrhythmias - AVOID quinidine/flecainide/amiodarone

175
Q

how is lithium overdose managed

A

mild-mod:
volume resus (saline)
severe:
haemodialysis
?sodium bicarb to promote lithium excretion

176
Q

how is warfarin overdose treated

A

vitamin K

177
Q

how is heparin overdose treated

A

protamine sulphate

178
Q

how is beta blocker overdose treated

A

bradycardic = atropine
resistant = glucagon

179
Q

how is ethylene glycol overdose treated (antifreeze)

A
  1. fomepizole
  2. ethanol = competes for enzyme
180
Q

how is methanol poisoning managed

A

fomepizole or ethanol
haemodialysis

181
Q

how is organophosphate poisoning managed

A

atropine

182
Q

how is digoxin overdose treated

A

digoxin-specific antibody fragments

183
Q

how is iron overdose treated

A

desferrioxamine (chelating agent)

184
Q

how is lead poisoning treated

A

dimercaprol
calcium edetate

185
Q

how is carbon monoxide poisoning treated

A

100% oxygen
hyperbaric oxygen

186
Q

how is cyanide poisoning treated

A

hydroxocobalamin

187
Q

how do live vaccines work and give 3 examples

A

weakened form of pathogen
full natural immune response
B+T cell
e.g. MMR, BCG, yellow fever

188
Q

describe how inactivated vaccines work and give 3 examples

A

pathogens that have been killed to elicit immune response
may require boosters
e.g. rabies, hep A, flu

189
Q

describe how toxoid vaccines work and give 3 examples

A

inactivated toxin
immune system response to non-toxic toxoid
require boosters
e.g. tetanus, diptheria, pertussis

190
Q

describe subunit/conjugate vaccines and give 3 examples

A

part of pathogen used to generate response
e.g. pneumococcus, hep B, haemophilus

191
Q

what is a monovalent, multivalent, polyvalent vaccine

A

monovalent = against single strain of virus
e.g. measles
multivalent/polyvalent = multiple antigenic components
e.g. influenza

Phase 2a (15 decks)

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