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Nagasaki Flashcard Extravaganza > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is the causative organism for a buruli ulcer?

A

Mycobacterium ulcerans

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2
Q

Where do buruli ulcers occur geographically?

A

West Africa/Australia

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3
Q

what is the treatment for Buruli Ulcer

A

Tx Rifampicin 600mg OD plus Clarithromycin 500mg BD - consider surgery if large or over a joint

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4
Q

What is the investigation for Buruli ulcer?

A

PCR

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5
Q

What are the WHO cardinal signs of leprosy?

A
  1. loss of sensation in a hypopigemented or reddish skin lesions
  2. thickened of enlarged peripheral nerve, with loss of sensation or motor weakness of muscles supplied by that nerve
  3. presence of AFBs on slit skin smear
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6
Q

Describe type of nerve damage in leprosy

A

Peripheral, can occur before or after the skin lesion, sensory/autonomic

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7
Q

Common motor function impairments in leprosy?

A

Claw hand, wrist drop, foot drop, lagophthalmos

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8
Q

Eye complications in leprosy

A
  • lagophthalmos
  • decreased corneal sensation
  • acute iritis
  • chronic iritis
    *cataract
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9
Q

What are the investigations in leprosy?

A

Clinical - skin, neurological
Slit skin smear/histology - ZN
Ear lobe good site (need fluid without blood, AFBs prefer cool environment)
Skin biopsy
Culture not useful

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10
Q

Are serological tests in leprosy useful?

A

Good sensitivity in MB but not PB. May be cross reactive in households

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11
Q

Where are the common geographical locations for leprosy?

A

Africa, SE Asia, Brazil

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12
Q

Nature of transmission of m.leprae

A

Human to human
Survives in environment for up to 45 days
Shed from nasal mucosa

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13
Q

Who acquires leprosy?

A

More male than female
Children and adults
5-8x in household, only 15-30% incident cases

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14
Q

Protective factors in leprosy acquisition

A

BCG (can also precipitate)
Improved socio-economic status

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15
Q

What type of organism is M Leprae?

A

Acid-fast, non-motile and non spore forming
Obligate intracellular parasite Can not be grown on artificial media
But multiply in mouse footpad and nine-banded armadillo
Optimum temperature requirement: 30-33oC - M. leprae growth in the peripheral nerves and cooler areas of the body
Tropism for macrophages, monocytes and Schwann cells

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16
Q

what are the 5 types of leprosy?

A

Tuberculoid leprosy (TT)
Borderline tuberculoid (BT)
Mid-borderline (BB)
Borderline lepromatous leprosy (BL)
Lepromatous leprosy (LL)

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17
Q

What are the history/immuno differences between TL and LL?

A

TT/BT * Abnormal immune response (granulomatous reaction) or ‘fighting’ against M. leprae
* Very few bacilli

BL/LL

  • Least cellular immunity against M. leprae (anergic)
  • Many bacilli
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18
Q

What are the clinical differences between TL and LL?

A

Tuberculoid type (TT) - Hyper-reactive -
* Infiltrated plaques
* Well-defined with sharp
borders
* Single lesion
* Localized, asymmetrical
* Loss of sensation at the site of skin lesion

Lepromatous type (LL) - Anergic -
Macules, papules, nodules, diffuse infiltration
Numerous lesions Symmetrical
Loss of sensation can occur at any site
Leonine facies, madarosis, saddle nose, bilateral infiltration of the earlobes

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19
Q

What is the epidemiology of leprosy?

A

Most cases occur in India
5% of people in endemic areas are asymptomatic carriers
Young adults

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20
Q

What are the two causative organisms in Leprosy

A

Mycobacterium leprae
Mycobacterium Lepromatosis

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21
Q

What is the microbiology of Mycobacterium Lepra/lepromatosis

A

Gram +ve
Acid fast bacilli
Obligate intracellular

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22
Q

What two animal vectors are associated with Leprosy

A

Armadillos
Red Squirrels

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23
Q

How is Leprosy spread?

A

Air droplets
Breast milk (rare)

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24
Q

What is the incubation period of leprosy?

A

3-5 years

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25
Q

What are the 3 immune mediated complications of leprosy (‘Leprosy Emergencies’)

A

Type 1 Reaction: Local reaction –> spontaneous worsening of existing lesions ( odematous and erythematous) and pain/loss of nerve function acutely!!!!!!)

Type 2 Reaction: Systemic Reaction –> General systemic inflammatory response; malaise, fever, fatigue, anorexia

Lucio’s Phenomenon: Occurs in M. Lepromatosis
Haemorrhagic rash

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26
Q

Which types of Leprosy are Paucibacillary

A

Tuberculoid Leprosy
Borderline Tuberculoid

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27
Q

Which types of leprosy are multibacillary

A

Mid Borderline Leprosy
Borderline Lepromatous
Lepromatous Leprosy

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28
Q

Which types of Leprosy are TH1 mediated?

A

TT, TB, BB

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29
Q

Which types of leprosy are TH2 mediated?

A

BL, LL

30
Q

How do you manage Multibacillary TB?

A

12/12 of:
Rifampicin 600mg PO MONTHLY
+
Clofazimine 50mg PO OD and 300mg MONTHLY
+
Dapsone 100mg OD

31
Q

How do you manage Paucibacillary Leprosy?

A

6/12 of:
Rifampicin 600mg PO Monthly
+
Dapsone 100mg OD
+
Clofazamine 50mg PO OD and 300mg MONTHLY

32
Q

What are the side effects of Clofazimine

A

– Skin pigmentation-
– Lesions and normal skin
– Icthyosis (Ichthyosis is a condition that causes widespread and persistent thick, dry, “fish-scale” skin. The skin of a person with ichthyosis is rough, dry and scaly and needs to be regularly moisturised.)

33
Q

What are the main side effects of Dapsone?

A

– Haemolytic anaemia Hb drop 1-2 gm
– Dapsone Hypersensitivity Syndrome

34
Q

What are the main Side effects of rifampicin?

A

– Urine discolouration
– Liver enzyme induction
- Hepatitis

35
Q

What cause Pitiryiasis versicolour and what is the treatment?

A

Malassezia species
Topical antifungals
Pigmentary changes may persist

36
Q

What is this?

A

Scabies mite

37
Q

What are the clinical features of scabies?

A

Itchy lesions
Infants tend to get axilla/limb lesions/sparing of face
Adults - hands, groin
Crusted scabies -> hyperkeratosis, less itch
Can be quite nodular

38
Q

Who is vulnerable to scabies?

A

HIV/elderly/HTLV
Outbreaks in closed communities, humanitarian disasters

39
Q

When is mass drug administration recommended for scabies

A

When prevalence > 10%

40
Q

How is scabies managed?

A

Permethrin (or another topical like Malathion)
Ivermectin if recalcitrant or crusted
Hot wash or sunbathe clothes and bedding
Treat household and partners

41
Q

What are the clinical features of yaws?

A

Spirochete causing yellow papilloma and ulcers in children, often around mouth

Affects bone or cartilage if untreated
Positive syphilis serology

Treat with benpen or SCA

42
Q

What is the vector for onchocerciasis?

A

blackfly/simulium transmit onchocerca colvulus filial worm

43
Q

What are the clinical symptoms of onchocerciasis?

A

Blindness, nodules, severe itch, depigmentation “leopard skin”

44
Q

Where is onchocerciasis found?

A

Central America, Yemen, South America, Africa

45
Q

How to test for onchocerciasis?

A

skin snipping, antibodies

46
Q

What is the treatment for river blindness?

A

Ivermectin (Mectizan - used for mass drug administration)

47
Q

what trep species is yaws?

A

pertenue

48
Q

what is the treatment for yaws?

A

single dose SCA or doxy

49
Q

Which types of leprosy have more bacilli, lesions and nerve involvement?

A

BL/LL

50
Q

Which nerves are affected most in leprosy?

A

– Sensory and autonomic nerve fibres
– Ulnar, median, radial cutaneous, facial, radial, – common peroneal, posterior tibial

Motor function impairment:
Claw hand, wrist drop, foot drop, lagophthalmos
Sensory loss
secondary damage: ulceration, loss of digits and limbs
Autonomic function impairment
Dry skin, cracking (worsens effect of sensory loss)

51
Q

What are the blinding complications in leprosy?

A
  • lagophthalmos
  • decreased corneal sensation
  • acute iritis
  • chronic iritis
  • cataract
52
Q

What are the leprosy serological tests?

A

All more sens in MB

M leprae antigen - PGL 1
ML flow test (more sens in MB, seropositive in endemic areas)
LID-1 test (cross reactive in household contacts)
Orangelife test (abx, cannot tell if past or current)
PCR from biopsy - sens but expensive

53
Q

What is the transmission of leprosy?

A

Human to human
survives in environment 45 days
Shed from nasopharynx

54
Q

What is incubation time of leprosy?

A

2-5 years tuberculoid
8-15 years lepromatous

55
Q

What is the treatment of leprosy?

A

Regimes
Single lesions - Rif/oflox/mino single dose
PB (2-5 lesions)- Rif/Dap 6/12 (this is changing to triple)
MB (>5 lesions) - Rif/Clo/Dap = 12/12

56
Q

what are the side effects of the three main leprosy drugs?

A

Rifampicin/Clofazimine/Dapsone
RIF - body fluids go goes orange, intermittent dosing. Bacteriocidal
Clofazimine - risk hyperpigmentation of lesions. Weakly bacteriocidal
Dapsone - methaglobinaemia, haemolysis - anaemia, skin reactions, DRESS. Bacteriostatic

57
Q

What are type 1 leprosy reactions?

A

Pathology
* increased cell mediated immunity towards M. leprae antigens
Skin lesions
* increased erythema, oedema * new lesions
Neuritis
* tender/painful nerves * muscle weakness
* loss of sensation

More in BT/BB/BL

Treat with pred

(Type 4 hypersensitivty)

58
Q

What is a type 2 leprosy reaction

A

Malaise & Fever Neuritis
Iritis
Other Systemic Involvement
–orchitis
–arthritis
–lymphadenopathy
–renal disease

LL and BL

Tx with aspirin - steroids/thalidomide if severe.

(type 3 hypersensitivy)

59
Q

What is LPEP (leprosy pep)?

A

Rifampicin (weight/age based) PEP
Children should have BCG too

60
Q

What is the microbiology and pathophysiology of leprosy?

A

Obligate intracellular organism; can’t be cultured in vitro (but grows in mice and armadillos)
* Aerobic
* Acid-fast bacillus
* Slowest growing of all known bacteria

  • Chronic granulomatous condition
  • Infection of macrophages and
    peripheral nervous system
  • (Schwann cells)
    Spectrum of disease dependent on host’s cell-mediated immune response
61
Q

What is this?

A

Mycetoma - 2 types
Bacterial
Actinomadura madurae
Streptomyces somaliensis, Actinomadura pelletieri and Nocardia species
Fungal
Madurella mycetomatis etc.

62
Q

How do you test for mycetoma?

A

Microscopy:

Granules/GRAINS - Colonies of fungi WITH BLACK DOTS. They produce a membrane containing melanin to protect themselves. This makes mycetoma resistant to treatment.

63
Q

What is the clinical presentation of mycetoma?

A

Papule nodule → swelling → form sinus tracts discharging pus + grains filled with organisms

64
Q

How is mycetoma managed?

A

ABx/Antifx/surgery

65
Q

How long can treatment be completed in leprosy beyond you the course to be effective?

A

50% eg 9 or 18 months

66
Q

What type of reaction is erythema nodosum leprosum

A

Type 2 systemic reaction

67
Q

what are the disability grades for leprosy?

A

WHO

  1. normal
    2.loss of feeling in hands or palms
  2. reduced vision or visible damage to hands or feet, or visible neurological phenom
68
Q

What are the interventions to prevent secondary impairment from leprosy?

A

Moisturising (cracked skin, autonomic neuropathy, more wounds)
Footwear
Hygiene
Physio/OT
Surgery
Analgesia
Psychological support

69
Q

Which nerve gets biopsied in leprosy?

A

Preferentially sural nerve as little function

70
Q

What do the different colour grains on microscopy for mycetoma mean in terms of aetiology?

A
  • Black grains are pathognomic for
    eumycetoma (fungal)
  • Red grains are pathognomonic for actinomycetoma
  • White grains can signal either eu- or actino-mycetoma - non-specific

Nagasaki Flashcard Extravaganza (34 decks)

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