derm middle tier Flashcards

1
Q

venous ulcer presentation

A
Commonly lower leg
Takes 2w+ to heal
Pain - worse when standing
Varicose veins
Large, shallow, irregular
Normal pulses
Warm skin
Oedema in other leg
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2
Q

venous ulcer pathophysiology

A

High pressure (in superficial veins) forces fibrinogen out of vessels → perivascular fibrin deposition → poor oxygenation of skin in this area

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3
Q

venous ulcer risk factors

are they common?

A
Due to sustained venous hypertension in superficial veins
Incompetent valves
DVT
Atherosclerosis 
Vasculitis - RA, SLE

common, more common with age

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4
Q

ulcer =

A

abnormal break in epithelial surface eg skin

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5
Q

arterial ulcer risk factors

A
Smoking
Arterial disease - atherosclerosis ! 
DM
Hypercholesterolemia 
History of claudication, hypertension, angina
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6
Q

arterial ulcer presentation

A
Punched out
Small, defined
Necrotic base
Painful - worse at night / legs elevated 
Higher up on leg / foot
Absent peripheral pulses
Cold, pale leg
No oedema
Occurs at pressure/trauma sites
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7
Q

what must not be given to arterial ulcer

A

compression bandages

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8
Q

what investigation results suggest arterial ulcer

A

ABPI (ratio of blood pressure at ankle to upper arm). arterial insufficiency <0.8

doppler ultrasound confirms arterial disease

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9
Q

neuropathic ulcer risk factors/causes

A

DM
Neurological disease
Leprosy

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10
Q

neuropathic ulcer presentation

A
Painless! 
Peripheral neuropathy
Variable size/depth
Warm skin
At pressure sites - soles, heels, toes
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11
Q
  • vasculitis
    ulcer
  • causes
A

Vasculitis = Inflammatory disorder of blood vessels → endothelial damage

Mainly idiopathic
Drugs
Infection
Inflammatory disorder
Malignant disease
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12
Q

vasculitis ulcer presentation

A
Usually lower legs
Symmetrical
Palpable purpura 
Non-systemic 
Do not blanch
Pyrexia
Arthralgia
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13
Q

general ulcer risk factors

A
Neuropathy eg DM
Lymphoedema
Vasculitis
Malignancy
Infection (TB, syphilis)
Trauma (pressure sores)
Drugs 

may be multiple

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14
Q

leg ulcer = most likely to be what

A

mainly venous disease

some - arterial disease

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15
Q

dermatitis artefacta

A

ulcer self induced by patient, usually as result of psychological suffering
skin/ ulcer biopsy

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16
Q

ulcer treatment

A
  • Treat cause
  • Focus on prevention —Nutrition
  • Risk factor control (eg drug addiction)
  • Bandages -
  • – Compression — Never for arterial ulcers
  • Keep it clean and covered
  • Antibiotics for infection
  • Analgesia
  • Steroids - if vasculitis
  • Surgery inc debridement , vascular reconstruction
17
Q

complications of necrotising fascitis

A

multi organ failure
mortality high
amputation

18
Q

treatment of necrotising fascitis

A

Aggressive and immediate treatment

Antibiotics

  • Group A strep (pyogenes ) aka type 2 necrotising factor == IV benzylpenicillin + clarithromycin/clindamycin
  • Unknown cause = broad spectrum IV antibiotics

Radical debridement
Amputation

19
Q

investigations and results for necrotising fascitis

A

X ray - soft tissue gas is seen

Bloods
FBC- v high wbc
Raised CRP

20
Q

presentation of necrotising fascitis

A
  • Intense pain in area ( Disproportionate to skin findings (initially skin spared))
  • Erythematous
  • Necrotic (due to vascular supply - may be black and slough (shedding) → dry gangrene
  • Blistering
  • Sometimes crepitus
  • Systemically unwell
  • – Fever
  • – tachycardia
21
Q

what is necrotising fascitis

types

A
  • Life threatening infection of the deep fascia causing necrosis of subcut tissue fascia and fat
  • Skin is initially spared but is eventually destroyed
  • Progresses rapidly

1 : mixture of aerobic and anaerobic bacteria
- Following abdominal surgery
diabetes

2 : Group hemolytic streptococcus (strep pyogenes) (this is aerobic)
- Previously healthy patients

22
Q

risk factors for necrotising fascitis

A

Abdominal surgery
Diabetes
comorbidities
Immunosuppression

23
Q

impetigo seen mainly on what ages

A

infants kids

24
Q

impetigo presents

A
Often on face, hands, feet
Itchy
Red
Growing 
Weeping
Crusting
25
Q

impetigo treatment

A

antibiotics

26
Q

gangrene =

types

A

Death of tissue from poor vascular supply

Types

  • Dry = Necrosis WITHOUT infection
  • Wet = Necrosis WITH infection
  • – Tissue becomes necrotic, usually after burn/ trauma injury
  • – More likely to be infected
27
Q

amyloidosis =

A

Misfolded amyloid fibril (protein) deposits

  • In multiple organs (systemic)
  • In one organ (localised)
28
Q

name 5 effects of amyloidosis on organs

A

Kidneys

  • Podocyte damage → proteinuria
  • Oedema (as result of hypoalbuminemia / lower oncotic pressure)
  • –Tiredness
  • – Weakness
  • – Loss of appetite
  • Hyperlipidaemia

Heart

  • Stiffens walls → HF
  • Interferes with electrical conduction → arrhythmias
  • – Oedema
  • – SOB

Intestines

  • Damages villi → less absorption
  • – Weight loss
  • – Nausea
  • – Diarreha
  • – Constipation
  • Enlarged liver, spleen, tongue (macroglossia)

Brain

  • Alzheimers
  • Decreased brain function
  • Increase risk of haemorrhage

Nerves

  • Damage in somatic (sensory and motor) and autonomic nerves
  • – Numbness

Skin
- Purpura esp periorbital