Blok Special Sense

1. Group14
Tutor : dr. Sri Wahyuni, M.Kes

2.  11020150009 Aulia Amani
 11020150024 Nada Nahda
 11020150033 Ainun Jariah Muliadi
 11020150059 Nur Zamzam Azizah
 11020150065 Afrilia Chaerunnisa
 11020150081 A. ST. Zuraidha P.A
 11020150089 Indah Chintya Maharani
 11020150096 Muhammad Rizky Hidayat
 11020150109 Reza Novriadi Khautsari
 11020150119 Asyaratun Qamila

3. 29-year-old woman came to the polyclinic
with red scaly spots on the face, back and chest
since 4 months ago. The complaint is accompanied
by itching and the patient feels like scratching but
is light. If treatment complaints heal but then
reappear. Symptoms get heavier after the patient
is fired from his job and has not returned to work,
since 3 bulant erakhir. On physical examination,
erythema and skuama macules are found to be
slightly coarse and partly refined. Been to the
health clinic repeatedly but not changed even
more and more and more severe complaints due
to stress sufferers. The patient's sister history has
the same complaint. Patients often feel pain in
large joints.

4.  Macula is the primary efflorescence that is
merely a change of skin color without form
changes, as in tinea versicolor, Hansen
morbus.
 Erythema is a red macula, as in dermatitis,
lupus erythematosus.
 Skuama is the release of the horn layer from
the skin surface. Can be either smooth scales
(TV), moderate (dermatitis) or rough
(psoriasis). Skuama can be white (psoriasis),
brown (TV), or like fish scales (iktiosis).

5.  A 29-year-old woman
 Complaints red scaly spots Since 4 months
ago
 On face, back and chest
 Itchy
 Recovers but reappears
 Heavy after being fired
 Obtained macules, erythema, skuama rough
and smooth
 Often pain in large joints
 The patient's sister had the same complaint

7. A) contains epidermal Langerhans
cells,scattered immature dendritic
cells (D), and skin-homing memory
T cells (T) in the dermis. Normal-
appearing skin
B) manifests slight capillary
dilatation and curvature, and a
slight increase in the numbers
of dermal mononuclear cells
and mast cells (M). A slight
increase in epidermal thickness
is usually present.

8. C) is characterized by progressive
increases in capillary dilatation numbers
of mast cells, macrophages (MP), and T
cells, and mast cell degranulation (small
arrows). In the epidermis, there is
increasing thickness with increasingly
prominent rete pegs, widening of the
extracellular spaces, transient
dyskeratosis, spotty loss of the granular
layer, and parakeratosis. The fully
developed lesion.
Reference : Fitzpatrick’s Dermatology in general medicine, 8e, vol.2: 198.
D) is characterized by fully developed
capillary dilatation . The epidermis of
the mature lesion manifests markedly
increased (approximately tenfold)
keratinocyte hyperproliferation
extending to the lower suprabasal layers,

10. 1. Wahid, Syarifuddin, A.Miskad, Upik. 2016. IMUNOLOGI Lebih Mudah Dipahami. Surabaya: Brilian Internasional. Hal. 59, 62, dan 72
2. Price, Sylvia A., Wilson, Lorraine. 2005. Patofisiologi Konsep Klinis Proses-proses Penyakit. Ed. 6. Vol. 1. Jakarta: EGC. Hal. 165.
3. Habif, Thomas. 2016. CLINICAL DERMATOLOGY A Color Guide to Diagnosis and Therapy.6th Ed. China: Elsevier Page 182.
Erythema and Itchy(pruritus)
Tissue damage
Mediator release by
makrofag and mast
cell
Vascular respon by
endotel
Vasodilatation
Erythema
Histamine
1
Pruritus
sensation

11. In physiology, the amount of skuama,
lost in normal humans between 500-1000 mg
/ day. Keratin peeling occurs most often in
the palms of the hands, scalp, and forehead
(approximately 2-3,5 gr / m2 per 24 hours).
Because the body catabolizes 50-60 grams of
protein per day, this physiological exfoliation
plays an important role in protein
metabolism as a whole

13.  In erythroderma there is an increase in
epidermal peel rate
 In psoriasis and seborrhoeic dermatitis there
is an increase in epidermal proliferation
resulting in a finite to coarse skuama
•Freederg IM. Exfoliative dermatitis. Fitzpatrick et all.1996. Fitzpatrick’s dermatology in general medicine. 4th ed. Newyork: Mcgraw-
Hill. Chapter-41.p;94-106,236-238
•Schӧn MP, Boehncke WH.2005. Psoriasis. N Engl J Med;352:1899-912.

15.  Appear in skin surface that have a lots of hair and
sebacea glands, and produce a lots of sebum, such as
head skin, glabella, back, chest, axilla, inguinal
 Lesion start with mild exfoliation until a yellow crust
appear and attached to face skin and hair. It can cause or
not alopecia

17. CD 8 (T Cell)
(IL-1â, IL-2, IL-10, IFN-
ã, TNF-á)
tendon insertion, ligaments,
fascia, synovium, spine and
sacroiliac joints.
Joint pain
GMCSF EGF, IL-6, IL-8,
IL-12, IL-17, dan IL-23
may result in physiological changes of normal skin
to more keratinocytes fast, Blood vessels become
dilated, meandering, angiogenesis, and vascular
hypermealability
1. Eko V. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. 2014;41(5):352-355.
2. Ilmu Penyakit Kulit Dan Kelamin. Universitas Indonesia; 2016.

19. Pamela RD. Pengaruh Stres Psikologis terhadap Fungsi Pertahanan Kulit. 2012;39(6):420-422.
There are three theories that can
potentially explain the negative effects of
psychological stress on the host defense
function on infection and neoplasia:3
1.Psychoneuroimunoendocrine
dysfunction: an increase in
proinflammatory neuropeptides and
cytokine production with or without the
Hypothalamus-Hypophisis-Adrenal
pathway.
2.Increased levels of endogenous plasma
glucocorticoids caused by activation of
the Hipotalamus-Hipofi sis-Adrenal
pathway.
3.Skin steroidogenic system, through
local production of Corticotropin
Releasing Factor (CRF) which is a
mediator of the onset of further effects of
psychological stress on the skin

21. Recurn
Onset Type of lesionFamily History
Refrence : Gudjonsson JE, Elder JT. Psoriasis. In: WolffK, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors.
Fitzpatrick’sdermatology in general medicine. 7,ed. United States of America: McGraw Hill: 169-93.

23. Related
Psoriasis is an inherited chronic skin disease with a strong genetic
factor
HLA B13 and HLA DQ9, HLA Cw6 also play a role
Psoriasis Susceptibility 1 or PSORS1 (6p21.3)
When both parents develop psoriasis, the risk of a person getting
psoriasis is 41%, 14% if only experienced by one of them, 4% if 1
sibling is affected, and drops to 2% if there is no family history.

25.  1) Eczema
 2) Furunkel
 3) Herpes Zoster
 4) Pediculosis of
Kapitis
 5) Corrective
Pediculosis
 6) Pitiriasis Versikolor
 7.) impetigo
 8) scabies
 9) Urtikaria
 10.) psoriasis

27.  This comprehensive approach is collected in
a data set on a disease course history known
as the disease status of the patient (SPP).
 SPP includes anamnesis, physical
examination (general and specific),
laboratory tests (general and specific),
special tests, resumes (summary), inspection
suggestions, occupational diagnoses,
differential diagnoses, prognosis and disease
travel monitoring. The complete SPP is made
as follows.

28. anamnesis includes the identification of the
patient, the main complaint and the course
of the disease.What needs to be asked in the
main complaint is a complaint that
encourages the patient to seek medical
help.The course of the disease includes:
- since when to start getting sick (how many
days, weeks, months),
- how and what kind of abnormalities at first
(red-red, freckles, wounds, etc.),
- where the first disorder arises (foot, head,
face, limb),

29. - whether creeping / not, or disappearing,
- whether itchy, sick, or how,
- whether liquid / dry out,
- the drugs that have been used, how the drug is
affected, whether the disease is improving,
worsening or settling.
About family should be asked:
- the socio-economic family, the number of family
members, the way of life, and the illness within
the family or in the individuals around it.
- Is the cause of the disease related to a cause,
such as a result of employment, the injury caused
by a particular object, a relationship with the
season, or the effects of a factor in the
environment.

30. Examination of the general condition is
important, and should be sought to relate to
the skin disease being suffered. Examination
of the skin itself should be done in a bright
place, if necessary with the help of a
magnifying glass. First, the localization of the
disorder must be determined, ie:
a. Regional: r. facial, r. thoracic, r. Abdominal
b. With the relative region: 1/3 proximal left
inferior extremity, middle third right arm,
etc.

31. Primary skin rash:
• - Makula
- Erythema
- Papula
- Nodules
- Vesicles
- Bulls
- Pustula
- Urtika
- Tumors
- Cysts
Secondary skin
rash:
• - Skuama
- Krusta
- Erosion
- Excoriation
- Ulcers

32. 1. Size
2. Overview
3. Shape
4. Localization/deployment:
- Solitar, Multiple, Regional, Discrete, Symmetrical,
Bilateral, Unilateral, Universal, Generalized.

33.  To ensure the diagnosis must be supported by
laboratory examination and specific
examination. Examinations that can be done
are:
1. Routine blood examination, feces and urine,
and blood chemistry.
2. Examination of wet smear such as
examination of hyphae (with 10% KOH),
trichomonas (NaC1 0.9o / o).

34. 3. Inspection of secretions or ingredients from
kinks with special staining, such as Gram (for
bacteria), Ziehl Nielsen for acid-resistant
bacillus, gentian violet for viruses, dark field
microscope for spirochete, bubble fluid
examination (for calculating eosinophils) and
cell check Tzanck.
4. Serologic examination for syphilis, yaws.
5. Wood examination of skin fungus
infections.
6. Checking of allergy: scratch test, drops,
stick, puncture, and injection test.
7.Histopathological examination.

37. Psoriasis is a skin disease characterized by
tightly defined erythema with coarse and
transparent coarse skuama, chronic and
residif
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.

38. The immediate etiology of psoriatic arthritis is
still unknown; can be caused by a combination
of several factors such as:
genetics immune system,
environmental factor,
hard trauma (deep-Koebner phenomenon),
psychological stress factors,
metabolic stress,
as well as consumption of alcohol, cigarettes,
drugs (beta blockers, lithium, anti malaria,
sudden steroid cessation).
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.

39. The pathogenesis of psoriatic arthritis is regulated by
CD8 (T cells), completely unrelated to B cells
commonly found in other autoimmune diseases.
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.
T CELL TO TARGET
NETWORKS (tendon
insertions, ligaments,
fascia, synovium, spine
and sacroiliac joints)
ACTIVE TEMPLE
OUT SITOKIN
AND KEMOKIN
ACTIVATE
MACROFAG AND
LEUKOSIT
INFLAMATION
TISSUE
DAMAGE

40.  Symmetrical Arthritis
 Asymmetrical Arthritis
 Distal Interphalangeal Predominant (DIP)
 Spondylitis
 Arthritis mutilans
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.

41. Diagnosis primarily from anamnesis and clinical
features. On inspection will be obtained:
 full body fatigue,
 pain,
swollen tendons, fingers and toes,
a picture of the fingers and toes like a sausage
called dactylitis,
stiff joints,
limitation of movement especially early
morning,
nail changes (onycholysis, nail pit),
red eyes and pain (conjunctivitis).
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.

42.  There is no special blood disorder,
 the rate of sedimentation of blood may rise
due to arthritis,
 negative rheumatoid factor
 HLA-B27 gene marker is positive in over 50%
of psoriatic arthritis patients
 Abnormal x-ray joints are usually seen at an
advanced stage, in the form of "pencil in a
cup"
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.

43. Pharmacology
 NSAIDS (Non Steroidal Anti Inflammatory Drugs):
Ibuprofen 400 mg orally (PO), 4 times/day;
Meloxicam 7,5-15 mg PO, 4 times/day;
 Methotrexate: may be given oral or intra-
muscular injection. Initial doses of 7.5 mg per
week to monitor symptoms of toxicity or
sensitivity
 Biological agents: TNF-α (etanercept) inhibitors
25 mg twice a week
 Etretrinate: a vitamin A derivative, effective for
severe cases but teratogenic
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.

44. Non Pharmacology
 In addition to drug therapy is also a diet to
control weight so as not to increase the
burden of the joints.
 Vitamin D supplements can improve and help
the formation of bone cells.
 Smoking, drinking alcohol, too fatty foods,
too sweet and salty should be avoided.
 Expand the consumption of vegetables and
fruits because the content of vitamins,
minerals and antioxidants are high.
Referensi: Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis Psoriatika. CDK-216/ vol. 41 no. 5, th.
2014.Hal.352.355.

46.  Erythroderma is a skin disorder characterized by
generalized redness or erythema covering 90% of
the body surface lasting several days to several
weeks. Exfoliativa dermatitis is considered
synonymous with erythroderma.

47. Male : female -> 2:1
Age > 40 years
The identification of psoriasis
underlying erythrodermic
disease is more than 1

48.  systemic allergy medications
 Expansion of skin diseases.
- Psoriasis
- Seborrhoeic dermatitis
 systemic diseases including malignancy

49. 1. Vascular dilatation skin blood flow>> 
heat loss rate >>  atient feeling cold &
shivering
2. Heat loss>>  liquid evaporation >> 
dehydration
3. Skuama >> (≥ 9 gr/m2)  loss of protein >>
 hypoalbimun & globulin >>
4. Vascular Permeability >> + loss of protein
 peripheral edema

50. 1. drug allergies
 skin disorders may also concern the
mucous membrane.
 allergies occur acutely within 10 days.
 At first skin is only universal erythema,
especially at the time of acute, after
reaching the healing phase then arises
skuama.

51. 2. Expansion of other skin diseases
 psoriasis
- his signature will disappear
- causing the initial symptoms  uneven
erythema.
In place of predilection of psoriasis  the skin
disorder is more erythematous and slightly
elevated than the surrounding area and the
skuama is thicker
 Seborrhoeic dermatitis in infants (Leiner's disease)
- the situation is generally good without complaints
erythema can be on the whole body with a rough
skuama.

52. 3. systemic diseases including malignancy
(Sezary's syndrome)
 red scorched erythema is universal with skuama
and very itchy.
 There is an infiltrate of the skin and edema.
 1/3 - ½ patients were splenomegaly, superficial
lymphadenopathy, alopecia, hyperpigmentation,
palmar hyperkeratosis et plantary, and distrofic
nails

53. 63/5000 looking for signs of
the etiology of history and
physical examination
multiple looks at biopsy punch;
repeated biopsy 3-6 months to
determine the exact diagnosis
additional tests were performed:
biopsy for immunofluorescence,
CBC, CD4: CD8 ratio, CXR, lymph
gland biopsy
think of
another DD
exact diagnosis and
appropriate
treatment
+
-
-
+
(CBC = pemeriksaan sel darah, CXR = x-ray thoraks)
Sumber: Champion RH ed. Rook’s, textbook of dermatology,
5th ed
+
-
-
-
+

54. 1. Laboratory
 anemia, leukocytosis, lymphocytosis,
eosinophilia, increased IgE, and increased
erythrocyte sedimentation.
 Electrolyte disturbance 2. Pemeriksaan
histopatologi
2. skin biopsy depends on the weight and
duration of the inflammatory process.
 In the acute stage, spongiosis and parakeratosis
protrude, resulting in edema.
 In chronic stadium, akantosis and rete ridge
extension are more dominant

55.  Group I: corticosteroid (prednisone 4 x 10 mg, healing
in a few days - weeks)
 Group II: corticosteroids (prednisone 4 x 10 mg - 4 x
15 mg daily); acetyretin for psoriasis; healing in
weeks
 Sezary's syndrome: corticosteroids (prednisone 30 mg
daily) or methylprednisolone is equivalent to
cytostatic (chlorambucil at a dose of 2-6 mg daily).
 Chronic erythroderma: given a diet high in protein
 Skin disorders should also be emollient to reduce
radiation due to vasodilation by erythema eg with
10% lanolin saline or urea cream 10%

56.  Fluid and electrolytes lost due to capillary
leak decreased blood protein levels of
oedem, muscle weakness, and
hypoalbuminemia.
 High-output heart failure  increased blood
flow to the skin. This condition usually
occurs in the elderly, especially with heart
abnormalities.
 Increased susceptibility to  infections due
to inflammation, fissure, and excoriation of
the skin.

57. Prognosis depends on etiology
 Drug eruption: disappears weeks after
discontinuation of the drug, with possibly
hepatomegaly.
 Psoriasis & atopic: may disappear within months,
or settle, with a high recurrence rate.
 Malignancy: more commonly chronic & refractory
 Sezary syndrome is poorly prognosis, male
patients will generally die after 5 years, while
female patients after 10 years

59.  Seborrhoeic dermatitis is a
chronic papulosquamosa
disease that affects infants
and adults often found in
body parts with high and
active sebaceous follicle
concentrations including
the face, scalp, ears,
upper body and flexural
(inguinal, infrared and
axilla).
•Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI. Fitzpatrick's dermatology in general medicine. 6th ed.USA:
McGraw-Hill; 2003.
•Djuanda A, et al. Ilmu penyakit kulit dan kelamin. Edisi 6. Jakarta: Badan Penerbit FKUI; 2010.

60. Peak = baby <3bulan and age 40-70 years old
male > female (3:1)
All races
Occurs in 85% of HIV cases
3-5% prevalence rate
The mild type most commonly found (15-20%
•Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI. Fitzpatrick's dermatology in general medicine. 6th ed.USA: McGraw-
Hill; 2003.
•Djuanda A, et al. Ilmu penyakit kulit dan kelamin. Edisi 6. Jakarta: Badan Penerbit FKUI; 2010.

61. Etiology???
Seborrhea
Microbial effects
Drug
Neurotransmitter abnormalities
Physical factors

62.  Acute and subacute:
superficial infiltrate
perivascular lymphocytes and
histiocytes, mild spongiosis,
mild psoriasiform hyperplasia,
follicular plugging by
orthokeratosis and
parakeratosis, and crusting
containing neutrophils at the
follicular ends of ostia
Chronic: capillaries and
dilated veins in the superficial
plexus, and psoriasiform
•Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI. Fitzpatrick's dermatology in general medicine. 6th ed.USA: McGraw-
Hill; 2003.
Sampaio A, Mameri A, Sousa Vargas J, Ramos-e-Silva M, Nunes AP, Silva Carneiro SC. Seborrheic dermatitis.
An Bras Dermatol [serial on internet]. 2011. 86(6):1061-1074. Available from: http://www.scielo.br/scielo.

65. •Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI. Fitzpatrick's dermatology in general medicine. 6th ed.USA: McGraw-
Hill; 2003.

67. Medikamentosa
Oral anti-histamine: 1x1 tablet CTM
Oilum coccos
Non-medical:
Prompt to wash hair daily with mild
shampoo (not containing anti-dandruff).
Education avoids triggers: how to clean hair,
dry hair, avoid stress, fatty foods, use hijab
that absorbs sweat.

70. Pharmacology
NSAID
Corticosteroid
Salicylic acid
Non
pharmacology
Avoidiing
trigger

72.  Controlled emotions
 cognitive behavior therapy CBT) avoiding
negative thinking
 Eat health food
 Doing exercise

73.  Fitzpatrick’s Dermatology in general medicine, 8e,
vol.2: 198.
 Wahid, Syarifuddin, A.Miskad, Upik. 2016. IMUNOLOGI
Lebih Mudah Dipahami. Surabaya: Brilian
Internasional. Hal. 59, 62, dan 72
 Price, Sylvia A., Wilson, Lorraine. 2005. Patofisiologi
Konsep Klinis Proses-proses Penyakit. Ed. 6. Vol. 1.
Jakarta: EGC. Hal. 165.
 Habif, Thomas. 2016. CLINICAL DERMATOLOGY A Color
Guide to Diagnosis and Therapy.6th Ed. China: Elsevier
Page 182.
 Freederg IM. Exfoliative dermatitis. Fitzpatrick et
all.1996. Fitzpatrick’s dermatology in general
medicine. 4th ed. Newyork: Mcgraw-Hill. Chapter-
41.p;94-106,236-238
 Schӧn MP, Boehncke WH.2005. Psoriasis. N Engl J
Med;352:1899-912.

74.  Harahap, Marwali. 2013. IlmuPenyakitKulit. Jakarta:
Hipokrates. Hal 14-16.
 Eko V. Komplikasi Psoriasis pada Sendi atau Artritis
Psoriatika. 2014;41(5):352-355.
 Ilmu Penyakit Kulit Dan Kelamin. Universitas
Indonesia; 2016.
 Pamela RD. Pengaruh Stres Psikologis terhadap Fungsi
Pertahanan Kulit. 2012;39(6):420-422.
 Gudjonsson JE, Elder JT. Psoriasis. In: WolffK,
Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell
DJ, editors. Fitzpatrick’sdermatology in general
medicine. 7,ed. United States of America: McGraw
Hill: 169-93.
 yuliastuti,dwinidya.jurnal psoriasis RS meilia
cibubur,depok,Indonesia. Halaman 901-902
 jurnal kedokteran , e-jurnal.uajy.ac.id halaman 13
dan 15
 Eprints.undip.ac.id.halaman 26-30

75.  Siregar, S. Saripati Penyakit Kulit. Jakarta. EGC Edisi 3
 Eko,Vincea. Komplikasi Psoriasis pada Sendi atau Artritis
Psoriatika.CDK-216/ vol. 41 no. 5, th. 2014.Hal.352.355.
 Wasitaatmadja Syarif M. Anatomi Kulit. Djuanda A. Ilmu Penyakit
Kulit dan Kelamin. 7th ed. Jakarta : Fakultas Kedokteran Universitas
Indonesia.
 Djuanda A. Dermatosis Eritroskuamosa. Ilmu Penyakit Kulit dan
Kelamin. 7th ed. Jakarta : Fakultas Kedokteran Universitas Indonesia.
 Sularsito SA, Djuanda S. Dermatitis. Djuanda A. Ilmu Penyakit Kulit
dan Kelamin. 7th ed. Jakarta : Fakultas Kedokteran Universitas
Indonesia.
 Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI.
Fitzpatrick's dermatology in general medicine. 6th ed.USA: McGraw-
Hill; 2003.
 Djuanda A, et al. Ilmu penyakit kulit dan kelamin. Edisi 6. Jakarta:
Badan Penerbit FKUI; 2010.
 Jurnal Universitas Sumatra Utara
 eko, Vincea. 2015. Komplikasi Psoriasis pada Sendi atau artritis
Psikotropika. Jakarta : Kalmed hal. 354-355