Pruritus, or itch, is a sensation that provokes the desire to scratch. Chronic pruritus lasts more than 6 weeks and can be caused by skin diseases or systemic diseases. Itch is transmitted through unmyelinated C fibers and is a distinct sensation from pain. Scratching provides temporary relief by stimulating myelinated fibers or damaging sensory nerve endings. Management of pruritus involves general skin care, topical agents like corticosteroids, calcineurin inhibitors, local anesthetics, and antihistamines, as well as treating any underlying cause.

1. +PRURITU
S
PRESENTER:
DR. KEZHALETO
MODERATOR:
DR. ANANTA

2. +INTRODUCTION
 Pruritus can be defined as an uncomfortable sensation and
emotional experience associated with an actual or perceived
disturbance to the skin that provokes the desire to scratch.
 Chronic pruritus is defined as pruritus lasting more then 6
weeks
 The sensation of itch was first described in 1893 by Radcliffe
Crocker.
 It is a dominant symptom of skin diseases and can also
occur in many systemic diseases
 Although often publicly perceived as trivial, pruritus is
socially disabling and a cause of serious impairment of
quality of life.

3. +
PATHOPHYSIOLOGY
 Itch, like pain is perceived by unspecialized free nerve endings
located close to the dermo-epidermal junction.
Pain => withdrawal reflex
Itch => scratch reflex
 Itch receptors are unmyelinated and confined to the skin and
cornea.
 Rothman proposed that itch and pain are transmitted along the
same nerve pathways i.e. unmyelinated polymodal C fibres
with:
 Low intensity stimulation-itch
 High intensity stimulation-pain

4. +
 Significant advances in recent years have helped to disprove
many of the conventional concept
 Itch and pain are separate sensory modalities
 Studies have identified ‘dedicated’ itch sensitive C fibers that
transmit itch and comprise no more than 5% of total C fibers.
 Of those itch-sensitive C fibres, 10% are histamine dependent
and 90% are histamine independent
 These C nerve fibers have:
 Exceptionally slow conduction velocity
 Unusually wide innervation territories
 Sensitive to pruritogenic and thermal stimuli, but not mechanical
stimuli. (raising the temperature lowers the threshold pruritus)
 Also transmitted via myelinated A-delta afferents

5. +
 Scratching
 A reflex functioning at a spinal level, modified greatly by higher centres.
 Scratch‐induced relief could be due to temporary suppression of
facilitating circuits in the relay synapses of the spinal cord by
stimulation of fast‐conducting myelinated afferents
 Alternatively, scratching could simply damage sensory nerve endings,
repair occupying several minutes.
 Sensitisation
 Defined as the increased response of primary sensory neurons to itch
and pain mediators
 Alloknesis
 Non pruritogenic stimuli in an area of CP elicit a sensation of itch
 Hyperknesis
 Enhanced itch sensation elicited by a normal itch stimulus

6. + NERVE PATHWAYS
PRURITOGEN

FREE N. ENDINGS

UNMYELINATED TYPE C FIBRES(1st order)

DORSAL HORN OF GREY MATTER OF SPINAL
CORD(2nd order neurons)

CONTRALATERAL SPINOTHALAMIC TRACT

POSTEROLATERAL VENTRAL THALAMUS => MULTIPLE AREAS OF BRAIN
.

7. +

8. +
Areas of the brain involved in pruritus
 Somatosensory cortex areas I and II - reflect the detection,
localization, and discrimination of itch.
 Somatosensory cortex area II, the insular cortex and the
claustrum - have discrete areas that respond to both presence of
itch and the intensity of itch
 Anterior cingulated cortex and the insular cortex - integrate the
sensory and emotional experience of pruritus
 Pre-motor area and the supplementary motor area - scratching
response is planned.
 Prefrontal cortex and striatum - motivation and craving to scratch
 Strong correlation between the relief of itch with scratching and
the activity of the brain’s reward circuits - the substantia nigra,
ventral tegmental area, and the raphe nucleus

9. MEDIATORS RECEPTOR CLINICALLY RELEVANT
MECHANISM OR DISEASE
DRUGS ACTING
AGAINST
Acetylcholine Muscarinic Atopic eczema Atropine
Histamine H1, H4 Urticaria, insect bite reactions Hydroxyzine, cetrizine
IL‐31 IL‐31RA/OSMR Atopic eczema, familial
primary cutaneous
amyloidosis
Nemolizumab
Endothelin 1
(ET-1)
Endothelin A receptor Release of nitric oxide,
vasodilatation
Ambrisentan, bosentan
Leukotriene B4 TRPV-1 channel and
BLT-2 receptor
Uremic pruritus, atopic dermatitis,
psoriasis
Capsaisin-desensitises
Nerve growth
factor (NGF)
Tropomyosin receptor
kinase A (TrkA)
Atopic eczema, psoriasis.
Receptors, peripheral sensitization
Entrectinib
Tryptase Proteinase-activated
receptor-2 (PAR-2)
Atopic eczema, cutaneous
mastocytosis
Substance P Neurokinin 1 receptor
(NK-1)
Atopic eczema, prurigo
nodularis, psoriasis
Aprepitant
Chemical mediators of itch

10. Mediators Receptor Clinically relevant
mechanism or disease
TNF-alpha TNF receptor Sensitizes nocioceptive nerve endings Infliximab,
adalimumab,
Thalidomide
Thromboxane A2 TP receptor Polycythaemia
Rubra Vera
Seratrodast,
Picotamide
Glutamate Gastrin releasing
peptide receptor
histaminergic-
independent transmission
Endorphins μ opioid receptor Cholestatic pruritus Naltrexone, Naloxone
Dynorphin κ opioid receptor Uraemic pruritus Nalfurafine-agonist
Natriuretic poly-
peptide B (Nppb)
Natriuretic peptide
receptor A (Npra)
excite downstream GRPR expressing
neurons
Lymphocytes:
• Th1
o IL-2 is pruritogenic.
o IFN-gamma upregulates IL-31 receptors.
• Th2
o IL-31 is pruritogenic

12. +
Intrinsic anti-pruritic system
 Two main pathways
 Ascending signal from the periaqueductal gray (PAG) to the thalamus
 Descending signal from the PAG to the dorsal horn
 At the dorsal horn, Bhlhb5 fibres interneurons transmit an
inhibitory signal from the pain pathway
 k-opiod receptors which are located both peripherally and
centrally
 Peripheral receptors including:
 CB1 and CB2 endocannaniboid receptors.
 Cold receptors (TRPM8).

13. +Classifications of chronic pruritus
 Neuroanatomical classification (based on aetiology)
 1. Pruritoceptive: originating in the skin
 2. Neuropathic: resulting from peripheral nerve damage
 3. Neurogenic: due to centrally acting mediators
 4.Psychogenic: predominantly psychological basis
 Differential diagnostic classification (underlying disease)
 Dermatological diseases
 Systemic diseases
 Neurological diseases
 Psychosomatic ⁄ psychogenic diseases
 Mixed
 Other (unknown cause)

14. +Systemic diseases associated with itching
Hepatobilliary disease Primary billiary cirrhosis, pruritus
gravidarum, extrahepatic billiary
obstruction, drug-mediated cholestasis
Renal disease Chronic renal failure, uremia
Hematopoetic disorders Polycythemia vera, iron deficiency anemia,
hodgkins lymphoma, leukemias,
mastocytomas, plasma cell dyscrasias
Metabolic and endocrine
disorders
Diabetes mellitus, carcinoid syndrome, hypo
and hyperthyroidism
Neurologic disorders Multiple sclerosis, cerebral tumors, cerebral
abscess
Infestations Hookworm, ascariasis, onchocerciasis
Psychogenic disorders
Miscellaneous Viral exanthem, post menopausal states, HIV

15. +
 Onset: acute or chronic
 Acute -seen in cutaneous diseases such as scabies, insect bite
-generally rules out systemic diseases
 Nature of sensation: burning, pricking, stinging
 Burning classically seen in dermatitis herpetiformis
 Pricking in aquagenic pruritus
 Stinging in insect bite reaction
 Continuous or intermittent
 most conditions present with continuous itching
 Causes of intermittent itch: Chronic urticaria, Aquagenic pruritus,
Psychogenic pruritus, CNS disorders such as multiple sclerosis
 Diurnal variation
 In most causes of organic pruritus, night-time worsening occurs e.g. scabies
 However psychogenic pruritus seldom worsens at night
HISTORY

16. +
 Localized itch
WITH RASH WITHOUT RASH
Psoriasis Notalgia paraesthetica
Irritant contact dermatitis Brachioradial pruritus
Asteatotic eczema Post-stroke pruritus
Nummular eczema Phantom itch
Pompholyx Multiple sclerosis
Dermatophytosis Diabetes mellitus
Stasis dermatitis Transverse myelitis
Brain tumor or abscess

17. +
 Generalized itch
WITH RASH WITHOUT RASH
Allergic contact dermatitis Renal failure
Atopic dermatitis Cholestasis
Bullous pemphigoid Thyroid disorders
Dermatitis herpetiformis Iron deficiency
Drug hypersensitivity Hodgkin’s lymphoma
Insect bite reaction Leukemia
Mastocytosis Multiple myeloma
Mycosis fungoides Polycythemia vera
Urticaria Carcinoid tumor
Scabies HIV
Sjogrens syndrome

18. +
 Occupational history
 For suspected cases of contact dermatitis
 Initiating or aggravating factors:
 Bathing- aquagenic pruritus.
 Exercise- cholinergic urticaria
 Cold temperature/skin cooling- cold urticaria
 Warm temperatures- worsening of AD
 Irritants such as detergents, solvents- in eczemas
 Drug history
 Other pertinent historical factors
 Family or personal history of atopy
 Social history-household and other contacts(relevant in scabies)
 Contact with pets
 Sexual history- relevance in HIV and HCV infections
 Allergies- topical and systemic

19. +SYSTEMIC REVIEW
GENERAL HEALTH Fever, sweats, chills, fatigue, loss of
appetite, weight loss
Lymphomas, leukemias
ENDOCRINE Polyuria, polydypsia, temperature intolerance,
tremors
 Thyroid disorders, Diabetes mellitus
OPHTHALMIC Eye signs, exophthalmos
Hyperthyroidism
GASTROINTESTINAL Nausea, vomiting, change in bowel habits,
hepatosplenomegaly,jaundice
Lymphomas, carcinoid syndrome, cholestasis,
uremia
HEMATOPOIETIC Pallor, bleeding, lymphadenopathy
Lymphomas, multiple myeloma, leukemia

20. +
GENITOURINARY Colour of urine, frequency, pregnancies
Uremia, pruritus gravidarum, diabetes
mellitus
NEUROLOGIC Headaches, paraethesias, visual disturbances
Multiple sclerosis, CNS tumors
MENTAL STATUS Sleep disturbances, mood lability, hallucinations
Psychogenic pruritus, cholestasis, uremia
SKIN Pigmentation, sweating, xerosis, jaundice
Uremia, thyroid disorders, cholestasis,
polycythemia vera
HAIR Texture, hair loss,
Thyroid disorders
NAILS Grooving, colour changes, curvature
Thyroid disorders

21. +Mucocutaneous examination
 Lesions associated with primary dermatoses should be searched
for and evaluated
 Secondary changes from scratching such as
 Excoriations
 Lichenification
 Secondary impetiginization
 Prurigo nodularis
 Lichen simplex chronicus
 Butterfly sign
 Relatively hypopigmented butterfly-shaped area seen on the mid-
upper back which is inaccessible to the hand
 If lesions present in this area, likely to be a primary dermatosis,
 Morphology of lesions at this site is not altered due to scratching

22. +INVESTIGATIONS
Investigations Relevant diseases
Complete blood count with
differential
polycythemia vera, hematologic
malignancies, iron deficiency
Erythrocyte sedimentation
rate
Inflammatory conditions
Blood glucose Diabetes
Blood urea nitrogen, creatinine Chronic renal failure
Alkaline phosphatase, serum bilirubin Cholestasis, primary biliary cirrhosis,
hepatitis C
Thyroid function tests Hyperthyroidism, hypothyroidism
Urinalysis UTI, Drugs induced, Diabetes, liver,
kidney diseases
Stool for occult blood if age > 40
years
malignancy in GI tract

23. +
Investigations Relevant diseases
Stool for parasites Genito‐anal pruritus
Hepatitis B & C antibodies Hepatitis, cold-induced urticaria and
urticarial vasculitis
HIV antibodies HIV
ANA Autoimmune diseases, urticarial
vasculitis
RA factor Autoimmune conditions.
Complement assay (C3, C4) urticarial vasculitis, hereditary
angioedema
IgE level Allergic condition, Atopic eczema
Chest X‐ray Hodgkin disease-lymphadenoathy
Ultrasound abdomen Liver, kidney diseases

24. +Skin biopsy
 A primary lesion unaltered by secondary changes from
scratching is ideal. e.g. from the mid-upper back
 Diagnosis can also be made on a biopsy of clinically normal
skin in a few cases in the absence of primary lesions:
 Drug hypersensitivity
 Urticaria
 Papular urticaria
 Scabies
 Pemphigoid
 DH
 Linear IgA dermatosis
 Mastocytosis
 Perilesional skin for DIF :
 Bullous pemphigoid
 DH
 Drug hypersensitivity

25. +
MANAGEMENT
 General measures for pruritus associated with dry skin:
 Avoid hot and prolonged baths
 Avoid irritant substances
 Avoid Hot and spicy food, alcohol
 Avoidance of excitement, strain, stress
 Use cotton clothing
 Skin moisturizer on a daily basis especially after showering and
bathing

26. +Topical agents
 Cooling agents :
 Relieves itch by activating A-delta cold afferents,
 Calamine lotion, menthol and phenol(1 to 2%)
 Corticosteroids :
 Useful if pruritus is associated with inflammatory dermatoses
 Anti-inflammatory
 Attenuate histamine and kinin-induced vasodilation
 Inhibits the formation of pruritogenic prostaglandins and leukotrienes
 Adverse effects: increased skin fragility, telangectasia
 Topical calcineurin inhibitors :
 suppress IL-2 production
 Tacrolimus(0.03-0.1%), Pimecrolimus(1%)
 Use with caution: combined with UV therapy, children <2 years,
immunocompromised patients

27. +
 Local anaesthetics:
 Pramoxine (1% or 2.5%), lidocaine and prilocaine (2.5%)
 However these drugs can cause contact dermatitis, and cardiac
arrythmias if absorbed systemically
 Antihistamines:
 Topical antihistamines include Diphenhydramine and
Mepyramine
 However their use is limited by contact sensitization
 Topical Doxepine:
 A tricyclic antidepressant with potent anti-H1 properties
 Adverse effects: drowsiness, allergic contact dermatitis
 5% cream applied 3 times a day can be used in AD

28. +
 Emollients :
 Useful in managing pruritus associated with xerosis
 Miscellaneous :
 Capsaicin:
 pungent principle in red pepper
 Acts by depletion of substance P from unmyelinated C fibers
 Compliance poor due to burning sensation in early stages of
treatment
 used as a 0.075 – 1.0% cream
- Notalgia paraesthetica
- Brachioradial pruritus
- Uremia (localized itch)

29. + SYSTEMIC THERAPY
ANTIHISTAMINES:
 H1 blockers are the agents of choice in pruritic conditions where
histamine is the principle mediator e.g. urticaria, insect bite reaction
 In other conditions such as AD there are conflicting reports of their
efficacy
 Positive effects in AD may be due to decreased mast cell degranulation
rather than receptor blockade
 H2 blockers have a role in the management of pruritus due to Hodgkin’s
lymphoma, polycythemia vera and chronic urticaria

30. +
ANTIHISTAMINES:
AGENT SEDATING METABOLISM EXCRETION PREGNANCY
CATEGORY
Chlorphenira
mine
+ Primary site liver Predominantly renal B
Hydroxyzine + Cetirizine is an active
metabolite
Over 70% renal
excretion
C
Promethazine + Significant hepatic
metabolism
Predominantly renal C
Fexofenadine - 5% from liver 11% from renal C
Cetirizine - Levocetirizine an active
metabolite
Over 70% renal
excretion
B
Levocetirizine - 14% from liver Largely renal B
Desloratadine - Very extensive 45% from renal C
Bilastine - No liver metabolism 33% from renal

31. +ANTIDEPRESSANTS
 Doxepine:
 A tricyclic antidepressant with H1 and H2 receptor antagonistic action.
Dose 25-300 mg/day
 Also blocks cholinergic receptors.
 Senile, psychogenic pruritus, chronic urticaria not responding to H1
blockers.
 Paroxetine:
 Selective serotonin re-uptake inhibitor
 Useful in once daily doses of 5-10 mg
 Paraneoplastic itch, Intractable itch not responding to conventional
therapy
 Mirtazapine:
 A tetracyclic antidepressant with additional H1 and 5HT3 receptor
blocking action
 Antipruritic action occurs in once daily doses of 15-30mg
 Paraneoplastic itch and cholestasis, Uremia, Intractable itch not
responding to conventional therapy

32. +
ANTICONVULSANT
 Gabapentin
 Precise mechanism of action is unclear
 Prevents release of neurotransmitters from pre-synaptic
nerve terminals by action on voltage-dependent calcium
channels
 Effective in uraemic pruritus, neuropathic itch
 Adverse effects are constipation, weight gain, drowsiness,
ataxia, and blurred vision
 300 mg – 1800 mg/day

33. +
OPIATE AGONISTS AND ANTAGONISTS
 u-opioid antagonists
 Naltrexone: long-lasting, selective blockade of mu-opiate receptors.
Used as 20-250mg OD orally
 Naloxone: IV infusion of 0.2μg/kg/min used in emergency treatment of
acute exacerbation of itch of cholestasis
 kappa-opioid agonist
 Nalfurafine hydrochloride
 Butorphanol
 kappa-opioid agonist and mu-opioid antagonist
 1 to 4 mg inhaled at bedtime
 Cholestasis, CRF, Aquagenic pruritus, CTCL, Intractable itch not
responding to conventional therapy

34. +
PHOTOTHERAPY
 UVB radiation alone or combined with UVA has been useful in:
 Patients with contraindications to systemic agents
 Other therapies have failed.
 Uremic pruritus, Atopic eczema, Cholestasis-induced pruritus,
Aquagenic pruritus, Prurigo nodularis
 Mechanism of action:
 Decreases mast cells in dermis
 Degeneration of itch transmitting C fibers
 Photoinactivation of pruritogens in the skin
 Decreases the number of langerhans cell
 Decrease the concentration of divalent ions in the skin
 Not advised for patients who are taking topical calcineurin
inhibitors

35. +
MISCELLANEOUS
 LEUKOTRIENE RECEPTOR ANTAGONISTS
 Zafirlukast, Montelukast
 MAST CELL STABILIZER
 Cromolyn sodium- AD
 THALIDOMIDE
 Suppresses TNF alfa – uremic pruritus
 ONDANSETRON
 5-HT3-receptor antagonist – cholestatic pruritus
 BEHAVIORAL THERAPY
 Stress-reduction techniques and coping mechanisms that interrupt
the itch–scratch cycle

36. + UREMIC PRURITUS
 Is a manifestation of CRF and rarely seen in ARF
 Pruritus is unrelated to the primary pathology causing CRF
 Seen in 20-50% patients, and 50–90% of patients undergoing
peritoneal dialysis or hemodialysis
 Pruritus range from localized and mild to generalized and severe,
and tends to be persistent

37. +
PATHOGENESIS
 Mechanism underlying uremic pruritus seems to depend on
many factors
 Dryness of skin
 secondary hyperparathyroidism
 Immune mediated
 Peripheral neuropathy
 Opioid imbalance
 Abnormal mast-cell proliferation
 elevated levels of serotonin
 During hemodialysis, contact of blood and dialysis membranes leads
to production of pruritogenic cytokines such as IL-2
 Neurogenic hypothesis- due to abnormal sprouting of nerve fibers at
the dermo-epidermal junction
 Hyperparathyroidism which can lead to secondary increase in the
number of mast cells

38. +
TREATMENT MODALITIES
 Topical:
 Emollients
 Capsaicin 0.025%
 Tacrolimus 0.03%
 Systemic:
 Phototherapy - antipruritic effect is noticed only after 1-2 months of
treatment
 Naltrexone 12.5 to 50 mg orally once daily
 Gabapentin 100–300mg 3 times a week
 Thalidomide- limited by adverse effects
 Antihistaminics and topical steroids are generally unhelpful
 The only curable and reliable treatment for renal pruritus is renal
transplantation.

39. +CHOLESTATIC PRURITUS
 Seen in 20-25% of patients with jaundice.
 More common in intrahepatic than extrahepatic cholestasis
 Rubbing rather than Scratching, so secondary excoriation,
eczematization and infection less common
 Itching is intractable and most severe at night
 Predilection for hands and feet, but may be generalized.
 Worse itch premenstrually, during hormone replacement therapy,
and in 0.5% of pregnant women
 Pruritogens thought to be involved:
 bile salts, bile acids, bilirubin, progesterone metabolites, histamine, and
endogenous opioids
 Recent studies suggest the enzyme autotaxin (ATX)

40. +
TREATMENT MODALITIES
 Cholestyramine
 Nonabsorbable anion exchange resins
 Rifampin
 P450 cytochrome enzyme inducer
 Inhibition of ATX expression
 Can be hepatotoxic, so liver tests should be monitored
 𝜇-OPIOID ANTAGONISTS
 Naltrexone 20-250mg OD orally
 Naloxone IV 0.2μg/kg/min used in acute exacerbation
 Ondansetron
 5-HT3-receptor antagonist
 Appears to affect opioid pathways
 Other therapies that may be effective are thalidomide, serotonin-
selective reuptake inhibitors, UV-B

41. +
HEMATOLOGIC PRURITUS
IRON DEFICIENCY:
 With or without anemia
 Other signs include glossitis and angular cheilitis
 Iron is necessary for activity of many enzymes
 Treatment- Iron supplementation, continued for 3 months after
haemoglobin levels are back to normal

42. +
POLYCYTHEMIA VERA (AQUAGENIC PRURITUS):
 30–50% of patients
 Characteristically precipitated usually by contact with water
 Other precipitating factors- sweat, alcohol, sudden change in
temperature
 Pruritus may precede diagnosis of PV by several years
 Possible mechanism - Platelet aggregation, and histamine
 Treatment modalities:
 Aspirin- treatment of choice
 Alkalinization of bath water with NaHCO3
 Topical capsaicin
 Antihistamines
 UVB phototherapy
 Others – Paroxetine, Cyproheptadine, Pizotifen, IFN-α

43. +
ENDOCRINE PRURITUS
THYROID DISORDER
 4–11% of patients of thyrotoxicosis
 Intractable itching, associated with a warm moist skin
 Increased blood flow and skin temperature - decreased itch
threshold
 Myxoedema and hypothyroidism associated pruritus is rare
 Related to dryness of skin - Emollients

44. +
DIABETES
 About 3–49% of patients
 Often associated with xerosis cutis.
 Diabetic polyneuropathy with correlated dysfunction of sweating
 Pruritus in perianal/genital region more frequently in diabetic
women due to Candida albicans or dermatophyte infection
 Management:
 Emollients such as urea-containing moisturizers
 Topical polidocanol or menthol
 Refractory cases- Oral antihistamines, doxepin, Ultraviolet
phototherapy

45. + ATOPIC ECZEMA
 Interplay between epidermal barrier dysfunction and upregulated
immune cascades
 Patients exhibit reduced thresholds for itch and alloknesis
 Increased innervation density and expression of inflammatory
mdiators (SP, GPRP, IL-31)
 Pathogenic bacteria and yeast, often colonizing atopic skin, may
also directly activate peripheral nerves, exacerbating itch
Management
 Topical
 Emollients
 Steroids
 Tacrolimus/Pimecrolimus

46. +
 Systemic
 Short term steroids
 Cyclosporine
 Azathioprine
 Phototherapy
 Nonsedating Antihistamines are ineffective

47. + PRURITUS IN PREGNANCY
 About 20% of pregnant women
 Causes include:
 Polymorphic Eruption of Pregnancy
 Pemphigoid gestationis
 Intrahepatic Cholestasis of Pregnancy
 Atopic Eruption of Pregnancy
 Pustular psoriasis(Impetigo herpetiformis)
 Management
 Mild/moderate topical corticosteroids
 Oral antihistamine – Chlorpheneramine, cetirizine
 UVB phototherapy - Psoralen is a known mutagen and teratogen
 Permethrin, benzoyl benzoate, ivermectin- for scabies
 Oral prednisolone can be used in intractable cases

48. +
SENILE PRURITUS (WILLAN’S ITCH)
 Seen in ~50% of individuals in the 7th decade of life
 Pathogenesis:
 Result of excessive dryness of skin
 Altered stratum corneum barrier function
 Manifestation of underlying systemic disorder or adverse drug
reaction.
 Management:
 Liberal application of emollients
 Avoidance of chemical or mechanical irritants
 Antidepressants such as Doxepine or Paroxetine

49. +
PARANEOPLASTIC PRURITUS
 May occurs early or even precedes the clinical evidence of the
malignancy
 Causes - hodgkin’s lymphoma, polycythemia vera
-chronic leukemia, myelomatosis, sézary syndrome,
non‐Hodgkin lymphoma, solid tumors
 Hodgkin’s disease:
 Most common symptom-about 30% of patients
 Thought to be caused by release of histamine
 Mangement – Oral antihistamine, mirtazapine

50. + PSYCHOGENIC PRURITUS
 Diagnosis of exclusion when organic causes have been ruled
out
 Some studies suggests psychogenic cause in 1/3rd of patients
with cutaneous complaints
 Psychogenic cause of pruritus:
 Anxiety disorder
 Depression
 Personality disorder
 Dermatological conditions with psychogenic cause:
 LSC
 Prurigo nodularis
 Pruritus ani/vulvae/scrotum

51. +
 Management :
 If anxiety underlying cause:
-Hydroxyzine
-Doxepine
 If depression underlying cause:
-Amitryptylline
-Fluoxetine
 If delusional ideation:
-Pimozide
-Haloperidol

52. + BRACHIORADIAL PRURITUS
 Pruritus in elbow, adjacent lower and upper arms, shoulder and
neck
 Compressions of the nerve root of the cervical spine - disc
herniations, osteophytes, cervical rib
 Worsened by sunlight and improved by cold applications
 Cutaneous findings vary from no obvious changes to mild
erythema, lichenification, excoriations, xerosis
 MRI of cervical spine should be done
 Management:
 Topical anaesthetics
 Gabapentin
 Topical capsaicin

53. + NOTALGIA PARAESTHETICA
 A disorder similar to brachioradial pruritus in presentation as well
as response to therapy
 Nerve root entrapment (T2 to T6) may play a role in the
pathogenesis
 Site: mid-scapular region
 Mild lichenification and pigmentation with or without macular
amyloidosis
 HPE may show amyloid deposition
 Management
 Topical Capsaicin

54. +
THANK
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