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Derm > Ch6: pruritus and dysaesthesia > Flashcards

Ch6: pruritus and dysaesthesia Flashcards

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1
Q

Things to look for on assessment when dealing with itch

A
  • Xerosis
  • Dermographism
  • Butterfly sign: difficult to reach area spared
  • Mid-upper back involvement: primary skin disease/back scratching device
  • Lymph nodes
  • Scabies
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2
Q

2007 Classification - International Forum for the Study of Itch:

A
  • Inflamed skin
  • Non-inflamed skin
  • Chronic secondary scratch induced lesions
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3
Q

Ix for pruritus

A
  • Skin scrapings
  • Biopsies may be helpful
  • DIF of peri-lesional
  • Initial bloods:
    • FBC, UEC, LFT
    • LDH
    • Fasting BSL
    • Thyroid
    • ESR, CRP
  • Additional other
    • IgE
    • Iron studies
    • BP
    • HbA1c
    • PTH + CMP
    • Viral hepatitis, HIV
    • Serum tryptase, histamine
    • u/A
    • Porphyrin screen
    • EPG, IEPG
  • Imaging:
    • CXR, CT
    • LN USS
  • Other
    • Patch testing
    • Prick testing
    • Cancer screen
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4
Q

Main ddx for itch

A
  • Inflamed dermatoses
    • Eczema: mediators are neuropeptides - substance P, CGRP, neurotrophic factors, opioid receptors, IL-2, IL-31, endothelin 1, PAR2
    • Psoriasis: substance P, nerve growth factor, IL-2
  • Infestations
    • Scabies: begins 3-6 weeks after first time infestation
  • Infections
  • Neoplastic
    • CTCL: IL-31 implicated. Rx strategies include gabapentin, mirtazapine, opioid antagonists
  • Genetic/naevoid
  • Other
  • Dermatoses induced by pruritis associated scratching or rubbing
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5
Q

Prurigo nodularis epidemiology

A

Middle aged women

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6
Q

Prurigo nodularis clinical

A
  • symmetric, extensor aspects of extremities
  • Butterfly sign
  • Flexures not affected
  • Morphology: dome-shaped papulonodules with central scale, erosion, ulceration, can get verrucous or fissured
  • If crust but no papulonodules: prurigo simplex
  • Often secondary to primary disease: atopic dermatitis, xerosis, systemic illness, psychological
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7
Q

What happens to nerves in prurigo nodularis

A

More nerve density and thickening

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8
Q

Prurigo nodularis differentials

A
  • Perforating disorder
  • Pemphigoid nodularis
  • Hypertrophic lichen planus
  • Hypertrophic lupus erythematosus
  • Scabies
  • Insect bites
  • Dystrophic EB
  • Multiple KAs
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9
Q

Prurigo nodularis histology and staining

A
  • Histo:
    • epidermal hyperplasia
    • thick, compact hyperkeratosis
    • erosions
    • fibrosis of the papillary dermis with vertically arranged collagen fibers, increased fibroblasts and capillaries
    • perivascular or interstitial mixed inflammatory infiltrate
  • Immunostain:
    • Pan-neuronal marker PGP 9.5 –> highlights that there is an increase in density of dermal nerve fibers
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10
Q

Prurigo nodularis treatment

A
  • treat underlying issues
  • topical anti-pruritics: menthol, pramoxine, polidocanol, palmitoylethanolamine, capsaicin (0.025-0.3% 4-6 times daily), calcipotriol, calcineurin inhibitors
  • oral anti-histamines
  • topical steroids under occlusion
  • IL-steroids
  • phototherapy
  • excimer laser treatment
  • Compulsive behaviour:
    • SSRIs and TCAs
    • Thalidomide: 50-200 mg daily
    • Gabapentin, pregabalin and neurokinin-1 receptor blocker aprepitant
    • Opioid blockers: naloxone, naltrexone, butorphanol (intranasal)
    • Cyclosporin?
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11
Q

LSC - what is it

A

Epidermal hypertrophy secondary to chronic scratching

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12
Q

LSC epidemiology

A

Adults

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13
Q

LSC clinical

A
  • well-defined plaques with exaggerated skin lines, leathery appearance, coalescing papules, hyperpigmentation, varying degrees of erythema
  • solitary or multiple
  • sites: posterolateral neck, occipital scalp, anogenital region, shins, ankles, dorsal aspects of hands, feet and forearms
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14
Q

Risk factors for LSC

A

xerosis, atopy, psoriasis, anxiety, OCD, localized neuropathic itch

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15
Q

LSC histology

A

compact hyperkeratosis, acanthosis with irregular elongation of rete ridges, hypergranulosis, vertically oriented collagen bundles

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16
Q

LSC treatment

A
  • same as prurigo nodularis
    • topical and intralesional steroids
    • Repeated application of hydrocolloid dressing
    • topicals: lidocaine, capsaicin, antipruritic agents
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17
Q

Scalp pruritus

A
  • can occur in absence of any objective changes
  • middle aged, with stress and fatigue
  • Rx: topical steroids, antipruritic agents
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18
Q

Pruritus ani epidemiology

A
  • 1-5% of population

- M:F 4:1

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19
Q

Causes of pruritus ani

A
  • primary
    • pruritis in the absence of any cutaneous, anorectal or colonic disorder
    • causes: diet such as excessive coffe intake, personal hygiene, psych
  • secondary
    • chronic diarrhoea –> if on chronic antibiotics –> liquid stools with pH of 8-10 –> lactobacillus
    • faecal incontinence/anal seepage
    • haemorrhoids
    • anal fissures or fistulas
    • rectal prolape
    • cutanoues issues
    • STDs
    • malignancy
    • infestations –> pinworm infection in kids is common
    • radiation therapy
    • neuropathic –> nerve compression, back issues
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20
Q

Rx of primary pruritus ani

A
  • Sitz baths, cool compresses, hygiene, fragrence free toilet paper or bidet –> then dry with blotting or a fan
  • application of zinc oxide
  • mild steroid cream –> can increase
  • topical calcienurin inhibitors
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21
Q

Pruritus vulvae and scroti

A
  • solely psychogenic in only 1-10%
  • worse at night, repeated rubbing leads to lichenification
  • evaluation same as pruritis ani
  • Acute pruritis: candidiasis, ACD, ICD
  • Chronic: dermatoses, malignancy, atrophic vulvovaginitis
  • Scrotal pruritis also been associated with lumbosacral radiculopathy
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22
Q

What is aquagenic pruritus

A
  • sensation occurs within 30 minutes of water contact, irrespective of temperature or salinity, and lasts for up to 2 hours
  • begin on lower extremities then generalize, spares the head, palms, soles and mucosae
  • unsure how it works –> elevated dermal and epidermal levels of Ach, histamine, serotonin and PgE2 has been seen
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23
Q

Causes of aquagenic pruritus

A
  • Primary
  • Secondary
    • Urticaria - cold, dermographism, cholinergic, aquagenic
    • Haematoloigic malignancy: PCV (ruddy complexion), haemochromatosis (diffuse hyperpigmentation), Hodgkin, MDS, essential thrombocythemia
    • Infiltrates: mastocytosis, HES
    • Drugs: anti-malarial, clomipramine, testosterone induced erythrocytosis
    • Aquagenic pruritis of the elderly
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24
Q

Aquagenic pruritus treatment

A
  • Alkalinization of bath water to pH of 8 with baking soda
  • Light therapy
  • Capsaicin - can decrease symptoms but long-term use not ideal
  • Systemic: cyproheptadine, cimetidine, cholestyramine
  • Secondary: anti-histamines
25
Q

Pruritus in scars cause

A
  • scar remodeling can last 6 months - 2 years
  • pruritis with wound healing is common, can be prolonged
  • due to:
      1. physical stimuli - mechanical stimulation of nerve endings
      1. chemical stimuli: histamine, vasoactive peptides and prostaglandins
    • C fibres, both myelinated and unmyelinated, will contribute to itch perception
26
Q

Pruritus in scars treatment

A
  • emollients
  • Topical and intra-lesional steroids
  • Silicone gel sheets
  • Oral anti-histamines
  • Oral pentoxifylline
27
Q

Post-thermal burn pruritus risk factors

A

deep dermal injury, female, psychological distress

28
Q

Post-thermal burn pruritus treatment

A
  • emollients
  • topical anaesthetics
  • massage therapy
  • bathing in oiled water
  • morphine
  • oral gabapentin more effective than cetirizine
29
Q

Fibreglass dermatitis

A
  • manufacturing or construction
  • hands, and other non-covered sites involved
  • cutaneous: looks like scabies, eczema, folliculitis, urticaria
30
Q

Renal pruritus epidemiology

A
  • rare in children
  • otherwise doesnt correlate with age
  • haemodialysis –> has decreased over years, likely secondary to improvement in dialysis methods
    • for those getting 3X a week, the pruritus peaks in the evening after 2 days without dialysis, is relatively high during dialysis and is lowest the following date
31
Q

Renal pruritus aetiology

A
  • Overall, it is poorly understood
  • histamines not really thought to be part of the process
  • ?Accumulation of compounds that cross the dialysis membranes slowly
  • Parathyroid gland activity –> however no correlation observed with PTH levels
  • Pruritus does not correlate with xerosis, SC hydration or sweat secretion
  • Peripheral neuropathy –> may be manifestation of this
  • Opioid accumulation
  • IL-31 has been reported –> topical tacrolimus food for this
32
Q

Renal pruritus management

A
  • Assess:
    • Serum PTH –> treat if appropriate
    • Quality of dialysis: Kt/V: urea clearance multiplied by dialysis time divided by volume of urea distribution is >1.2
    • If itch persists - gabapentin after each dialysis can be tried
  • General skin care measures
  • Topicals
    • Capsaicin
    • Gamma-linoleenic acid - 2.2% QID
    • Pramoxine
    • Cromolyn sodium
  • Systemic
    • First line
      • Gabapentin 100-300 mg daily
      • Pregabalin - 25-75 mg daily
      • Phototherapy
    • Second line
      • Naltrexone - 25-100 mg daily
      • Nalfurafine 2.5-5 microg PO or IV (K-opioid receptor blocker)
    • Others:
      • Charcoal
      • Montelukast
      • Cromolyn
      • Thaldiomide - 100 mg daily
      • Ketotifen
      • Doxepin
      • Sertraline - 25-100 mg daily
      • Pentoxifylline
      • Lidocaine
      • EPO
      • Cholestyramine
    • Ultimate: renal transplant
33
Q

Causes of cholestatic pruritus, and pathogenesis

A
  • Most common:
    • Primary biliary cholangitis
    • Primary sclerosing cholangitis
    • Choledocholithiasis
    • Bile duct carcinoma
    • Cholestasis
    • Chronic HCV

Aetiology

  • ubnknown
  • ?bile acids –> but not always elevated
  • increased opioidergic neurotransmission or neuromodulation in the CNS may contribute
  • More recent studies indicate: lysophosphatidic acid (LPA) and autotaxin (ATX, lysophospholipase D) are associated with increased itch
34
Q

Cholestatic pruritus clinical

A
  • generalized, migratory and not relieved by scratching
  • worse on hands, feet, body regions constricted by clothing
  • worse at night
  • can be an early symptom that develops years before any other manifestation of the liver disease
35
Q

Cholestatic pruritus treatment

A
  • Treat underlying cause
  • Intra-hepatic cholestasis of pregnancy: UDCA (ursodeoxycholic acid) reduces itch and serum bile acid levels - due to improvement of hepatobiliary secretion - 13-15 mg/kg or 1 g daily
  • first line for others:
    • Cholestyramine 4-16 g po daily- binds bile acids in the small intestine and faecally excretes them
  • Second line:
    • rifampin: 300-600 mg daily reduces ATX expression on a transcriptional level
  • Third line
    • Naloxone 0.2 microg/kg/min with 0.4 mg IV bolus
    • Naltrexone 25 mg BD PO
    • Nalfurafine 2.5-5 microg daily
  • Fourth line:
    • Sertaline 50-100 mg daily
  • Last: liver transplant
  • Other options:
    • Phototherapy, bright light therapy
    • Nalmefene: mu opioid blocker, start at 2 mg on day 1, 5 mg day 2, 10 mg day 3 –> can incr to 120 mg daily
    • Butorphanol nasal spray: 1-2 mg daily, also opioid blocker
    • Ondansetron
    • Paroxetine
    • Dronabinol - cannabinoid B1 receptor agonist
    • Phenobarbital - 2-5 mg/kg daily
    • Stanozol
    • Propofol
    • Lidocaine
    • Thalidmoide
  • Procedural
    • Nasobiliary drainage
    • Other methods to remove pruritic factors: plasmapharesis, plasma separation, anion adsorption
36
Q

Iron deficiency pruritus clinical

A

Generalized or localized
Particularly perianal and vulvar region
Improves with iron supplementation

37
Q

PCV associated pruritus

A
  • Aquagenic pruritus can precede diagnosis by several years, eventually affects 30-50% of patients –> should always consider this diagnosis in aquagenic pruritus
  • 95% of patients with PCV have a JAK2 mutation –> results in activation and agonist hypersensitivity in basophils –> may result in the aquagenic pruritus
  • MOA: ?platelet aggregation –> histamine release –> pruritus
38
Q

PCV pruritus treatment

A

Rx: aspirin, can provide relief for 12-24 hours, alternatives: phototherapy, SSRI (small series), JAK inhibitor ruxolitinib, IM inferon-alpha, anti-histamines

39
Q

Paraneoplastic itch

A
  • Paraneoplastic itch: systemic reaction to the presence of a tumour or a haematological malignancy, neither induced by the local presence of cancer cells nor by tumour therapy
  • Most commonly seen with myeloproliferative neoplasms, Hodgkin disease, NHL
  • Recalcitrant pruritus should be evaluated for an underlying malignancy
  • Intensity and extent do not correlate with tumour involvement
  • MOA:
    • ?toxic products from necrotic tumour cells entering circulation
    • tumours producing chemical mediators
    • allergic reaction to tumour specific antigens
    • increased proteolytic activity
    • histamine release
    • Biliary obstruction
    • Central nervous system invovlvement
    • From treatments - surgery, chemo, radio, etc
40
Q

Itch associated with Hodgkin disease and MOA

A
  • Noctural generalized pruritus, with chills, sweating and fever –> some argue should become a B symptom
  • Severe, persistent pruritus is a poor prognostic factor
  • MOA:
    • Reed-Sternberg cells secrete IL-5 –> eosinophils
    • Histamine release, leukopeptidases, bradykinin
    • Hepatic involvement?
41
Q

Hodgkin disease treatment

A
  • Lymphoma treatment
  • Topical steroids
  • Oral mirtazapine
  • Aprepitant –> NK1 receptor blocker
42
Q

Thyroid changes that result in itch

A
  • hyperthyroidism –> severe generalized

- Hypothyroidism –> dry skin –> asteatotic eczema with pruritus, can also get local or generalized pruritus

43
Q

Diabetes itch

A
  • generalised pruritus
  • can get localized: genital and peri-anal areas –> diabetic women with poor glycaemic control
  • predisposition to candidiasis
  • Diabetic neuropathy –> burning and prickling sensations as well
44
Q

Pruritus in HIV and AIDs

A
  • occasionally can be presenting symptom
  • HIV: develop pruritic dermatoses such as pruritic papular eruption, eosinophilic folliculitis, severe seb derm, psoriasis, scabies, insect bite reactions, etc
  • Intractable pruritus and HIV viral load has been observed
  • Immunologic markers associated with pruritus in HIV patients:
    • elevated IgE
    • peripheral hypereosinophilia
    • Th2 type cytokine profile
45
Q

Pruritus in HIV treatment

A
  • topical steroids and antihistamines
  • anithistamines with anti-eosinophilic potential may be better –> cetirizine
  • UVB
  • ART –> can help, but sometimes can flare skin conditions
  • Thalidomide: 100-300 mg/day
46
Q

Medications that cause pruritus (remember liver, skin, nervous system, mediators)

A
  • Any medications that affect the liver:
    • Cholestasis: oestrogens, captopril, sulfonamides, erythromycin
    • Hepatotoxicity: panadol, steroids, minocycline, augmentin, halothane, phenytoin, sulfonamides
  • Any medications that affect the skin:
    • Xerosis: retinoids, tamoxifen, beta-blockers, clofibrate, beta-blockers
    • Phototoxicity: psoralens
  • Any medications that affect the nervous system:
    • Opioids
    • Recreational drugs
    • Anti-depressants: SSRIs
  • Any medications that result in increased mediators:
    • ACEI –> increased bradykinin
    • NSAIDs –> increased leukotriene
    • Hitamine –> betahistine
  • Other:
    • EGFR inhibitors
    • PD-1s
    • TK inhibitors
    • Chloroquine –> MRGPR stimulation
    • Starch –> deposition
    • Idiopathic: clonidiine, gold salts, lithium, bleomycin
47
Q

Dysaesthesia definition

A

unpleasant abnormal sensation

48
Q

List all the types of localized neurologic pruritus

A
  • Trigeminal trophic syndrome –> face
  • Brachioradial pruritus –> arm
    • Radial dorsal antebrachial cutaneous nerve
    • intermittent pruritus or burning pain on the dorsolateral aspects of the forearms and elbows
    • degenerative osteoarthritis on x-ray in 50%, rarely associated with spinal cord tumour
    • UV light exacerbates, may report relief with ice
  • Cheiralgia paraesthetica –> dorsum of hand
    • Mononeuropathy of the superficial branch fo the radial nerve
    • Numbness, tingling, burning
    • Trauma or pressure –> tight watch, etc
  • Notalgia paraesthetica –> medial scapular borders
    • Posterior rami T2-6 –> degenerative change in 60% of affected patients. These nerves take a right angle course through the multifidus spinae muscle –> entrapment and injury
    • Rarely associated with MEN Type 2a (childhood or adolescence)
    • Hyperpigmented patch due to chronic rubbing (correlates with dermal melanophages)
    • Focal macular amyloidosis
  • Meralgia paraesthetica –> lateral thigh
    • Lateral femoral cutaneous nerve –> pressure on this as it passes under the inguinal ligament
    • Allodynia associated as well
    • Risk factors: obesity, pregnancy, prolonged sitting, tight clothing, carrying heavy wallets in trouser pockets, lumbar radiculopathy
  • Digitalgia paraesthetica –> fingers
    • Digital nerves of fingers (can be toes too)
    • Trauma or pressure
49
Q

Neurologic pruritus treatment

A
  • topical capsaicin 0.025-0.3% 3-6 times a day for >4-6 weeks
  • Topical anaesthetics or steroids
  • Oral gabapentin or pregabalin
  • Acupuncture
  • Imaging
  • Referral to ortho and neurology
  • Physical therapy, nerve blocks, surgical decompression
50
Q

Burning Mouth Syndrome (Orodynia) epidemiology and aetiology

A
  • Epi: middle-aged or older adults, F>M
  • Aetiology:
    • Malignant lesion
    • Exogenous: ill-fitting dentures, any medications that cause xerostoma
    • Infectious: candidiasis
    • Papulosquamous: contact dermaitits
    • Metabolic: iron, zinc, folate, B12
    • Endocrine: diabetes, hypothyroidism, menopause
51
Q

Burning Mouth Syndrome (Orodynia) clinical

A
  • Bilateral: anterior 2/3 of tongue, palate and lower lip
  • Types:
      1. 35%: absence of symptoms on awakening, gets worse throughout the day
      1. 55%: constant
      1. 10%: days of remission that follow no identifiable pattern
52
Q

Burning Mouth Syndrome (Orodynia) treatment

A
  • Treat underlying cause
  • TCAs, low dose benzos, gabapentin
  • Anti-depressant
  • Topicals: capsaicin, lidocaine, anaesthetics, tetracycline, hydrocortizone, Maalox
  • CBT and alpha-lipoid acid 600 mg daily
53
Q

Burning scalp syndrome

A
  • diffuse, burning pain, pruritus, numbness, tingling of the scalp
  • Secondary causes: seb derm, LPP, ACD, ICD, DLE
  • Assoc: depression and anxiety
  • Rx: gabapentin, TCA, topical capasaicin
54
Q

Dysaesthetic anogenital pain syndromes

A
  • most common cause: haemorrhoids and fissures
  • Other: trauma, infection, testicular torsion, malignancy
  • Syndromes:
    • Levator ani: intermittent burning pain or tenesmus of the rectal or perineal area, aggravated by sitting or elimination
    • Procatlgia fugax: stabbing pain
    • Coccydynia: localized to the coccyx, intermittent or persistent pain
    • Male genital pain syndrome: intermittent, continuous or episodic pain during penetration, urination, ejaculation, etc
    • Koro syndrome: acute anxiety, fear of genitalia are inwardly retracting and pain
55
Q

Trigeminal neuralgia

A
  • Recurrent paroxysms of sharp pain - seconds to minutes, trigeminal distribution
  • Unilateral (right sided more common)
  • can occur several times a day
  • can be triggered by teeth, eating, talking
  • Secondary causes: MS, trauma, tumour
  • MRI: 80-90%: compression of trigeminal nerve root by a vascular loop
  • Rx: carbamazepine in 70-90% works well, oxcarbazepine, lamotrigine, baclofen, botox, surgical: microvascular decompression and ablation
56
Q

Trigeminal trophic syndrome

A
  • Self-mutilation triggered by dysaesthesia together with hypaesthesia from damage to the sensory portion of the trigeminal nerve
  • Nasal tip is spared, as it is supplied by the external nasal branch of the anterior ethmoidal nerve
  • clinicl: small crust that develops into crescentic ulcer
  • Underlying nerve damage: iatrogenic due to therapeutic ablation for trigeminal neuralgia, stroke, HSV, trauma, craniofacial surgery
  • Ddx:
    • malignancy
    • infections
    • inflamamtory: granulomatosis with polyangiitis, PG
    • Factitial disease
  • Rx:
    • carbamazepine
    • gabapentin, amitryptyline
    • pimozide
    • protective barriers
    • surgical repair of the defect with innervated skin flaps
57
Q

Complex regional pain syndrome

A
  • upper extremities, particularly hands, involved
  • disproportionate pain
  • accentuated pain and sensation, can have vasomotor dysfunction, hypertrichosis, hyperhidrosis, nail dystrophy, motor dysfunction
  • Refer to neuro
58
Q

Congenital Insensitivity to pain and related conditions

A
  • basically have cuts etc everywhere and increased risk of infection because they don’t feel pain
  • Stains for neuronal markers: PGP-9.5 –> absence of innervation to sweat glands, BV, arrector pili muscles

Morvan disease, Riley-Day syndrome., CIP with anhidrosis

Derm (57 decks)

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