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MSRA Content > Level 2 - Renal, Dermatology > Flashcards

Level 2 - Renal, Dermatology Flashcards

1
Q

Definition of HUS?

A
  • Triad of acute renal failure, microangiopathic haemolytic anaemia (schistocytes, burr cells) and thrombocytopenia
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2
Q

Damage in HUS?

A
  • Endothelial damage to glomerular capillaries
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3
Q

Pathology in typical HUS? How is it acquired?

A

o Secondary to GI infection with E.coli 0157 (produces verocytotoxin which localises in endothelial cells of kidney and causes intravascular thrombogenesis)

o Coagulation cascade activated which consumes platelets and MHA results from damaged to red blood cells when they circulate through microcirculation

o Acquired through contact with farm animals, eating uncooked beef or less often, Shigella

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4
Q

Pathology in atypical HUS?

A

o Not-diarrhoea associated and often familial

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5
Q

When does HUS usually present?

A
  • Typical HUS usually in <3 year olds
  • Commonest cause of AKI, peaks in summer months
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6
Q

Risk factors for HUS?

A

o Rural populations

o Warmer summer months

o 6 months – 5 years

o Contact with farm animals

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7
Q

Symptoms and signs of typical HUS?

A

o Follows a prodrome of diarrhoea which turns bloody

o Often fever, abdominal pain, vomiting

o Haemorrhagic Colitis → Haemoglobinuria → Oliguria → CNS signs → Encephalopathy → Coma

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8
Q

DDx of HUS?

A
  • Other causes of diarrhoea – gastroenteritis, appendicitis, IBD
  • DIC
  • HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelet count)
  • TTP
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9
Q

What is seen on blood tests in HUS? What other tests are needed?

A
  • Bloods

o FBC (raised WCC, low platelets, haemolytic anaemia, thrombocytopenia) and blood film (fragmented red cells), CRP, clotting

o U&Es (AKI), LFTs

o High LDH

  • Stool microscopy and culture
  • Urine microscopy and culture
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10
Q

Management of HUS?

A
  • Inform local Health Protection Unit
  • Early supportive treatment

o Appropriate fluid and electrolyte management

o Antihypertensive therapy

  • Dialysis when required
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11
Q

Complications of HUS?

A

Intestinal perforation, pancreatitis, severe colitis, altered mental state, seizures, AKI, CKD, Haematuria, hypertension and proteinuria

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12
Q

Why does HUS need follow up?

A
  • Follow-up as may be persistent proteinuria and hypertension
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13
Q

Definition of nephrotic syndrome?

A
  • Clinical syndrome defined as:

o Proteinuria

o Oedema

o hypoalbuminemia

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14
Q

Pathology of nephrotic syndrome?

A
  • Increased permeability of serum protein through the damaged basement membrane in the renal glomerulus
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15
Q

How is nephrotic syndrome classified?

A
  • Classified as steroid sensitive, steroid resistant or steroid dependent
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16
Q

Aetiology of nephrotic syndrome?

A
  • 90% cause is unknown
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17
Q

Primary glomerular causes of nephrotic syndrome?

A

 Minimal change disease – 85% in children

 Focal segmental glomerulonephritis (FSGN)

 Membranous glomerular disease

 Membranoproliferative glomerulonephritis

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18
Q

Secondary glomerular causes in nephrotic syndrome?

A

 Infection – HIV, HepB/C, syphilis, malaria

 SLE, HSP, Lupus

 Diabetes

 Alport’s syndrome

 Malignancies

 Toxins (snake bites, bee stings) and heavy metals

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19
Q

Symptoms and signs of nephrotic syndrome?

A
  • Periorbital oedema, leg/ankle oedema, ascites and breathlessness
  • Oliguria
  • Proteinuria, oedema, hypoalbuminemia
  • Dyslipidaemia, abnormalities in coagulation/fibrinolysis, reduced renal function
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20
Q

Investigations performed in nephrotic syndrome? and why?

A
  • Urine dipstick

o Check for protein & microscopic haematuria

  • Urine MSU

o Microscopy, culture and sensitivities to exclude UTI

  • Bloods

o FBC, CRP, ESR, U&E’s (creatinine, low albumin)

o Complement levels

o Autoimmune screen

o HepB/C screen

  • CXR and renal USS
  • Renal biopsy
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21
Q

General management of nephrotic syndrome?

A
  • Sodium and fluid restriction
  • High-dose diuretics
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22
Q

Management of steroid sensitive nephrotic syndrome?

A

o Oral prednisolone for 4 weeks then wean over 4 months

 If steroid toxicity, use cyclophosphamide

o Pneumococcal and influenza vaccination

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23
Q

Management of steroid-resistent nephrotic syndrome?

A

o Management of oedema with diuretics, salt restriction and ACE inhibitors (enalapril)

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24
Q

What is Steven Johnson Syndrome? Range of severity?

A
  • Immune-complex-mediated hypersensitivity disorder
  • Ranges from mild skin and mucous membrane lesions to a severe, sometimes fatal systemic illness: toxic epidermal necrolysis (TEN)
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25
Q

Spectrum of disorders in SJS? Classification?

A
  • SJS, SJS/TEN overlap and TEN form a spectrum of severe cutaneous adverse reactions (SCAR) that can be differentiated by the degree of skin and mucous membrane involvement
  • The classification is based on the percentage of body surface area detached
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26
Q

Epidemiology of SJS?

A
  • Incidence is 2-3 cases/million population/year
  • More common in individuals with HIV
  • Females > males
  • Most 10-30 years old
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27
Q

Aetiology of SJS?

A
  • Approximately 75% of SJS/TEN are caused by medications and 25% by infections and ‘other’ causes
28
Q

What medications cause SJS?

A
  • Allopurinol, carbamazepine, sulphonamides, antiviral agents, phenobarbital, phenytoin, valproic acid, lamotrigine
29
Q

What infections causes SJS?

A
  • HSV, EBV, HIV, influenza, bacterial, fungal
30
Q

Symptoms and signs of SJS?

A
  • Starts with a URTI
  • May be associated with fever, sore throat, chills, headache, arthralgia, vomiting and diarrhoea and malaise
  • Mucocutaneous lesions develop suddenly and clusters of outbreaks last from 2-4 weeks. The lesions are usually not pruritic
31
Q

Describe the lesions in SJS? Pattern? Types? Signs?

A

o Lesions most commonly palms, soles, dorsum of hands and extensor surfaces

o Begin as macules develop into papules, vesicles, bullae, urticarial plaques, or confluent erythema

o Centre of lesions may be vesicular, purpuric, or necrotic

o Appearance of a target

o Nikolsky sign is positive (mechanical pressure to skin leading to blistering within minutes or hours)

32
Q

Other symptoms in SJS?

A
  • Oromucosal ulceration
  • Dysuria or an inability to pass urine
  • Painful red eye, purulent conjunctivitis, photophobia, blepharitis
33
Q

Investigations in SJS?

A
  • Serum electrolytes, glucose and bicarbonate essential to assess severity and dehydration
  • Clinical diagnosis classification
  • Skin biopsy

o Bullae are sub epidermal

o Epidermal cell necrolysis may be seen and perivascular areas are infiltrated with lymphocytes

34
Q

Acute management of SJS?

A

o Identify and remove causative drug or underlying cause.

o Use of the ALDEN (Algorithm for assessment of Drug-induced Epidermal Necrolysis) may be useful

o A rapid assessment of prognosis should be made using the SCORTEN

35
Q

Supportive therapy in SJS?

A

o Attention to airway and haemodynamic stability.

o Severe fluid loss

  • IV fluid replacement and electrolyte correction.

o Analgesia

o Skin lesions are treated in the same way as for burns.

 Mouth: mouthwashes; topical anaesthetics are useful in reducing pain and allowing the patient to take in fluids.

 Eye care: frequent ophthalmology assessment and frequent eye drops, including antibiotic and steroid when required

36
Q

What is thrush?

A
  • Candida is a yeast-like fungus which is part of the normal commensal flora of the human gastrointestinal tract and the vagina
37
Q

Risk factor for thrush?

A
  • Complication of nappy rash
38
Q

Symptoms of nappy rash/thrush??

A
  • Bright red rash with clearly demarcated edge
  • Satellite lesions beyond border
  • Inguinal folds usually involved
  • May have oral thrush too
39
Q

Diagnosis of nappy rash?

A

Diagnosis is made clinically

40
Q

Management of nappy rash?

A
  1. Frequent nappy changes
  2. Barrier ointment cream, expose to air
41
Q

When would suspect thrush in nappy rash?

A

Worse in flexures or satellite lesions (a portion of the rash of cutaneous candidiasis in which a beefy red plaque may be found surrounded by numerous, smaller red macules located adjacent to the body of the main lesions)

42
Q

Management of thrush in nappy rash?

A
  1. Topical antifungal e.g. nystatin ointment 6-hourly (if severe, may benefit from oral antifungal simultaneously)
43
Q

What is thrush?

A
  • Candida is a yeast-like fungus which is part of the normal commensal flora of the human gastrointestinal tract and the vagina
44
Q

Risk factor for thrush?

A
  • Complication of nappy rash
45
Q

Symptoms of thrush??

A
  • Bright red rash with clearly demarcated edge
  • Satellite lesions beyond border
  • Inguinal folds usually involved
  • May have oral thrush too
46
Q

Diagnosis of thrush?

A

Diagnosis is made clinically

47
Q

Management of thrush?

A
  1. Frequent nappy changes
  2. Barrier ointment cream, expose to air
48
Q

When would suspect thrush in nappy rash?

A

Worse in flexures or satellite lesions (a portion of the rash of cutaneous candidiasis in which a beefy red plaque may be found surrounded by numerous, smaller red macules located adjacent to the body of the main lesions)

49
Q

Management of thrush?

A
  1. Topical antifungal e.g. nystatin ointment 6-hourly (if severe, may benefit from oral antifungal simultaneously)
50
Q

What is nappy rash? Other names?

A
  • Acute inflammatory reaction of the skin in the nappy area, which is most commonly caused by an irritant contact dermatitis. It is also known as ‘napkin dermatitis’ or ‘diaper dermatitis’
51
Q

PAthology of nappy rash?

A
  • Skin barrier function compromised by skin maceration (excessive hydration), friction between the skin and nappy, prolonged skin contact with urine and faeces, and resultant increased skin pH - Increase skin permeability and activate faecal enzymes which further act as skin irritants
52
Q

What common secondary infections occur in nappy rash?

A
  • Possible secondary infection with Candida albicans and bacteria (most commonly Staphylococcus aureus and streptococci)
53
Q

Prognosis of nappy rash?

A

Uncomplicated nappy rash should settle with appropriate management in primary care, and typically lasts about three days. Can get secondary infections (thrush, viral).

54
Q

Risk factors for nappy rash?

A
  • Prolonged skin contact with urine and faeces
  • Type of nappy used
  • Soaps, detergents, or alcohol-based baby wipes.
  • Mechanical friction from skin contact with nappies or over-vigorous cleaning.
  • Pre-term infants
  • Diarrhoea
55
Q

Symptoms of nappy rash?

A
  • Itchy and painful
  • Well-defined areas of confluent erythema and scattered papules
  • Over convex surfaces in contact with the nappy (the buttocks, genitalia, suprapubic area, and upper thighs)
  • Sparing of the inguinal skin creases and gluteal cleft
  • Glazed appearance if acute
56
Q

DDx of nappy rash?

A
  • Allergic contact dermatitis, perianal streptococcal dermatitis, infantile seborrheic dermatitis
  • Atopic Eczema, eczema Herpeticum
  • Psoriasis
57
Q

Investigations in nappy rash?

A
  • Clinical diagnosis and no investigations needed
  • Skin swab for culture and sensitivity if secondary bacterial infection
58
Q

Self-management of nappy rash?

A
  • High absorbency nappy
  • Ensure the nappy fits properly
  • Leave nappies off for as long as possible
  • Dry gently after cleaning — avoid vigorous rubbing.
  • Do not use soap, bubble bath, lotions, talcum powder, or topical antibiotics which can have an irritant effect.
59
Q

Drug therapy in nappy rash?

A

Emollients Topical hydrocortisone 1% cream

60
Q

Prognosis of nappy rash?

A

Uncomplicated nappy rash should settle with appropriate management in primary care, and typically lasts about three days. Can get secondary infections (thrush, viral).

61
Q

What is impetigo? When are lesions infectious?

A
  • Highly-contagious Staph aureus or B-haemolytic Strep superficial skin infection.
  • May be primary or complicate other skin disease (e.g. HSV infection, eczema, scabies).
  • Nasal carriage is often source of infection
  • Autoinoculation occurs and lesions are infectious until dry
62
Q

Epidemiology of impetigo?

A
  • Most common in infants and young children
63
Q

Risk factors for impetigo?

A
  • More common when pre-existing skin condition
  • Overcrowding
  • Poor hand hygiene
64
Q

Symptoms of impetigo?

A
  • Lesions well defined, usually start around nose & face
  • Erythematous macules become vesicular/pustular and then rupture to give classical honey-coloured crusted lesions
  • Superficial flaccid blisters can occur
65
Q

Investigations in impetigo?

A
  • Examination should confirm diagnosis
  • If very severe, skin swabs could be done
66
Q

Management of impetigo?

A

Consider hydrogen peroxide 1% cream (apply two or three times daily for 5 days) for people who are not systemically unwell or at a high risk of complications.

Otherwise:
- Topical fusidic acid for localised infections
- Oral flucloxacillin QDS for 7 days if severe
- Hygiene advice
- Avoid going to nursery or school until lesions are dry

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