Medical Shorts Flashcards
Symmetrical well-defined salmon-pink plaques
Silvery micaceous scale
Located:
Extensors
Behind ears
Scalp
Umbilicus
Sites of trauma: Kobner phenomenon
May see skin staining form treatment:
Coal tar (brown)
Dithranol (purple)
This is Psoriasis
Other DDx
Bowmen’s disease (squamous cell carcinoma in situ)
Lichen planus
Dermatitis
Nails changes in Psoriasis
Discolouration
Pitting
Onycholysis
Subungual hyperkeratosis
Subtypes of Psoriasis
Guttate: drop-like lesions on the trunk, commoner in children following streptococcal throat infection
Pustular: generalised or palmo-plantar
Erythroderma
Flexural: not scaly
Pathogenesis of psoriasis
Type IV cell-driven hypersensitivity
Hyperkeratosis
Parakeratosis
Intra-epidermal micoacscesses (of Munro)
Psoriatic Arthritis
Seronegative arthritis develops in 10-40%
Asymmetric oligoarthritis (2-4 joints)
Distal arthritis
Symmetric polyarthritis may mimic Rheumatoid Arthritis
Spondylitis
Arthritis mutilans: severe form of rheumatoid or psoriatic arthritis –> resorption of bones and the consequent collapse of soft tissue
Management of Psoriatic Arthritis
General
MDT: GP, Dermatoligst, Specialist nurse
Avoid precipitants: Ethanol, beta-blockers, smoking, stress
Topical
Emollients: Epaderm, Dermol, Diprobase
Steroids: Betometasone
Vit D analogues: Calcipotriol (Combination+ betometasone = dovobet)
Coal Tar
Dithranol
Phototherapy
PUVA
Narrow-band UVB
Systemic
Ciclosporin, Methotrexate
Retinoids: acetretin
Biologics: Anti-TNF
Erythematous lichenified patches
Predominantly the flexors
Excoriations
Painful fissures
This is Dermatitis
DDx
Just hands = contact / irritant dermatitis
Atopic eczema
Discoid: well-demarcated patches on trunk and limbs
Sebhorrhoeic dermatitis
Management of Dermatitis
General
MDT: GP, Dermatologist, Specialist nurse
Avoid precipitants
Anti-histamines can help pruritis (break cycle)
Antibiotics for any infections (Flucloxacillin)
Topical
Emollients: Dermol, Epaderm, Diprobase
Soap substitutes: Dermol, Epaderm
First-line: steroids
Second line: Tacrolimus
Phototherapy
Systemic steroids if very severe
Cutaneous Manifestations of Diabetes Melitus
Hands
Cheiroarthoprathy: thickened skin and limited joint mobility of the hands and fingers, leading to flexion contractures
Prayer sign: inability to flatten hands
Granuloma annulare: flesh coloured papules in annular configuration, usually on dorsum of hand
Capillary glucose testing marks on finger tips
Injection Sites
Shoulders, abdomen and thighs
Lipodystrophy
Shins
Necrobiosis lipoidica diabeticorum: well-demarcated waxy, bruise-like plaques, prominent blood vessels, 90% female
Feet
Charcot’s joint
Ulcers: heel, metatarsal head, digits
Other
Infections: candida, cellulitis
Eruptive tendon xanthoma seocndary to hyperlipidaemia
Granuloma Annulare
Flesh-coloured papules in annular configuration
Usually on dorsum of hand
Associated with Diabetes Melitus
Cheiroarthropathy
Demonstration of the Prayer Sign
Tight waxy skin that limits finger extension
Necrobiosis Lipoidica Diabeticorum
Well-dermarcated waxy, bruise-like plaqyes
Prominent blood vessels
Assoc with diabetes melitus
90% females
Neuropathic arthropathy (or neuropathic osteoarthropathy)
Progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity due to loss of sensation
Tendon Xanthoma
Seconday to hyperlipideaemia
Pearly nodule with rolled telangiectactic edge
On face, or sun-expsoed areas
Most common skin cancer
Slowly gorwing destructive: “rodent ulcer”
Do not metastasise
Mx:
Superficial: surgical removal
Deep: surgical removal + radiotherapy
Ulcerated lesion with an everted edge
Sun-exposed areas
Actinic keratosis —> Bowen’s —-> Squamous cell carcinoma
Actinic keratosis: irregular, crusty, warty lesion
Bowen’s: red/brown scaly plaques
Risk Factors
Sun exposure
Immunosuppression e.g. ciclosporin
Genetic: xerodermapigmentosum
Chronic trauma: Marjolin’s ulcer
Mx
Surgery and radiotherapy
Malignant Melanoma
Fair skin with freckles (Fitzpatrick I)
Blue eyes, lights hair
Lesion:
Asymmetrical
Boarder: irregular
Colour: non-uniform
Diameter >6mm
Evolving / elevating
Examine regional LNs
Fundoscopy
Liver
Glass eye + Ascites = Occular melanoma
Risk Factors
Sun exposure, esp. when young
Low Fitzpatrick skin type
Increase number of mole
FHx
Increased age
Immunosuppression
Glass eye AND Ascites
= Ocular Melanoma
Classification of Malignant Melanoma
Superficial spreading: 80%
Lentigo maligna melanoma: elderly patients
Acral lentiginous
Nodular
Amelanotic: delayed diagnosis
Management of Malignant Melanoma
Staging
Breslow Depth
Clarke’s levels
Mx
Excision biopsy for staging
Seconday excision margin depends on stage
+/- lymphadenectomy
+/- adjuvant chemo
Mohs Surgery
Most effective technique for treating many basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs)
The procedure is done in stages, including lab work, while the patient waits.
This allows the removal of all cancerous cells for the highest cure rate while sparing healthy tissue and leaving the smallest possible scar.
Neurofibromatosis
Skin
Cafe-au-lait spots: 6 or more, >15mm in diameter
Axillary freckling
Nuerofibromas: gelatinois violaceous nodules
Eyes
Lisch nodules: melanocytic hamartomas of the iris
Extras
Visual acuity: optic glioma
Back: scoliosis
BP: renal artery stenosis and phaeochromocytoma
Palpable nerves
Peripheral neuropathy
Lisch Nodules
Melanocytic hamartomas of the iris
Complications of Neurofibromatosis
Epilepsy
Sarcomatous change: 5%
Scoliosis: 5%
Learning difficulty: 10%
Management of Neurofibromatosis
MDT: GP, neurologist, specialist nurse, Surgeons
Excision of problematic neurofibromas
Monitor complications
Yearly BP and cutaenous review
Treat epilepsy
Genetic counselling
Causes of Neurofibromatosis
Autosomal Dominant
NF1: Chromosome 17
1 in 2,500
NF2: Chromosome 22
1 in 35,000
Differential of Cafe-au-lait Spots
Neurofibromatosis
McCune Albright
Cafe-au-lait spots
Polyostotic fibrous dysplasia
Endocrinopathy –> precocious puberty
Tuberous sclerosis
Tuberous Sclerosis
Autosomal Dominant
Chromosome 16
Skin
Facial adenoma sebaceum: perinasal angiofibromata
Periungual fibromas: hands and feet
Shagreen-patch: roughended leathery skin over sacrum
Ash-leaf macule: hypopigmented macule on trunk (fluroresce with UV / Wood’s lamp)
Cafe-au-lait spots
Extras
Fundus: retinal phakomas (dense white patches)
Lungs: cystic lung disease
Abdomen: renal enlargement due to cysts or transplanted kidney
Signs of phenytoin use (80% epileptic): ginigval hypertrophy, hisutism
Invx
Skull films: railroad track calcification
CT/MRI brain: tuberous mass in cortex
Abso USS: renal cyst
Ech: Cardiomyopathy (rhabdomyomas)
Alport’s Syndrome
X-linked dominant pattern
Defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM)
Presents in childhood
Mmicroscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus: protrusion of the lens surface into the anterior chamber
Retinitis pigmentosa
Renal biopsy: splitting of lamina densa seen on electron microscopy
Hereditary Haemorrhagic Telangiectasia
= Osler-Weber-Rendu Syndrome
Autosomal dominant
Telangiectasia
AVMs: lungs, liver, brain
Inspection
Multiple telangiectasia on face, lips and buccal mucosa
Cyanosis: can have larhe pulmonary AVMs
No signs of CREST
DDx
HHT
Scleroderma
Chronic liver disease
Ataxia telangiectasia
Compliations
Haemorrhage: epistaxis, GI haemorrhage, Haemoptysis, SAH
High-output cardiac failure
Increased risk of Colorectal cancer with SMAD4 mutation
(A) telangiectasia on the periungal regions of the fingers
(B) telangiectasia on the lips
(C) telangiectasia on the oral mucosa
(D) bleeding foci in the Kisselbach’s plexus
(E) microtelangia on the tongue
(F) clubbing fingers with one small hemangioma
Peutz-Jeghers
Autosomal dominant mutation of STK11 gene on chromosome 19
Mucocutaneous macules
GI hamartomatous polyps
Small pigmented macules on lips, oral mucosa, palms and soles
DDx
Peutz-Jeghers
Carney Complex
McCune-Albright
Simple freckles
Complications
GI hamartomas: GI bleeding and intussusception
PAncreatic endocrine tumours
Increased risk of colorectal carcinoma
Erythema Multiforme
Symmetrical targetoid lesions
esp. Extensor surfaces of peripheries
Initial lesions are sharply demarcated, round, red/pink and flat (macules), which become raised (papules/palpable) and gradually enlarge to form plaques (flat raised patches) up to several centimetres in diameter
DDx of lesions with central clearing:
Erythema multiforme,
Discoid eczema
Tinea
Causes
Infection
- HSV (70%)
- Mycoplasma
Drugs
- Sulfonamides
- NSAIDs
- Allopurinol
- Penicillin
- Phenytoin
Stevens-Johnson syndrome and TEN are distinct severe forms of EM
Erythema Nodosum
Tender bkue/red smooth shiny nodules
Commonly found on shins but can be anywhere with subcutaneous fat
Older lesions leave a bruise
Extras
Parotid swelling: Sarcoidosis
Red, sore throat: Streptococcal infection
Joint pain, oral ulceration: Behcet’s
Causes
Systemic
- Sarcoidosis
- IBD
- Behcet’s
Infection
- Steptococcal infection
- TB
Drugs
- Sulphonamides
- OCP
Rheumatoid Arthritis Hands
Joints:
PIP and MCP joints (especially 2nd and 3rd MCP)
Ulnar styloid
Triquetrum
As a rule, the DIP joints are spared
Late changes include:
Subchondral cyst formation: the destruction of cartilage presses synovial fluid into the bone
Subluxation causing:
Ulnar deviation of the MCP joints
Boutonniere and swan neck deformities
Hitchhiker’s thumb deformity
Carpal instability: scapholunate dissociation, ulnar translocation
Ankylosis
Swan-neck deformity
Hyper-extension of PIP
Flexion of DIP
Due to lateral bands drifting dorsally
exacerbate hyperextension at PIP
unable to extend at DIP, unopposed profundus causes flexion at DIP
rheumatoid arthritis (classical association)
post-traumatic: particular post mallet finger injury
scleroderma
psoriatic arthritis
systemic lupus erythematosus arthropathy
Boutonniere Deformity
Flexion at PIP
Extension at DIP
Due to central tendon slip
Pathology of Rheumatoid Arthritis
Genetic predisposition (HLA-DR B1 )
Environmental trigger (Epstein-Barr virus postulated as a possible antigen, but not proven)
Lead to an autoimmune response that is directed against synovial structures and other organs
Activation and accumulation of T CD4 cells in the synovium starts a cascade of inflammatory responses
Inflammatory response leads to pannus formation
Pannus is an oedematous thickened hyperplastic synovium infiltrated by lymphocytes T and B, plasmocytes, macrophages and osteoclasts.
Pannus will gradually erode bare areas initially, followed by the articular cartilage. It causes a fibrous ankylosis which eventually ossifies
Diagnosing Rheumatoid Arthritis
Diagnosis is based on a combination of clinical, radiographic and serological criteria.
ACR - EULAR classification criteria for Rheumatoid Arthritis 4 requires a score of >6/10 for a diagnosis of RA to me made:
A- Joint Involvement
0: Large Joint
1: 2-10 large joints
2: 1-3 small joints (with or without involvement of large joints)
3: 4-10 small joints (with or without involvement of large joints)
5: >10 joints (at least 1 small joint)
B- Serology
0: negative RF and negative ACPA
2: low-positive RF or low-positive ACPA
3: high-positive RF or high-positive ACPA
C- Acute Phase Reactants
0: normal CRP and Normal ESR
1: abnormal CRP and Abnormal ESR
D- Duration of Symptoms
0: <6 weeks
1: >6 weeks
Definition of Rheumatoid Arthitis
Rheumatoid arthritis is a chronic autoimmune multisystemic inflammatory disease
which affects many organs but predominantly attacks the synovial tissues and joints.
Signs of Rheumatoid Arthritis on Examination
Hands
Wrist
Elbow
Shoulder
Hip
Knee
Feet
Skin: steroid use
BP and pulse: AF
Eyes: episcleritis, keratoconjunctivitis sicca, anaemia
Neck: atlanto-axial subluxation
Heart: pericardial rub
Lungs: pulmonary fibrosis, effusion
Abdomen: splenomegaly (Felty’s)
Urine dip: nephrotic syndrome or DMARDs
X-ray changes in rheumatoid arthritis
Soft tissue swelling
Periarticular osteopenia
Loss of joint space
Periarticular erosions
Deformity
Management of Rheumatoid Arthitis
MDT: GP, Physio, Occupational Therapist, Rheumatologist, Orthopod
Conservative
Physiotherapy
OT: aids and splints
Medical
WHO analgesic ladder
Steroids: IM, PO or intra-articular
DMARDs
Biologics
Other
CV risk optimisation
Preventing PUD and osteoporosis
Surgical
Carpal tunnel decompression
Tendon repairs
Arthroplasty
Ulna stylectomy
NICE
1) Combination of DMARDs (including methotrexate and at least one other DMARD, plus short-term glucocorticoids) as first-line treatment as soon as possible
2) Offer short-term treatment with glucocorticoids for managing flares in people with recent-onset or established disease to rapidly decrease inflammation
3) Offer analgesics (for example, paracetamol, codeine or compound analgesics)
Oral NSAIDs/COX-2 inhibitors should be used at the lowest effective dose for the shortest
Co‑prescribe with a proton pump inhibitor (PPI)
4) Retuximab
5) Methotrexate
Acromegaly
Spade-like hands
Tight ring
Signs of Acromegaly on Examination
Hands
Spade-like (compare to size of own hand)
Tight rings
Increase skin fold thickness
Boggy, sweaty palms
Thenar wasting and loss of sensation over index and middle finger = Carpal Tunnel Syndrome
Hypertensive
Face
Coarse facial features
Large nose
Big ears
Macroglossia
Widely spaced teeth: “smile and show me your gums”
Prognathism: inspect jaw from side
Look up nose for scars: pituitary surgery
Extras
Eyes: bitemporal hemianopia
Neck: goitre and JVP
Armpis: acanthosis nigrans
Abdomen: organomegaly
Myopathy: stand from chair
Completion
Urine dip for glycosuria
ECH: LVH and ischaemia
Previous photographs
History for Acromegaly
Headaches
Changes in vision
Changes in appearance
Ring size
Pain or parastheasia in the hands
Snoring, feeling tired (Obstructive sleep apnoea)
Polyuria
Polydypsia
Chest pain, SOB
Diagnosing Acromegaly
Urine dip: glycosuria
ECG: LVH, ischaemia
Bloods
IGF-1
Glucose tolerance test: non-suppression of growth hormone
Check other pituitary hormones: TFT, PRL,
Glucose
Imaging
CXR: cardiomegaly
MRI: pituitary fossa
Visual fields
Complications
Diabetes
Cardiovascular disease
Colorectal cancer
Managing Acromegaly
MDT approach: GP, endocrinologist, neurosurgeon, specialist nurse, ENT surgeon
1st line: trans-sphenoidal excision
Complications: meningitis, diabetes insipidus,m panhypopituitarism
2nd line: medical
Somatostatin analogues: octreotide
GH antagonist: pegvisomany
Dopamine agonists: Cabergoline
3rd line: radiotherapy
Follow-up: Yearly with bloods, visual fields, ECG and MRI head
Signs of Cushings on Examination
Hands
Thin skin
Evidence of cause: Rheumatoid arthritis
Arms: Hypertension
Face
Moon face / cushingoid face
Acne
Hirsutism
Abdomen
Central obesity
Purple straie
Extras
Proximal myopathy: stand from sitting
Back: inter-scapular fat pad
Palpate spine for tenderness (crush #)
Kyphosis
Causes of Cushing’s Syndrome
ACTH-independent
Most common: steroid use
Adrenal adenoma / carcinoma / hyerplasia
Carney complex (pigmentation)
ACTH-dependent
Pituitary tumour = Cushing’s disease
Ectopic ACTH from small cell lung cancer
Investigations for Cushing’s
Confirm increase in cortisol
24h free cortisol
Loss of diurnal variation: midnight cortisol
Low-dose dexamethasone suppression test
High dose dexamethasone test
MRI pituitary fossa
+/- Whole body CT
Bilateral inferior petrosal sinus vein sampling - distinguish between ectopic ATCH and pituitary source (raised with stimulus = pituitary)
Can also be used to detect affected side
Complications of Cushing’s Disease
Steroid comolications
Osteoporosis
Cardiovascular disease
Signs of Addison’s on Examination
Medic alert bracelet
Hyper-pigmentation: palmar creases, scars, nuccal mucosa
Postural hypotension
Extras:
Signs of AI disease (Diabetes, Votiligo, hypothyroidism)
Signs of TB
Investigations for Addison’s
Bloods
U+Es: Hyponatraemia with Hypokalaemia
Hypoglycaemia
Antibody against 21-hydroxylase
8am cortisol: low
8am ACTH: high
SynACTHen test: no increase in cortisol
CXR: TB
AXR: adrenal calcification
Management of Addison’s
Acute
0.9% normal saline to rehydrate
100mg hydrocortisone IV
Treat cause of admission e.g. infection
Chronic
Replace hydrocortisone and fludrocortisone
Patient education and advice
Dont stop steroids suddenly
Increase dose during illness
Wear medic alert bracelet
Carry steroid card
Avoid NSAIDs
Complications of Steroid Treatment
Side Effects of Steroids
MSK
Proximal myopathy
Osteoporosis (consider bisphosphonates)
Endocrine
HPE suppression
Obesity
Diabetes melitus
Metabolic
Sodium and water retention
Hypertension
Hypokalaemia
Immune
Immunosuppression
CNS
Depression
Pyschosis
Eye
Cataracts
Glaucoma
GI
Peptic ulcer (give PPI)
Hemiballismus
Involuntary flinging motions of the extremities
Continuous and random
Isolated to one side
Cause
Damage to the subthalmic nucleus
Usually a small infract in diabetic
Can be caused by multiple sclerosis
Mx
Self resolving
Haloperidol
Benign Essential Tremor
Autosomal Dominant
Action / postural tremor
Worse with movement
Exacerbating factors: Caffeine, Anxiety
Relieving factors: Alcohol, Sleep
Mx
Propanolol
Primidone (anti-epileptic)
