Medical Shorts Flashcards

1
Q
A

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

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2
Q

Nails changes in Psoriasis

A

Discolouration

Pitting

Onycholysis

Subungual hyperkeratosis

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3
Q

Subtypes of Psoriasis

A

Guttate: drop-like lesions on the trunk, commoner in children following streptococcal throat infection

Pustular: generalised or palmo-plantar

Erythroderma

Flexural: not scaly

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4
Q

Pathogenesis of psoriasis

A

Type IV cell-driven hypersensitivity

Hyperkeratosis

Parakeratosis

Intra-epidermal micoacscesses (of Munro)

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5
Q

Psoriatic Arthritis

A

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

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6
Q

Management of Psoriatic Arthritis

A

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

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7
Q
A

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

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8
Q

Management of Dermatitis

A

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

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9
Q

Cutaneous Manifestations of Diabetes Melitus

A

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

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10
Q
A

Granuloma Annulare

Flesh-coloured papules in annular configuration

Usually on dorsum of hand

Associated with Diabetes Melitus

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11
Q
A

Cheiroarthropathy

Demonstration of the Prayer Sign

Tight waxy skin that limits finger extension

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12
Q
A

Necrobiosis Lipoidica Diabeticorum

Well-dermarcated waxy, bruise-like plaqyes

Prominent blood vessels

Assoc with diabetes melitus

90% females

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13
Q
A

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

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14
Q
A

Tendon Xanthoma

Seconday to hyperlipideaemia

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15
Q
A

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

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16
Q
A

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

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17
Q
A

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

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18
Q

Glass eye AND Ascites

A

= Ocular Melanoma

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19
Q

Classification of Malignant Melanoma

A

Superficial spreading: 80%

Lentigo maligna melanoma: elderly patients

Acral lentiginous

Nodular

Amelanotic: delayed diagnosis

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20
Q

Management of Malignant Melanoma

A

Staging

Breslow Depth

Clarke’s levels

Mx

Excision biopsy for staging

Seconday excision margin depends on stage

+/- lymphadenectomy

+/- adjuvant chemo

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21
Q

Mohs Surgery

A

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.

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22
Q

Neurofibromatosis

A

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

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23
Q
A

Lisch Nodules

Melanocytic hamartomas of the iris

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24
Q

Complications of Neurofibromatosis

A

Epilepsy

Sarcomatous change: 5%

Scoliosis: 5%

Learning difficulty: 10%

25
Q

Management of Neurofibromatosis

A

MDT: GP, neurologist, specialist nurse, Surgeons

Excision of problematic neurofibromas

Monitor complications

Yearly BP and cutaenous review

Treat epilepsy

Genetic counselling

26
Q

Causes of Neurofibromatosis

A

Autosomal Dominant

NF1: Chromosome 17

1 in 2,500

NF2: Chromosome 22

1 in 35,000

27
Q

Differential of Cafe-au-lait Spots

A

Neurofibromatosis

McCune Albright

Cafe-au-lait spots

Polyostotic fibrous dysplasia

Endocrinopathy –> precocious puberty

Tuberous sclerosis

28
Q

Tuberous Sclerosis

A

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)

29
Q

Alport’s Syndrome

A

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

30
Q
A

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

31
Q
A

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

32
Q
A

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

33
Q
A

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
34
Q
A

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

35
Q

Swan-neck deformity

A

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

36
Q

Boutonniere Deformity

A

Flexion at PIP

Extension at DIP

Due to central tendon slip

37
Q

Pathology of Rheumatoid Arthritis

A

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

38
Q

Diagnosing Rheumatoid Arthritis

A

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

39
Q

Definition of Rheumatoid Arthitis

A

Rheumatoid arthritis is a chronic autoimmune multisystemic inflammatory disease

which affects many organs but predominantly attacks the synovial tissues and joints.

40
Q

Signs of Rheumatoid Arthritis on Examination

A

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

41
Q

X-ray changes in rheumatoid arthritis

A

Soft tissue swelling

Periarticular osteopenia

Loss of joint space

Periarticular erosions

Deformity

42
Q

Management of Rheumatoid Arthitis

A

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

43
Q
A

Acromegaly

Spade-like hands

Tight ring

44
Q

Signs of Acromegaly on Examination

A

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

45
Q

History for Acromegaly

A

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

46
Q

Diagnosing Acromegaly

A

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

47
Q

Managing Acromegaly

A

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

48
Q

Signs of Cushings on Examination

A

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

49
Q

Causes of Cushing’s Syndrome

A

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

50
Q

Investigations for Cushing’s

A

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

51
Q

Complications of Cushing’s Disease

A

Steroid comolications

Osteoporosis

Cardiovascular disease

52
Q

Signs of Addison’s on Examination

A

Medic alert bracelet

Hyper-pigmentation: palmar creases, scars, nuccal mucosa

Postural hypotension

Extras:

Signs of AI disease (Diabetes, Votiligo, hypothyroidism)

Signs of TB

53
Q

Investigations for Addison’s

A

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

54
Q

Management of Addison’s

A

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

55
Q

Complications of Steroid Treatment

A
56
Q

Side Effects of Steroids

A

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)

57
Q

Hemiballismus

A

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

58
Q

Benign Essential Tremor

A

Autosomal Dominant

Action / postural tremor

Worse with movement

Exacerbating factors: Caffeine, Anxiety

Relieving factors: Alcohol, Sleep

Mx

Propanolol

Primidone (anti-epileptic)

59
Q
A