SSS Week 5

Nail Clubbing clinical features + treatment

1. usual small diamond window cannot be seen when the index fingers are brought together with the distal phalanges placed adjacent to each other

2. soft nail beds

3. increased nail convexity

4. thickening of the finger

Treatment: treat underlying disease

Causes of nail clubbing

Resp

• interstitial lung disease

• lung cancer

• tb

• sarcoidosis

• abscess, emphysema

• CF

Cardio

• congenital heart disease

• subcute bacterial endocarditis

• AA

Endocrine

• hyperthyroidism

• thyroid cancer

• secondary parathyroidism

GIT

• IBD - crohns and UC

• hepatocellular carcinoma

• achalasia

• celiac disease

• liver cirrhosis

other

• hodgkin lymphoma

• asbestos

Koilonychia

spoon-shaped fingernails

• concavitiy in fingernail itself, resulting in a depression in the nail

associated with iron deficiency, sometimes be seen in normal infants, but disappears as child ages

Alopecia Areata description (clinical features, stages, aetiology)

• autoimmune

• non-scarring alopecia

• subtypes: totalis and universalis

clinical features

• discrete annular areas of hair loss anywhere on body

• more likely on scalp, eyebrows and beard

aetiology

• inflammation of anagen hair bulb causing hair growth to halt and catagen to be induced

• onset or reoccurrence triggered by stress, trauma, infection, and hormonal changes

STAGES

• sudden onset of hair loss

• increasing areas of hair loss which have a smooth surface, with scattered exclamation mark hairs

Trichotillomania

compulsive pulling out of hair

• can signify stress-relieving habit , or depression, and impulse control

there is normal hair growth in balding areas

DDx

• alopecia areata and tinea capitis

Scarring vs non-scarring alopecia

Scarring refers to irreversible destruction and replacement of hair follicles with scar tissue, which leads to permanent hair loss eg. can occur in SLE/lupus

Non-scarring refers to temporary hair loss where hair follicles remain intact and can regrow

Telogen effluvium (acute vs chronic) and how to confirm

• premature shift into telogen phase from anagen in response to shock to the system. which results in shedding prematurely (in exogen)

Acute vs chronic telogen effluvium

Acute - may follow childbirth or stopping pill, any acute illness, major surgery or severe dieting

Chronic - less common, it may be primary and idiopathic or

secondary to

• hypothyroidism

• hyperthyroidism

• malnutrition

• cancer

• TB

• iron deficiency anemia

• drug side effect

Anagen effluvium

direct injury to anagen hair growth by drugs (chemo), toxins or inflammation

inflammation - alopecia areata a cause

Hirsutism vs Hypertrichosis

hirsutism

• increased hair growth in women, male pattern of hair in the moustache and beard areas or occurring more thickly than usual on the limbs … usually genetic

• ANDROGEN DEPENDENT

• lower face and midline of trunk that are preferentially affected by androgens

hypertrichosis

• widespread overgrowth of NON-ANDROGEN-DEPENDENT hair, seen with drugs like cyclosporin and phenytoin

• areas like FOREHEAD and FOREARMS have increased hair growth (rather than lower face and midline of trunk that are preferentially affected by androgens)

DDx for non-scarring alopecia

1. alopecia areata

2. androgenetic alopecia

3. traction alopecia

4. trichotillomania

Androgenetic alopecia (clinical features and aetiology)

• occurs with advancing age

• progressive miniaturisation of pigment scalp hair to fine hypopigmented hair

• (thick terminal hair to thin vellus hair)

• genetic predisposition

DIC pathogenesis, clin features, aetiology

arises as a complication of different serious and life-threatening diseases

1. caused by uncontrolled activation of coagulation cascade

2. depletes platelets and clotting factors

3. increased haemorrhage into urine, stool and skin

acute clin features

• bruises

• mucous membrane involvement

• internal haemorrhage

• malaise and high fever purpuric rash affecting extremities

• petechiae and purpura

chronic clin features

• thromboembolism

• DVT

acute

• infection

• septicemia (sepsis)

• tissue injury eg. burns

chronic

• cancer

• tb infection

• CKD

• PE

8 signs of liver cirrhosis

1. pruritis —> cholestasis? hard to treat

2. bruising (inability of liver to produce clotting factors)

3. palmar and facial erythema

4. jaundice

5. spider naevi

6. feminisation (impaired metabolism of oestrogen)

7. photosensitivity, skin erosions and mucosal changes eg. pellagra

8. leukonychia or half and half nails

Bacterial endocarditis (+ risk factors, + cutaneous signs)

infection of endocardium - usually strep viridians or staph aureus

Risk factors

• rheumatic heart disease

• iv drug abuse

• previous cardiac surgery

• congenital heart disease

Cutaneous signs

1. splinter haemorrhages

2. osler’s nodes - tender red papule on pads of fingers and toes

3. janeway lesions - macular erythema of palms

4. septic emboli - pustular and purpuric lesions of lower legs and toes

5. roth’s spots - haemorrhages of conjunctiva

General signs of cardiac disease

• peripheral and central cyanosis

• erythema due to compensatory polycythaemia

• finger clubbing

• flushing of nail bed in time with aortic incompetence

• diagonal ear lobe crease in coronary artery disease

• peripheral oedema

• elevated JVP

SKIN SIGNS of sarcoidosis

Lupus pernio - asymptomatic violaceous or erythematous (red, purple) indurated plaques or papules or nodules, distributed on nose, cheeks, chin and ears

erythematous nodosum - a type of panniculitis, painful nodules most common on anterior surface of lower extremities (like shins)

ALSO seen in TB, IBD and strep infection

DIABETES PRESENTATIONS

1. necrobiosis lipoidica

   • early plaques are violaceous (of a violet colour) but atrophy and become brown-red or slightly yellow, blood vessels are visible under the skin

   • mostly appearing on shins

   • refractory to treatment (resistant?)

2. diabetic dermopathy

   • brownish scars on skin, mostly on shins

     

3. granuloma annulare

   • skin coloured or light pink annular lesions over knuckles

   • composed of dermal nodules fused into a rough circle

   

4. candida infections

5. staph infections

6. eruptive xanthomas - crops of yellow papules with erythematous base

7. neuropathic foot ulcers

8. skin tags

9. acanthosis nigricans - hyperpigmented velvety thickening of skin folds

Xanthelasma - investigations and treatment

xanthelasna palpebrarum a common example used this week

what investigations - lipids, U&E, liver, glucose, TFT

treatment is lipid lowering medication & surgery

Specific manifestations of graves disease (hyperthyroidism) + other classic signs

1. pretibial myxoedema - either diffuse or nodular swelling of shins

2. ophthalmopathy

3. acropachy - triad is: digital clubbing, soft-tissue swelling of hands and feet, periosteal reaction in long bones.

• diffuse hair loss

• heat intolerance and sweatiness

• facial flushing

• palmar erythema

• itch

acropachy (what is it a manifestation of)

triad is: digital clubbing, soft-tissue swelling of hands and feet, periosteal reaction in long bones.

and is a manifestation of hyperthyroidism

Classical signs of hypothyroidism

• dry yellowish skin

• diffuse hair loss

• loss of outer third of eyebrows

• loss of body ahir

• puffiness of eyelids, hands and face

• itch

• absence of sweating

• bruising and purpura

• brittle nails

• cold sensitivity

Skin signs of Cushing’s syndrome

• facial roundness (moon face) and plethora (redness)

• buffalo hump

• central adipositiy

• striae

• fragile skin

• telangiectasia

• bruising

• acne

• excess facial and body hair

Signs and symptoms of addisons disease

• fatigue

• weakness

• weight loss

• nausea

• abdo pain

• diarrhoea

• vomiting

• mood disturbances

3 cutaneous signs of GIT disease

1. dermatitis herpetiformis

   • pruritis vesicles, papules and bullae on elbows, knees and lumbosacral areas, needs to biopsy to confirm

2. erythema nodosum

3. pyoderma gangrenosum (also a internal malignant sign)

   • begins as a papule and breaks down to form rapidly enlarging ulcer, raised purple undermined edges , needs biopsy to differentiate infective vs malignant cause

chronic cutaneous (discoid) LE

• well defined red scaly plaques

• occurs on sun exposed areas

• secondary changes of hyper or hypopigmentation and atrophic scarring → scarring can cause alopecia

treatment

• sun protection

• topical corticsteroids

• systemic agents eg. hydroxychloroquine, methotrexate

SLE

• butterfly rash

• severe photosensitivity

• mucosal erosions and ulcer

Scleroderma

connective tissue disorder characterised by symmetrical hardening of skin which can be local or systemic

progression

initial oedema → eventual contractures and atrophy with ulceration of fingers and toes

1. Localised or limited

type of limited systemic scleroderma: CREST syndrome which is characterised by

• Skin involvement: mainly hands, face, forearms.

• Internal organ involvement: usually milder, often lungs (pulmonary hypertension) or GI tract.

• Hallmark features: Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangiectasia (CREST).

2. Extensive/diffuse

scleroderma which involves skin of distal limbs and face as well as arms, legs and trunk

this one is associated with severe systemic disease particularly affecting the kidney, GIT and lugns

other clinical signs present in extensive/diffuse scleroderma include

• Thickened, indurate white plaques occurring anywhere on the skin surface.

• They may have an erythematous or purple peripheral rim.

• Linear lesions which may extend the length of an arm or leg sometimes causing contractures

• Hyperpigmentation and hypopigmentation

Investigations for bullous pemphigoid, treatment

investigations

• skin autoantibodies

• skin biopsy and direct immunofluorescence

treatment

• potent topical steroids or oral steroids

• long term alternatives include doxycycline, or nicotinamide (steroid sparing agents)

Vitiligo classical presentation

Milky white patches of skin

Disfiguring condition where colour is lost from the skin. It is usually patchy but in rare cases can be widespread.

Pigment loss in vitiligo is complete, so the skin is white and sunburns easily. The edge of the lesion in vitiligo is always sharp and well defined.

Aetiology of pruritis and tests

FBC - infection, WBC, eosinophil count

U&E - if suspect renal failure

LFT - liver failure

CRP, ESR - inflammatory markers

Ferritin

TSH

could also be due to malignancy

3 cutaneous signs of internal malignancy (+skin signs for no.3)

1. acanthosis nigricans - gastric adenocarcinomas, with other adenocarcinomas

2. pyoderma gangrenosum - the purple raised edge, starts as papule or pustule that breaks down into a rapidly enlarging ulcer

3. dermatomyositis

   1. periorbital macular violaceous erhythema (heliotrope rash)

   2. scaly, reddish papules on dorsum of interphalangeal joints (gottron’s papules)

   3. violaceous rash involving sun exposed sites

   4. rugged cuticles and nail fold telangiectasia

   5. poikiloderma (skin atrophy, telangiectasia, pigmentation)

   6. photosensitivity

4. generallised pruritis

5. superficial thrombophlebitis

6. erythroderma

7. sweets syndrome

   • Sudden onset of painful oedematous, erythematous to blue plaques

     on face, neck and limbs.

   • Plaques may be vesicular or pustular

   • Often a fever and neutrophil leucocytosis

   • associated with haematological malignancy, some solid neoplastic tumours and… strep throat infection

Chronic leg ulcers aetiology + treatment

chronic so full thickness skin defect >4 weeks