study guide skin semester 3 tayang 29 Des 2015

GENERAL CORE COMPETENCY

1. Patient Care

Demonstrate capability to provide comprehensive patient care that is compassionate, appropriate, and effective for the management of health problems, promotion of health and prevention of disease in the primary health care settings 2. Medical knowledge base

Mastery of a core medical knowledge which includes the biomedical sciences, behavioral sciences, epidemiology and statistics, clinical sciences, the social aspect of medicine and the principles of medical ethics, and apply them. 3. Clinical skill

Demonstrate capability to effectively apply clinical skills and interprete the findings in the investigation of patient.

4. Communication

Demonstrate capability to communicate effectively and interpersonally to establish rapport with patient, family, community at large, and professional associates, that results in effective information 1xchange, the creation of therapeutically and ethicallysound relationship.

5. Information management

Demonstrate capability to manager information which includes information access, retrieval, interpretation, appraisal, and application to patient’s specific problem, and maintaining records of his or her practice for analysis and improvement.

6. Professionalism

Demonstrate a commitment to carrying out professional responsibilities and to personal probity, adherence to ethical principles, sensitivity to diverse patient population, and commitment to carrying out continual self-evaluation of his or her professional standard and competence.

7. Community-based and health system-based practice

Demonstrate awareness and responsiveness to larger context and system of health care, and ability ti effectively use system resources for optimal patient care.

BLOCKS OUTCOMES

LEARNING OUTCOMES CURRICULUM CONTENT

1. Describe the functional structure of the skin and its appendices and hearing systems

2. Identify typical skin manifestation related to skin and hearing disorders 3. Identify the risks and

compatibility of topical treatment in dermatology 4. Diagnose and manage

common skin and hearing systems disorders

5. Refer patient with

life/disability threatening, refractory and unidentified skin and hearing systems disorders

6. Educate the patient and their family about skin health.

1.1 Describe the functional structure of the skin and its appendices and hearing systems.

2.1 Common pathological bases of skin disorders.

2.2 Skin manifestation (effluorescenses) in common skin disorders.

3.1 Identify the risks and compatibility of topical treatment in dermatology.

4.1 Symtoms and sign of common skin and hearing systems disorders. 4.2 Clinical diagnostic of common skin and hearing systems disorders 4.3 Management of common skin and

hearing system infection

5.1 Refer patient with life/disability threatening, refractory and unidentified skin and hearing syatems disorders

6.1 General principles of skin health 6.2 Education and prevention of common

~ CURRICULUM ~

Aims:

 Manage common skin disorders knowledges in the context of primary health care settings

 Identify skin disorders which may require referral Learning outcomes:

 Describe the functional structure of the skin and its appendices and hearing systems

 Identify typical skin manifestation related to skin disorders

 Identify the risks and compatibility of topical treatment in dermatology

 Diagnose and manage common skin and hearing systems disorders

 Refer patient with life/disability threatening, refractory and unidentified skin and hearing systems disorders

 Educate the patient and their family about skin health. Curriculum contents:

 Functional structure of the skin and its appendices and hearing systems.

 Common pathological bases of skin disorders.

 Primary skin manifestation in common skin disorders

 Risks and compatibility of topical treatment in dermatology.

 Secondary skin manifestations.

 Symtoms and sign of common skin disorders, clinical diagnose of common skin disorders, management of common skin disorders : Papulo-erythrosquamosa, Tumor of the skin, Drug eruption of the skin, Pigmentary and sebaseous gland disorders, Insect bite and infestation, Dermatitis, bacterial infection, vaginitis and cervicitis.

 Symtoms and sign, clinical diagnose and management of common hearing systems disorders : pericondritis, wax, foreign bodies, bulous myringitis; membrane tymphani perforation, OMS, labirinitis, paresis nervus Facialis, ear trauma/othematoma, barotrauma, motion sickness, PGPKT, hearing loss, noise induced hearing loss.

 Referal of patient with life/disability threatening, refractory, or unidentified skin and hearing systems disorders

 General principles of skin and hearing systems health

 Education and prevention of common and contagious skin and hearing systems diseases.

~ PLANNERS TEAM ~

~ LECTURERS ~

NO NAME DEPARTMENT PHONE

1 dr. Ni Nyoman Suryawati, Sp.KK Dermatovenereology 0817447279 2 _{Dr. dr. Ni Made Linawati,M.Si Histology} 081337222567 3 _{Dr. dr. Made Wardana, SpKK (K) Dermatovenereology} 08563704591 4 Prof dr Made Swastika Adiguna SpKK

(K)

Dermatovenereology 08123828548 5 Dr. dr. AA Gde Putra Wiraguna,SpKK

(K)

Dermatovenereology 081338645288 6 Dr. dr. IGA Praharsini, SpKK Dermatovenereology 081238888794 7 Dr. dr. Luh Mas Rusyati, SpKK Dermatovenereology 081337338738 8 dr. Herman Saputra, SpPA Patology anatomy 081558028879 9 Dra. I A Alit Widhiartini, Apt, M.Si Farmacy 0816572852 10 dr.IGN Surya Trapika Farmacology 081337991177 11 dr. IGA Elies Indira, Sp.KK Dermatovenereology 081338718384 12 dr.IGA Dwi Karmila, Sp.KK Dermatovenereology 08123978446 12 dr. Luh Putu Ratih Vibriyanti K, Sp.KK Dermatovenereology 081337808844 13 dr. Ni Made Dwi Puspawati, Sp.KK Dermatovenereology 08123766268

14 dr. Lely Rahayu, SpTHT-KL ENT 08113809882

15 dr. Andi Dwi Saputra, Sp.THT ENT 081338701878

16 dr.Eka Putra Setiawan, Sp.THT ENT 087861361255 17 dr. I Made Wiranadha, Sp.THT –KL ENT 08123968294 18 dr. IG Kamasan Arijana, Msi Med Histology 085339644145 19 dr.I Made Krisna Dinata, M.Erg Physiology 08174742566

20 dr. Yuliana, M.Biomed Anatomy 0816555671

NO NAME DEPARTMENT

1 dr. Ni Komang Suryawati, SpKK (K) (Head) Dermatovenereology 2 Dr. dr. Ni Made Linawati,M.Si (Secretary) Histology 3 Dr. dr. Made Wardana, SpKK (K) Dermatovenereology 4 dr.Made Lely rahayu, Sp.THT-KL ENT

~ FACILITATORS ~

Regular Class

No

Name

Grou

p

Departme

nt

Phone

Room 1. dr. Made Agus Dwianthara

Sueta, Sp.B-KBD

A1 Surgery 081338648424 3nd floor: R.3.09 2. dr. Nyoman Suryawati , M.Kes,

Sp.KK A2 Dermatology 0817447279 3nd floor:R.3.10 3. dr. I Gusti Ayu Sri Darmayani,

Sp.OG

A3 Obgyn 081338644411 3nd floor: R.3.11 4. dr. I Made Suka Adnyana,

Sp.BP-RE

A4 Surgery 081236288975 3nd floor: R.3.12 5. dr. Luh Nyoman Alit Aryani,

Sp.KJ

A5 Psychiatry 085737717244 3nd floor: R.3.13 6. dr. Dudut Rustyadi , Sp.F A6 Forensic 08123994234 3nd floor:

R.3.14 7. dr. I Dewa Ayu Inten Dwi

Primayanti, M.Biomed

A7 Fisiology 081337761299 3nd floor: R.3.15 8. dr. I Made Sudipta, Sp.THT- KL A8 ENT 08123837063 3nd floor:

R.3.16 9. dr. Putu Budhiastra, Sp.M(K) A9 Opthalmology 085238238999 3nd floor:

R.3.17 10. dr. A.A.Ngurah Subawa , Msi A10 Clinical

Pathology

08155735034 3nd floor: R.3.19

English Class

No Name Group Department Phone Room

1. dr Ni Nyoman Metriani Nesa, M.Sc.,Sp.A

B1 Pediatric 081337072141 3nd floor: R.3.09 2. Dr. dr. Desak Made Wihandani,

M.Kes

B2 Biochemistry 081338776244 3nd floor: R.3.10 3. dr. Anak Agung Ayu Yuli

Gayatri, Sp.PD B3 Interna 08123803985 3nd floor:R.3.11 4. dr. I Gede Ngurah Harry Wijaya

Surya, Sp.OG

B4 Obgyn 0814386935 3nd floor: R.3.12 5. Prof.Dr.dr.I Putu Gede

Adiatmika, M.Kes

B5 Fisiology 08123811019 3nd floor: R.3.13 6. dr. Dyah Kanya Wati, Sp A (K) B6 Pediatric 085737046003 3nd floor:

R.3.14 7. dr. I Gusti Ayu Indah Ardani,

Sp.KJ

B7 Psychiatry 08123926522 3nd floor: R.3.15 8. dr. Putu Yuliandari, S.Ked B8 Microbiology 089685415625 3nd floor:

R.3.16 9. dr. I Kadek Swastika , M Kes B9 Parasitology 08124649002 3nd floor:

R.3.17 10. dr. Ni Putu Sriwidyani , Sp.PA B10 Anatomy

Pathology

081337115012 3nd floor: R.3.19

TIME TABLE ENGLISH CLASS (B)

BLOCK SKIN AND HEARING SYSTEMS AND DISORDERS

3

rd

_{Semester Medical Faculty Udayana University 2015 -2016}

Days /

Date Time Activity Venue Lecturers

Des 29, 2015

Tuesday 08.00-08.30 (30’) 08.30-09.00 (30’)

Lecture 1 : Introductionary to Block Skin and Hearing and Disorders

Lecture 2 : Functional structure of the skin and it’s appendices Class Room Suryawati Linawati Fasilitator Linawati

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) _SGD Discussion

Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Des 30, 2015 Wednesday 08.00- 15.00 (see BCS schedule) BCS: Efforesensi Prak : mikroscopic structure of the skin and appendages and hearing system

Class room Histology lab

Dwi Puspawati Linawati / Arijana

Des 31, 2015 Thursday

08.00-09.00 (60’) Lecture 3 : Common Pathophysiological bases of the skin and hearing system disorders

Class Room

Herman

Fasilitator

Herman

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) _SGD Discussion

Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Jan 4, 2016 Monday

08.00-09.00 (60’) Lecture 4 : Benign skin tumor (veruka, moluskum, kista, kondiloma

akuuminata), and vaginitis, servicitis

Class Room

Wiraguna/ Dwi Puspawati Fasilitator

Wiraguna/ Dwi Puspawati

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) _SGD Discussion

Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Jan 5, 2016

Tuesday 08.00-09.00 (60’)

Lecture 5 : Drug eruption (exantematous drug reaction, fixed drug reaction, erythema nodosum, erythema multiforme )

Class Room

Prof Suastika A/ Ratih

10.30-12.00 (90’) _SGD Discussion

Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Jan 6, 2016 Wednesday

08.00-09.00 (60’) Lecture 6:

Papuloerythrosquamosa

Class Room

Rusyati/Karmila Fasilitator

Rusyati/ karmila

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Jan 7, 2016 Thursday

08.00-09.00 (60’)

Lecture 7 : Dermatitis (numularis,

neurodermatitis, napkin eksema, perioral, urtikaria, dermatitis fotokontak, angioederma/angioedema) Class Room Wardana/ Suryawati Fasilitator Wardana/ Suryawati

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Jan 11, 2016 Monday

08.00-09.00 (60’)

Lecture 8: Pigmentary and Sebaceous gland disorders (hipo/hiperpigmentasi, miliaria, hidradenitis supuratif)

Class Room Elies/ Praharsini

Facilitator

Elies/ Praharsini

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Jan 12, 2016 Tuesday

08.00-09.00 (60’) _{Lecture 9: Bacterial} Infection (impetigo, skrofuloderma, erisipelas, selulitis, eritrasma)

Class Room Karmila/ Ratih

Fasilitator

Karmila/ Ratih

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

Jan 13, 2016 Wednesday

08.00-09.00(60’) Lecture 10: Insect bite and infestation (pedikulosis,

kapitis and pubis, scabies) Class Room

Praharsini/ Elies

Facillitator

Praharsini / Elies

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project Presentation (skin)

-14.00-15.00 (60’) Plenary Session Class Room

Jan 14, 2016 Thursday

08.00-08.30 (30’) 08.30-09.00 (30’)

Lecture 11: Rational topical treatment in dermatology Lecture 12:

Dermatofarmacology

Class Room Alit Widhiartini Surya T Facillitator

Alit, Surya T

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

Presentation (skin)

-14.00-15.00 (60’) Plenary Session Class Room

Jan 15, 2016 Friday

08.00-08.30 (30’) 08.30-09.00 (30’)

Lecture 13: Anatomical of Hearing Systems

Lecture 14: Histology of Hearing Systems Class Room Yuliana Arijana/ Ratnayanti Facilitator Yuliana, Arijana

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’)

Plenary Session Class Room

Jan 18, 2016 Monday

08.00-08.30 (30’) 08.30-09.00(30’)

Lecture 15: Physiology of Hearing systems

Lecture 16: Otic Drug

Class Room

Krisna Dinata Alit Widhiarthini

Facilitator

Krisna, Alit W

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) _{Plenary Session} Class Room

Jan 19, 2016 Tuesday

08.00-09.00 (60’) Lecture 17: Pericondritis, Wax, Foreign bodies,

Bulous Myringitis Class Room

Lely Rahayu

Facilitator

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-Lely Rahayu 14.00-15.00 (60’)

Plenary Session Class Room

Jan 20, 2016 Wednesday

08.00-09.00 (60’) Lecture 18: Membrane tymphani perforation,OMS, labirinitis, paresis nervus fasialis

Class Room

Andi dwi Saputra

Facilitator

Andi dwi Saputra

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

-14.00-15.00 (60’) Plenary Session Class Room

Jan 21, 2016 Thursday

08.00-08.30 (30’)

08.30-09.00(30’)

Lecture 19: Ear Trauma/ othematoma, barotrauma, Motion Sickness, PGPKT Lecture 20: Hearing loss, noise induced hearing loss

Class Room

Eka Putra

Wiranadha

Facilitator

Eka Putra , Wiranadha

09.00-10.30 (90’) Independent Learning

-10.30-12.00 (90’) SGD Discussion Room

12.00-12.30 (30’) Break

-12.30-14.00 (90’) Student Project

Presentation (hearing)

-14.00-15.00 (60’) _{Plenary Session} Class Room

Jan 22, 25, 26, 27,

2016

08.00 - 13.00 BCS 2, 3, 4 dan 5 L. Bersama, pharmacy L, RK.302 Jan 28,

2016 Thursday

EXAM. PREPARATION

Jan 29, 2016 Friday

TIME TABLE REGULAR CLASS (A)

BLOCK SKIN AND DISORDERS

3

rd

_{Semester Medical Faculty Udayana University 2015-2016}

Days /

Date Time Activity Venue Lecturers

Des 29, 2015 Tuesday

09.00-09.30 (30’) 09.30-10.00 (30’)

Lecture 1 : Introductionary to Block Skin and Disorders Lecture 2 : Functional structure of the skin and it’s appendices Class Room Suryawati Linawati Facilitator Linawati 10.00-11.30 (90’) Student Project (searching _{for references)}

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Des 30, 2015 Wednesday

09.00 – 16.00 (see BCS schedule)

BCS 1: Effloresensi Prak : mikroscopic structure of the skin and appendages and hearing system

Class room Histology lab

Dwi Puspawati Linawati / Arijana

Des 31, 2015 Thursday

09.00-10.00 (60’)

Lecture 3 : Common Pathophysiological bases of the skin and hearing system disorders

Class Room Herman

Fasilitator Herman 10.00-11.30 (90’) Student Project (searching _{for references)}

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 4, 2016 Monday

09.00-10.00 (60’)

Lecture 4 : Benign Skin tumor (veruka, moluskum, kista, kondiloma

akuminata), and vaginitis, servicitis

Class Room Wiraguna/ Dwi Puspawati

Facilitator

Wiraguna/ Dwi puspawati 10.00-11.30 (90’) Student Project (searching _{for references)}

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

Jan 5, 2016 Tuesday

09.00-10.00 (60’)

Lecture 5 : Drug eruption (exantematous drug reaction, fixed drug reaction, erythema nodosum, erythema multiforme )

Class Room

Prof Suastika A/ Ratih

Fasilitator

Prof Suastika A/ Ratih 10.00-11.30 (90’) Student Project (searching _{for references)}

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 6, 2016 Wednesday

09.00-10.00 (60) Lecture 6:

Papuloerythrosquamosa Class Room

Rusyati/Karmila

Facilitator Rusyati/ karmila

10.00-11.30 (90’) Student Project

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 7, 2016 Thursday

09.00-10.00 (60’)

Lecture 7 : Dermatitis (numularis,

neurodermatitis, napkin eksema, perioral, urtikaria, dermatitis fotokontak, angioderma/angioedema)

Class Room Wardana / Suryawati

Facilitator

Wardana/ Suryawati

10.00-11.30 (90’) Student Project

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 11, 2016 Monday

09.00-10.00 (60’)

Lecture 8: Pigmentary and Sebaceous gland disorders (hipo/hiperpigmentasi, miliaria, hidradenitis supuratif)

Class Room Elies/ Praharsini

Facilitator Elies/ Praharsini

10.00-11.30 (90’) Student Project

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 12, 2016 Tuesday

09.00-10.00 (60’)

Lecture 9: Bacterial Infection (impetigo, skrofuloderma, erisipelas, selulitis, eritrasma) Class Room Karmila/ Ratih Facilitator Karmila/Ratih

10.00-11.30 (90’) Student Project

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

Jan 13, 2016 Wednesday

09.00-10.00 (60’) Lecture 10: insect bite and infestation (pedikulosis, kapitis and pubis, scabies)

Class Room Praharsini/Elies

Facillitator Praharsini/ Elies 10.00-11.30 (90’) Student Project _{Presentation (skin)}

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 14, 2016 Thursday

09.00-09.30 (30’) 09.30-10.00 (30’)

Lecture 11: Rational topical treatment in dermatology Lecture 12:

Dermatopharmacology

Class Room Alit widhiartini Surya T

Facillitator Alit w, Surya T 10.00-11.30 (90’) Student Project _{presentation (skin)}

-11.30-12.00 (30’) Break

-12.00-13.30 (90’) Independent Learning

-13.30-15.00 (90’) SGD Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 15, 2016 Friday

09.00-09.30 (30’) 09.30-10.00 (30’)

Lecture 13: Anatomical of Hearing Systems Lecture 14: Histology of Hearing Systems Class Room Yuliana Arijana/ Ratnayanti Facilitator Yuliana, Arijana

10.00-11.30 (90’) Independent Learning

-11.30-12.00 (30’) SGD

-12.00-13.30 (90’) Break

-13.30-15.00 (90’) Student Project hearing Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 18, 2016 Monday

09.00-09.30 (30’) 09.30-10.00 (30)

Lecture 15: Physiology of Hearing systems

Lecture 16: Otic drug

Class Room

Krisna Dinata Alit W

Facilitator

Krisna, Alit W

10.00-11.30 (90’) Independent Learning

-11.30-12.00 (30’) SGD

-12.00-13.30 (90’) Break

-13.30-15.00 (90’) Student Project hearing Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 19, 2016

Tuesday 09.00-10.00 (60’)

Lecture 17: Pericondritis, Wax, Foreign bodies, Bulous myringitis Bulosa

Class Room Lely Rahayu

Facilitator

10.00-11.30 (90’) Independent Learning

-11.30-12.00 (30’) SGD

-12.00-13.30 (90’) Break

Lely Rahayu

15.00-16.00 (60’) Plenary Session Class Room

Jan 20, 2016 Wednesday

09.00-10.00 (60’)

Lecture 18: Membrane tymphani perforation, OMS, labirinitis, paresis nervus fasialis

Class Room

Andi Dwi Saputra

Facilitator

Andi Dwi Saputra

10.00-11.30 (90’) Independent Learning

-11.30-12.00 (30’) SGD

-12.00-13.30 (90’) Break

-13.30-15.00 (90’) Student Project hearing Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 21, 2016 Thursday

09.00-09.30 (30’) 09.30-10.00 (30’)

Lecture 19: Ear Trauma/ othematoma, barotrauma, Motion Sickness, PGPKT Lecture 20: Hearing loss, noise induced hearing loss

Class Room

Eka Putra Wiranadha

Facilitator

Eka Putra, Wiranadha

10.00-11.30 (90’) Independent Learning

-11.30-12.00 (30’) SGD

-12.00-13.30 (90’) Break

-13.30-15.00 (90’) Student Project _{Presentation (hearing)} Discussion Room

15.00-16.00 (60’) Plenary Session Class Room

Jan 22, 25, 26, 27, 2016

08.00 - 13.00 BCS 2, 3, 4 dan 5 L. Bersama, Physiology L, Pharmacy L, RK.302 Jan 28, 2016

Thursday

EXAM. PREPARATION

Jan 29, 2016

Friday EXAMINATION

FAS LEC

PRACTICUM AND BCS SCHEDULE ( 3

th

_Semester)

30-12-2015 R.kuliah 22-01-2016 R.kuliah 25-01-2016 R.kuliah 26-01-2016 R.kuliah 27-01-2016 R.kuliah Efflore sensi kulit, kuku, mukosa, rambut, dermogra fisme (dr. Dwi Puspawati) Labora tory investiga tion (KOH, Giemsa,wo od lamp) ( dr. Suryawati, dr. Karmila) Perawatan luka, kompres, bebat kompresi pd vena varikosum (dr Luh Mas Rusyati, dr Ratih ) Insisi abses, Eksisi tumor, rozerplasti kuku, ekstraksi komedo (dr.Wardana) Manuver valvalva, pembersihan MAE dg usapan, pengambilan serumen dan benda asing di telinga (dr. Andi S)

08.00 – 09.00 A, B A,B A,B A,B A,B

09.00 – 10.00 A, B A,B A,B A,B A,B

10.00 – 11.00 C, D C,D C,D C,D C,D

11.00 – 12.00 C, D C,D C,D C,D C,D

12.00 - 13.00

Histology lab Histology lab Physiolog y & Pharmacy Lab Physiology/ Pharmacy Lab Physiology Lab Histology Practicum skin and hearing organ (dr.Lina Wati/ Arijana) Patologi Anatomi Practicum skin and hearing systems (dr. Herman) Topical Prepa Ration in skin and Otic drug (Dra. IA Alit

W)

Farma cology practicum in Skin and hearing (dr.

Surya trapika)

Physiology practicum (dr. Krisna)

08.00-09.00 C C C C C

09.00-10.00 D D D D D

10.00-11.00 A A A A A

11.00-12.00 B B B B B

Group A: SGD A1, A2, A3, A4, A5. Group B: SGD A6, A7, A8, A9, A10. Group C: SGD B1, B2, B3, B4, B5. Group D: SGD B6, B7, B8, B9, B10.

~ STUDENT PROJECT ~

No Topics Supervisors Time of

presentation

1 Hemangioma Dr. Luh Mas

Rusyati, Sp.KK/ dr. Karmila, Sp.KK

January 13, 2016 A : 10.00 - 10.45 B: 12.30 – 13.15

2 Leg Ulcer Dr. Suryawati,

Sp.KK/ dr. Ratih, Sp.KK

January 13, 2016 A : 10.45 - 11.30 B: 13.15 – 14.00

3 Albino dr. IGA Praharsini,

Sp.KK/ dr. IGA Elies Indira, Sp.KK

January 14, 2016 A : 10.00 - 10.45 B: 12.30 – 13.15 4 Prevention of Sexual

Transmitted Disease and Human Immunodeficiency

Virus

Dr. AA Wiraguna/ dr Dwi Puspa

January 14, 2016 A : 10.45 - 11.30 B: 13.15 – 14.00

5 Deafness dr. Eka Putra,

Sp.THT/ dr. Wiranadha, Sp.THT

January 21, 2016 A : 10.00 - 10.45 B: 12.30 – 13.15 6

Fistula Preauricular

dr. Lely Rahayu, Sp.THT-KL

January 21, 2016 A : 10.45 - 11.30 B: 13.15 – 14.00 Regulation for Strudent Project

1. Each small group discussion must make 1 scientific writing (see topic for each group)

2. Each small group discussion must ready to present their scientific writing (due to the above schedules)

3. The assesment of student project (SP) for each student would be the combination of :

i. Facilitator (supervisor) scoring with 60% qualification (during SP formation), should be collect per group by student / facilitator to dr.linawati (Histology 4th _flr)

ii. Evaluator scoring with 40%, from SP presentation, should be collect per group by supervisor / student after SP presentation to dr.linawati (Histology 4th _flr)

4. Report Format

II. Introduction

III. Content

a. Etiology b. Pathogenesis c. Clinical feature d. Diagnosis

e. Therapy/ Prevented

IV. Conclution

V. References ( vancouver style) (min. 8)

15- 20 halaman; 1,5 spasi; Times New Romance; jilid warna hijau

Cover  Tittle

Grup Discussion

Name and Student Registration Number

Faculty of Medicine, Udayana University 2015 Student Project Topic

No Group Topic

1 A1 - Hemangioma

2 A2 - Leg ulcer

3 A3 - Albino

4 A4 - Prevention of STD and HIV?

5 A5 - Hemangioma

6 A6 - Leg ulcer

7 A7 - Albino

8 A8 - Prevention of STD and HIV?

9 A9 - Deafness

10 A10 - Fistula preauricular

11 B1 - Hemangioma

12 B2 - Leg ulcer

13 B3 - Albino

14 B4 - Prevention of STD and HIV?

15 B5 - Hemangioma

16 B6 - Leg ulcer

17 B7 - Albino

18 B8 - Prevention of STD and HIV?

19 B9 - Deafness

Paper Assessment Form

Block The Skin and Hearing systems and Disorders

Name : ... Student Reg. Number : ... Facilitator : ... Title : ... Supervisor’s (Facilitator) scoring with 60% qualification :

No Item Assessment Range Score (%) Score

1. Ability to find the literature 0-20

2. Communication/Attitude 0-30

3 Quality of material 0-40

4 Student’s interest and motivation 0-10

TOTAL 100

Supervisor,

(...) NIP.

Paper Assessment Form

Block The Skin and Hearing Systems and Disorders

Name : ... Student Reg. Number : ... Facilitator : ... Title : ... Evaluator’s scoring (presentation) with 40% qualification :

No Item Assessment Range Score (%) Score

1. Quality of material 0-60

3 Critical thinking 0-30

TOTAL 100

Evaluator,

(...) NIP.

ASSESSMENT METHODES

NO TOPIC ASSESSMENT/

METHOD 1

2 Introductionary to Block Skin and DisordersFunctional structure of the skin and it’s

appendices MCQ (5)

3 4 5

Common Pathological bases of the skin disorders

Rational topical treatment in dermatology and hearing systems

Dermatofarmacology and hearing systems

MCQ (5) MCQ (5) MCQ (5) 6 Skin manifestation (effloresences) in common

skin disorders

MCQ (5) OSCE (coordination

with OSCE team) 7 Dermatitis (numularis, fotocontact,

neurodermatitis, napkin eksema, perioral, urtikaria)

MCQ (5)

8 9

Papulo-erythrosquamosa Drug eruption of the skin

MCQ (5) MCQ (5) 10 Pigmentary and sebaceous gland disorders MCQ (5) 11 Bacterial infection (impetigo, scrofuloderma,

erisipelas, selulitis, eritrasma, hidradenitis) MCQ (5) 12 Eksisi tumor and curetase OSCE (coordination

with OSCE team) 13 Insect bite and infestation (Scabies, creeping

eruption, pediculosis)

MCQ (5) 14 Tumor of the skin, vaginitis, servicitis MCQ (5) 15 Abcess incision OSCE (coordination

with OSCE team) 16 Laboratory investigation OSCE (coordination

with OSCE team) 17 _{Anatomical of Hearing Systems} MCQ (5) 18 Histology of Hearing Systems MCQ (5) 19 _{Physiology of Hearing systems} MCQ (5)

20 Otic Drug MCQ (5)

21 Pericondritis, wax, foreign bodies, and bulous

timpani,OMS,LABIRINITIS,paresis nervus fasialis

23 Ear trauma/ othematoma, barotrauma,motion sickness,PGPKT

MCQ (5) 24 Hearing loss, noise induced hearing loss MCQ (5) 25 Manuver valsalva, pembersihan MAE dengan

usapan, pengambilan serumen dengan kait/kuret, pengambilan benda asing di telinga

OSCE (coordination with OSCE team)

~ MEETING ~

Meeting of the student representatives

The meeting between block planners and student group representatives will be held on Friday, Jan 15 , at 10.00 until 11.00 at Class Room. In this meeting, all of the student group representatives are expected to give suggestions and inputs or complaints to the team planners for improvement. For this purpose, every student group should choose one student as their representative to attend the meeting.

Meeting of the facilitators

The meeting between block planners and facilitators will take place on Friday, Jan 15 at 10.00 until 11.00 at Class Room. In this meeting all the facilitators are expected to give suggestions and inputs as evaluation to improve the study guide and the educational process. Because of the importance of this meeting, all facilitators are expected to attend the meeting.

~ PLENARY SESSION ~

For each learning task, the student is requested to prepare a group report. The report will be presented in plenary session. Lecturer in charge will choose the group randomly. The aim of this presentation is to make similar perception about the topic that has been given.

~ ASSESSMENT METHOD ~

Assessment will be performed on Friday, January 29th _{2016 for both Regular class} and English class. There are 100 questions for the examination that consist of Multiple Choice Question (MCQ).

The borderline to pass exam is 70. The proportion of final results are: Final exam (MCQ) : 80%

Small group discussion : 5% Student project (SP) : 15%

BLOCK RULES:

1. Cheating during block activity (paper plagiat, during block exam, etc) is prohibited, violent of the rules would be considered to decrease 10 % of final result.

~ LEARNING PROGRAMS ~

ABSTRACTS OF LECTURES

Day 1

Lecture 1. Introduction to The Block Skin and

Hearing Systems and

Disorders

Suryawati

Lecture 2. Functional Structure of the Skin and Its Appendices

Linawati

The skin consist of three layers firmly attach to one another. (1) The outer is epidermis, derived from ectoderm; (2) the deeper dermis, derived from mesoderm; and (3) the hypodermis or subcutaneous layer, corresponding to the superfisial fascia in gross anatomy. The epidermis is stratified squamous epithelial layer which consists of four distinct cell types; keratinocyte, melanocytes, langerhans cells and merkel cells. The epidermis consist of in five layer or strata : (1) stratum basale, (2) stratum spinosum, (3) stratum granulosum, (4) stratum lusidum and (5) stratum corneum. Skin appendages consist of hair, nail, sebaseous gland, sweat gland and nails.

Skin is generaly classified into two types : (1) thick skin and thin skin. Thick skin (more than 5 mm thick) covers the palms of the hands and the soles of the feet and has a thick epidermis and dermis. Thin skin (1 to 2 mm in thickness) lines the rest of the body; the epidermis is thin.

The skin has several functions : (1) Protection (mechanical function); (2) as a water barrier; (3) Regulation of body temperature (conservation and dissipation of heat); (4) Non spesifik defense (barrier to microorganism); (5) Excretion of salts; (6) synthesis of vitamin D; (7) as sensory organ

The epidermis and dermis display a tight fit interface at the dermal-epidermal junction, where a basal lamina and hemidesmosomes are located. A primary epidermal ridge interlocks with a subjacent primary dermal ridge. An epidermal interpapilary peg, projecting downward from the primary epidermal ridge, interlocks with the primary dermal ridge, which is subdivided into two secondary dermal ridges. A number of dermal papillae project upward from the surface of each secondary dermal ridge into the epidermal region, interlocking with downward projections of the epidermis. This arrangement is predominant in hairless thick skin. Dermal papillae are numerous and branched. In thin skin, papillae are low and their number is reduced.

Day 2

Lecture

BCS 1

:

Effloresensi

Puspa

Distribution of the rash, arrangement and morphology of individual rash, distribution of the lesion: symmetrical, asymmetrical, exposed area, sun exposed area, scalp region, hand, extensor aspect, flexor aspect.

Arrangement and configuration of the lesion: grouped (as in insect bites, dermatitis herpetiformis, herpes simplex, common warts), annular or arciform (as in granuloma annulare, mycosis fungoides, tinea circinata, erythema annulare centrifugum), linear pattern (as in Koebner phenomenon, Psoriasis, lichen planus, plane wart, molluscum contagiosum; epidermal naevus, sporotrichosis, lichen striatus, lichen simplex, morphoea, lichen sclerosis, phytophotodermatitis).

Morphology of lesion: Individual lesion described with the help of magnifying glass. To find out the early primary lesion and to inspect it closely. Note the shape(geometric shape, oval), colour(salmon-pink, erythematous, skin colour, yellow), size, margin (sharpness of edge, well-defined, ill-defined), the surface characteristics (dome-shaped, umbilicated, spike like), temperature and smell.

It is a good practice if affordable to have thorough examination of the whole body especially for new consultation and for the elderly. Sometimes, examination of the back and buttock of the elderly may pick up unexpected lesions, even the patient himself or herself may not notice them e.g. persistent chronic annular erythematous rash in the buttock found in a case of tuberculoid leprosy.

The major types of primary lesions are:

 Macule. A small, circular, flat spot less than [frac25] in (1 cm) in diameter. The color of a macule is not the same as that of nearby skin. Macules come in a variety of shapes and are usually brown, white, or red. Examples of macules include freckles and flat moles. A macule more than [frac25] in (1 cm) in diameter is called a patch.

 Vesicle. A raised lesion less than [frac15] in (5 mm) across and filled with a clear fluid. Vesicles that are more than [frac15] in (5 mm) across are called bullae or blisters. These lesions may may be the result of sunburns, insect bites, chemical irritation, or certain viral infections, such as herpes.

 Pustule. A raised lesion filled with pus. A pustule is usually the result of an infection, such as acne, imptigeo, or boils.

 Papule. A solid, raised lesion less than [frac25] in (1 cm) across. A patch of closely grouped papules more than [frac25] in (1 cm) across is called a plaque. Papules and plaques can be rough in texture and red, pink, or brown in color. Papules are associated with such conditions as warts, syphilis, psoriasis, seborrheic and actinic keratoses, lichen planus, and skin cancer.

 Nodule. A solid lesion that has distinct edges and that is usually more deeply rooted than a papule. Doctors often describe a nodule as "palpable," meaning that, when examined by touch, it can be felt as a hard mass distinct from the tissue surrounding it. A nodule more than 2 cm in diameter is called a tumor. Nodules are associated with, among other conditions, keratinous cysts, lipomas, fibromas, and some types of lymphomas.

 Wheal -Urtica. A skin elevation caused by swelling that can be itchy and usually disappears soon after erupting. Wheals are generally associated with an allergic reaction, such as to a drug or an insect bite.

 Telangiectasia. Small, dilated blood vessels that appear close to the surface of the skin. Telangiectasia is often a symptom of such diseases as rosacea or scleroderma.

The major types of secondary skin lesions are:

 Ulcer. Lesion that involves loss of the upper portion of the skin (epidermis) and part of the lower portion (dermis). Ulcers can result from acute conditions such as bacterial infection or trauma, or from more chronic conditions, such as scleroderma or disorders involving peripheral veins and arteries. An ulcer that appears as a deep crack that extends to the dermis is called a fissure.

 Scale. A dry, horny build-up of dead skin cells that often flakes off the surface of the skin. Diseases that promote scale include fungal infections, psoriasis, and seborrheic dermatitis.

 Crust. A dried collection of blood, serum, or pus. Also called a scab, a crust is often part of the normal healing process of many infectious lesions.

 Erosion. Lesion that involves loss of the epidermis.

 Excoriation. A hollow, crusted area caused by scratching or picking at a primary lesion.

 Scar. Discolored, fibrous tissue that permanently replaces normal skin after destruction of the dermis. A very thick and raised scar is called a keloid.

 Lichenification. Rough, thick epidermis with exaggerated skin lines. This is often a characteristic of scratch dermatitis and atopic dermatitis.

 Atrophy. An area of skin that has become very thin and wrinkled. Normally seen in older individuals and people who are using very strong topical corticosteroid medication.

Day 3

Lecture 3: Common Pathological bases of Skin disorders

Herman S

Little more than 100 years ago, the noted pathologist Rudolph Virchow considered the skin as protective covering for more delicate and functionally sophisticated internal viscera. Then, and for the century that followed, the skin was considered primarily a passive barrier to fluid loss and mechanical injury. During the past three decades, however, of scientific inquiries have demonstrated the skin to be a complex organ in which precisely regulated cellular and molecular interactions govern many crucial responses of the skin to our environment.

Accurate description of the clinical appearance of the skin at a macroscopic level is often critical for diagnosis. Correlation between the gross and histologic appearances is often essential in formulating diagnoses and in understanding p

athogenesis. Accordingly, efforts are made in the following pages to depict and describe clinical lesions whenever possible and to relate these findings to the microscopic appearance of lesions.

Day 4

Lecture 4:

Benign skin tumors,

V

aginitis and

C

ervicitis

Wiraguna/ Dwi Puspa

Benign tumors of the skin is a dermatosis which consists of multiple entities. Examination of skin tumors, not only determine the malignant or benign , but also determine the origin of the tumor cell component of the skin. Tumors can be derived from epidermal keratinocytes or accessory gland cells. Epidermal nevus is a benign skin tumor that is a proliferation of epithelial hamartoma include; verukosa epidermal nevus derived from keratinocytes, sebaceous nevus derived from sebaceous gland, nevus komedonikus derived from pilosebaceous units, eccrine nevus derived from eccrine glands and apocrine

nevus that derived from apocrine glands. Expression of epidermal nevus mosaicism considered to have a genetic mutation occurs not only on the skin but also other networks. Lesions follow Blaschko lines which indicate the presence of mutations postzigotik. In general, large lesions and the wide distribution of lesions in the head and neck have internal organ involvement and is known as the epidermal nevus syndrome. Epidemiology, pathology and clinical course of the disease can vary depending on the clinical variations of tumor cell origin .

Infection of Human Papilloma Virus ( HPV ) can cause mucosal and skin epithelial proliferation and cause warts. Warts can be classified by anatomic location or its morphology , such as verruca vulgaris , verruca plana and palmo plantar warts . Humans are the only hosts and intermediaries. Warts Treatment based on clinical appearance , location and the patient's immune status, common warts are more difficult to treat in patients with immunosuppression. Because warts are linked as a cofactor cancer, it is necessary to be evaluated histologically .Molluscum is caused by poxviruses , MCV 1-4 and its variants. In children, the infection is caused by MCV 1. In patients who have HIV infection, MCV type 2 cause infection in most cases. Molluscum is easily transmitted through skin contact -chiefly on wet skin . Treatment is determined based on the clinical situation, in immunocompetent pediatric patients, sometimes no treatment is required.

Sexually transmitted infections (STIs) can be caused by various etiologies that have various clinical symptoms. Etiologic agent of STIs in women such as Neisseria

gonorrhoeae, Trichomonasvaginalis and Candida albicans infections can produce vaginal

discharge and cause vaginitis or cervicitis. The diagnosis can be confirmed by laboratory tests such as microscopic examination, culture or the latest diagnostic methods such as nucleic acid amplification test. Besides syndromic approach can be useful in tertiary care centers that do not have a complete diagnostic tool. Early diagnosis and appropriate therapy gives good prognosis accompanied by prevention of sexual transmission through treatment of sexual partners, sex abstinencia and safe sexual behavior.

Day 5

L

ecture

5

:

Drug eruption (

exantematous drug reaction, fixed drug reaction,

erythema nodosum, erythema multiforme

)

Suastika A/ Ratih

Exanthematous drug reaction are the most common form of adverse cutaneous drug eruption. They are characterized by erythema, often with small papules throughout. They tend to occur within the first two weeks of treatment but may appear later, or even within 10 days after the medication has been stopped. Lesions tend to appear first proximally, especially in the groin and axilla, generalizing within 1 or 2 days. Pruritus is usually prominent. The most common cause is an antibiotisc semisynthetic penicillins and trimethoprim-sulfamethoxazole.

Fixed drug reaction are common. Fixed drug eruptions are so named because they recur at the same site with each exposure to the medication. In most patients, six or fewer lesions appear, frequently only one. Uncommonly, fixed eruptions may be multifocal with numerous lesions. They may present on the body, but half occur on the oral and genital mucosa. Clinically, a fixed eruption begins as a red patch that soon evolves to an iris or target lesion identical to erythema multiforme, and may eventually blister and erode. Characteristically, prolonged or permanent post inflammatory hyperpigmentation results, althought a nonpigmenting variant of a fixed drug eruption is recognized.

Erythema nodosum is the most commonly diagnosed form of inflamatory panniculitis, with most cases occuring in young adult women. The eruption consists of bilateral, symetrical, deep, tender, bruise-like nodules, 1-10 cm in diameter, located pretibially. Initially the skin over the nodules is red, smooth, slightly elevated, and shiny. The onset is generally acute, frequently associated with malaise, leg edema and arthritis or athralgias.

Erythema multiforme minor is a self-limited recurrent disease, usually in young adults, occuring seasonally in the spring and fall, with each episode lasting 1-4 weeks. The individual clinical lesions begin as sharply marginated, erythematous macules, which become raised, edematous papules over 24 to 48 h. The lesions may reach several centimeters in diameter. Typically EM minor is usually associated with a preceding orolabial herpes simplex virus infection.

Day 6

Lecture

6

: Papuloerytroskuamosa

(psoriasis, pityriasis rosea and erythrodermi)

Luh Mas Rusyati/ Karmila

Erythrosquamous skin disease are disease with efflorescence in the form of erythema and squama. These diseases include psoriasis, pityriasis rosea, seborrheic dermatitis and erythrodermi.

Psoriasis is a common scaly erythematous disease of unknown cause showing wide variation in severity and distribution of skin lesions. It usually follows an irregular chronic course marked by remissions and exacerbations of unpredictable onset and duration. Factors that may lead to more lesions include drug reactions, respiratory infections, cold weather, emotional stress, surgery, and also viral infections. The goal of therapy in psoriasis is to achieve remission in which all or almost all lesions have disappeared. Topical therapy should be used if possible. Systemic therapy is used if topical therapy has failed. If psoriasis is limited to a few plaques, topical corticosteroids or tar should be used initially. Application of topical corticosteroids under an occlusive or intralesional injection of corticosteroid may result in rapid clearing of limited lesions.

Seborrheic dermatitis or also known as pityriasis sicca is a very common chronic dermatosis characterized by redness and scaling, occurring in regions where the sebaceous glands are most active such as the face, scalp, presternal area and in the body folds. Mild seborrheic dermatitis causes flaking which is familiar in the term of dandruff. Generalized seborrheic dermatitis, failure to thrive, and diarrhea in infants should bring to mind Leiner’s disease which also accompanied by a variety of immunodeficiency disorders.

Pityriasis rosea is a mild inflammatory exanthema characterized by salmon coloured papular and macular lesions that are first discrete but may be confluent. The individual patches are oval or circinate, and are covered with finely crinkled, dry epidermis which often desquamates, leaving a collarate of scalling. When stretched across a long axis, the scales tend to fold across the lines of stretch forming the so called “hanging curtain” sign. The disease most frequently begin with a single herald or mother patch, the efflorescence of new lesions spreads rapidly, and after 3-8 weeks they usually disappear spontaneously.

Erythrodermi is characterized by erythema over the whole of the body. It can be triggered by widely sebhorreic dermatitis, widely psoriasis vulgaris, or drug eruptions.

Day 7

Lecture 7: Dermatitis (numularis, neurodermatitis, napkin eksema, perioral,

urtikaria, fotokontak)

Numular dermatitis

Nummular dermatitis is defined as an eruption of round (discoid) eczematous patches almost exclusively of the extremities often the lower legs in men and the forearms and dorsal aspects of the hands in women. The lesions are well demarcated and measure 1–3 cm, only occasionally being larger. They may be acutely inflamed with vesicles and weeping, but are more often lichenified and hyperkeratotic. The pathogenesis has not been fully elucidated. Pruritus may be intense and excoriations are often prominent. Nummular dermatitis usually takes a very chronic course. Options comprise medium-to high-potency topical corticosteroid ointments, topical tacrolimus or pimecrolimus, and emollients. Tar preparations have also been used successfully. However, a number of patients will require phototherapy to clear the lesions.

Lichen simplex chronicus (circumscribed neurodermatitis)

Paroxysmal pruritus is the main symptom. Lichen simplex chronicus is a result of long-continued rubbing and scratching, more vigorously than a normal pain threshold would permit, the skin becomes thickened and leathery. Chronic scratching of a localized area is a response to unknown factors; however, stress and anxiety have long been thought important. It is important to stress the need for the patient to avoid scratching the areas involved if the sensation of itch is ameliorated. High-potency agents should be used initially and the treatment can be shifted to the use of medium-to lower-strength topical steroid creams as the lesions resolve. Topical doxepin, capsaicin, or pimecrolimus cream or tacrolimus ointment provides significant antipruritic effects and is a good adjunctive therapy. Intralesional injections of triamcinolone suspension, using a concentration of 5 or (with caution) 10 mg/mL, may be required.

Diaper (napkin) dermatitis

Diaper dermatitis is the cumulative result of several factors, in particular dampness and exposure to urine and feces. Prolonged use of diapers, dampness, and the factors detailed above lead to the breakdown of the horny layer barrier function. An alkaline pH also facilitates the development of secondary C. albicans infection. Diaper dermatitis is strictly confined to the diaper area, presenting with mild to pronounced erythema, erosions and scaling. Refractory diaper dermatitis may require a biopsy to exclude some of the above conditions. In the acute phase, mild corticosteroid preparations are helpful. Topical imidazole creams are added for secondary infection with Candida spp. The major goal of long-term management is avoidance of the causative factors. Frequent changing of highly absorbent disposable diapers is associated with a lower incidence and severity of diaper dermatitis, and it leads to a more physiologic pH. Emollients containing white paraffin or soft zinc pastes provide both protective and soothing effects.

Perioral Dermatitis

Perioral dermatitis is characterized by small discrete papules and pustules in periorificial distribution. Patients often reveal a history of an acute steroid-responsive eruption around the mouth, nose and/or eyes that worsen when the topical corticosteroid is discontinued. If the topical corticosteroid are being used, they should be discontinued. Patients should be educated about the link between application of topical corticosteroid and exacerbation of the dermatitis. In the most cases, treatment includes oral tetracycline, doxycycline or minocycline for a course 8-12 weeks, including a taper over the last 2-4 weeks. Topical antibiotic therapy most commonly with topical metronidazole, should be initiaed concurrently wiyh the systemic antibiotic. Other options include topical clindamycin or erythromycin, topical sulfur-based preparations, and topical azelaic acid.

Photoallergic Contact Dermatitis

Certain substances are transformed into irritants or sensitizers (photosensitizers) after irradiation with UV or short-wave visible radiation (280–600 nm). The photoactivated molecules may be transformed into new substances capable of acting as irritants or haptens. Photoallergic reactions are based on immunological mechanisms, and can be provoked by UV radiation only in a small number of individuals who have been sensitized by

same immunological mechanism as contact allergic reactions. The action spectrum for photoallergy is generally in the UVA range. Many photocontact allergens have been identified with varying degrees of confirmatory evidence, and these are perfumes, topical non-steroidal anti-inflammatory agents, phenothiazines, sulphonamides used for topical treatment, bithionol and hexachlorophene (in toilet soaps, shampoos and deodorants), quinines.

Photoallergic reactions can resemble sunburn, but usually show the same spectrum of features seen with allergic contact dermatitis. The dermatitis is localized to exposed areas of the skin, usually with well-demarcated margins where the skin is covered by clothing, for example at the collar and ‘V’ of the neck, below the end of the sleeves and trouser leggings. The area below the chin is usually spared.

Urticaria (Wheals)

Urticaria is a vascular reaction of the skin characterized by the appearance of wheals, generally surrounded by a red halo or flare and associated with severe itching, stinging, or pricking sensations. These wheals are caused by localized edema. Lesions may be a few millimeters in diameter or as large as a hand, and the number can vary from a few to numerous. The hallmark of wheals is that individual lesions come and go rapidly, by definition, in general within 24 hours. Angioedema swellings occur deeper in the dermis and in the subcutaneous or submucosal tissue. They may also affect the mouth and, rarely, the bowel. The areas of involvement tend to be normal or faint pink in color, painful rather than red and itchy, larger and less well defined than wheals, and often last for 2 to 3 days. Etiologic factors including drug, food, food additives, infections, emotional stress, menthol, neoplasm, inhalant, alcohol, hormonal imbalance, and genetics.

A comprehensive history is essential in every patient with urticaria. Patients should be given advice and information on common precipitants, treatments and prognosis. Antipruritic lotions and the avoidance of aggravating factors, including NSAIDs, may be sufficient for some, but many will need additional interventions, including systemic medications. Antihistamines are the mainstay of management for most patients with urticaria, although not all patients will respond and only about 40% of those attending tertiary care clinics will clear or almost clear at licensed doses. For severe reactions, including anaphylaxis, respiratory and cardiovascular support is essential. A 0.3 mL dose of a 1: 1000 dilution of epinephrine is administered every 10–20 min as needed. In young children, a half-strength dilution is used.

Day 8

Lecture 8: Pigmentary and

sebaseous gland

disorders

Elies/ Praharsini

Acne vulgaris is a chronic inflammatory disease of the pilosebaceous follicles, characterized by comedones, papules, pustules, nodules, and often scars. The comedo is the primary lesion of acne. Acne affects primarily the face, neck, upper trunk and upper arms. Acne is primarily a disease of the adolescent, with 85% of all teenagers being affected to some degree.Treatment consist of systemic and topical antimicrobials, systemic and topical retinoids, and systemic hormonal therapy.

Melasma is characterized by brown patches, typically on the malar prominences and forehead. There are three clinical patterns: 1) centrofacial, 2) malar, and 3) mandibular. Melasma occurs during pregnancy, using oral contraceptives or with hormone replacement therapy (HRT). Treatment: exposure to sunlight should be avoided and a complete sunblock with broad-spectrum UVA coverage should be used daily. Bleaching creams with hydroquinone are the gold standard. The combination of hydroquinone, tretinoin, topical steroid has been called Kligman’s formula and is excellent.

Day 9

Lecture 9: Bacterial infection

Karmila/ Ratih

Bacterial infection of the skin and it’s appendages are manifested as folliculitis, furunculosis, carbuncles, pyogenic paronichia, impetigo, staphylococcal scalded skin syndrome (SSSS), ecthyma, erysipelas and cellulitis. These bacterial infections above commonly caused by staphylococcal infection (S.aureus, S.epidermidis ) and streptococcal infection (S.aureus, S.pyogenes, S.β-hemolyticus group A, S.β-agalactiae, S.pneumoniae). The treatment of these bacterial infections needs local and systemic antibiotics.

Day 10

Lecture 10.

Insect bite

,

Infestation (scabies, creeping eruption)

, Pediculosis,

Cycticercosis cellulosa, Bedbugs and Mosquito bites

Praharsini/ Elies

Scabies is transmisibble ectoparasite skin infection characterized by superficial burrow, intense pruritus and secondary infection. Scabies is worldwide problem and all ages, races and socioeconomic groups are susceptible. There is variation in prevalence rates in some developing countries ranging from 4% to 100 %. The caused is Sarcoptes

scabiei varian homonis.

The intense pruritus is accentuated at night. Typical sites of involvement include the interdigital webbing of hands, flexural aspect of the wrist, axillae, buttock and genital area. Primary lesions is small erythematuos papules, variable numbers of excoriation, visicles., indurated noduls, excematous dermatitis and secondary bacterial infection. The pathognomonic sign is burrow.

Treatment options include either topical or oral medication. Topical option include permetrim cream, lindane, sulfur, crotamiton, benzyl benzoate. Oral option includes ivermectin, but is not avalaible in Indonesia.

Creeping eruption is term applied to twisting, winding linier skin lesions produced by the burrowing of larvae of various nematoda parasites . People who go bare footed on the beach, children playing on sandhoxes, carpenter and gardener are often victims.

The most common areas involved are the feet, buttock, genital and hands, accompanied by light local itching and the appareance of papules at the site of infection. After few days, the larvae migrate in the skin, creating bizzare erythematous curved lines.

Topical treatment include cryotherapy, topical theabendazole compounded as a 10 % suspension or 15 % cream.

The 3 mayor lice that infest humans are Pediculus humanus var. capitis (head lice), Pthirus pubis (Crab louse), and Pediculus humanus var. Corporis (Body Louce). Patient with louse infestation present with scalp pruritus, excoriations, cervical lymphadenopathy, and conjungtivitis. Head louse infestation crossses all social and geographic boundaries, occuring in affluent suburban schools and inner city school alike. Clinical manifestation is immediate urticarial lesion, a small 2-to 3 mm red macula or papul developing hours to days later, or the classic macula cerulae. Pubis infestation often ia acquired as a sexually transmitted disease. Treathment of louse infestation are topical pediculides ( permethrin, lindane, malathion) and envirommental control.

water, and is primarily a food borne disease. Humans are T. solium reservoirs. They are infected by eating undercooked pork that contains viable cysticerci. The condition known as cysticercosis in humans occurs due to the ingestion of tape worm eggs, either from external sources or from the person's own feces. In some cases the cysts will eventually cause an inflammatory reaction presenting as painful nodules in the muscles and seizures when the cysts are located in the brain.

The disease is most prevalent in countries in which pigs feed on human feces. A positive diagnosis is established where the parasite will be found. Albendazole and praziquantel is effective, however the status of CNS, spinal and ocular involvement needs to be thoroughly assessed prior treatment. None of these regimens clears the calcified parasites, however need to be surgically removed.

Bedbugs have flat oval bodies and retroverted mouthparts used for taking blood meals. They breed through a process referred to as traumatic insemination, where the male punctures the female and deposits sperm into her body cavity. Bedbugs hide in cracks and crevices then descend to feed while the victim sleeps. It is common for bedbugs to inflict a series of bites in a row (breakfast, lunch and dinner), bites may mimic urticaria and patients with popular urticaria commonly have antibodies to bedbug antigens.Bullous and urticarial reactions occur. Bedbugs are suspected vectors for chagas disease and hepatitis B, although data are sparse. Bedbugs often infest in bats and birds and these hosts may be responsible for infestations in houses. Management of the infestations may require elimination in houses. The area treated with an insecticides such as dichlorvos or permethrin.

Mosquitoes are vectors of malaria, encephalitis and yellow and dengue fevers. Their bite can also cause allergic reactions in sensitive individuals.

Image of a Mosquito Biting a Human

Mosquito bites are a common cause of popular urticaria. More severe local reactions are seen in young children, individuals with immunodeficiency and those with new exposure to indigenous mosquitos. Both necrotizing fasciitis and the hemophagocytic syndrome have been reported following mosquito bites and exaggerated hypersensitivity reactions to mosquito bites. Those with mild reactions to a mosquito bite can take antihistamines to reduce itching and swelling. Over time, some individuals develop immunity to the saliva of a mosquito and do not experience any symptoms at all upon being bitten.

Day 11

Lecture 11: Rational Topical Treatment in Dermatology

Alit Widhiartini

Dermatological therapy usually involves the use of topical therapy that was known since ancient times. Many agents are applied to the skin either for cosmetic or therapeutic purposes. However it is important that the basic principles underlying effective therapy should be well-understood. There are many factors to be considered, these include patient’s

age, hormonal status, and history. The anatomy and physiology of the skin and its appendages change with age and especially in woman, hormonal status may considerably influence the skin texture. The nature of the lesion, e.g. wet or dry, will determine the choice of the vehicle, the kind of topical preparation exactly, in which the active ingredient (drug) will be administered. The concepts of “If it’s wet, dry it;if it’s dry, wet it” will be clarified in detail during the small group learning.

The basic principles of topical therapy from the view point of pharmacotherapy, will guide the general practitioner to develop confidence in using topical therapy for common skin disorders such as wound dressing, acne, intralesional therapy, etc.

Lecture 12 : Dermatofarmacology

Surya Trapika

Therapy for cutaneous diseases often introduced by citing the skin’s role as a supportive interface between human’s external and internal milieu and as a barrier to potentially harmful agents in the environment. The fact that most dermatologic disorders are not life threatening should not lessen a physician’s responsibility for having to make as correct a therapeutic decision as is currently possible.

The general pharmacokinetic principles governing the use of drugs applied to the skin are the same involved in other routes of drug administration. Quantification of the flux of drugs and drug vehicles through these barriers is the basis of pharmacokinetic analysis of dermatologic therapy, techniques for making such measurements are rapidly increasing in number and sensitivity.

Topical medications usually consist of active ingredients incorporated in a vehicle that facilitates cutaneous application. Important consideration in selection of a vehicle include the solubility of the active agent in the vehicle, the rate of release of the agent from the vehicle. The ability of the vehicle to hydrate the stratum corneum, the stability of the therapeutic agent in the vehicle and interactions, chemical and physical of the vehicle, stratum corneum and active agent

The risks of less than through evaluation of simple dermatologic problems apply when problems become more complex. The drugs usually used in dermatologic disorders such as antibacterial agents, antifungal agents, topical antiviral agents, ectoparasiticides agents, agents affecting pigmentation, acne preparations, agents for psoriasis, antiinflamatory agents, keratolytic & destructive agents, antipruritic agents and trichogenic agents.

Day 12

Lecture 13. Anatomy of the Ear

Yuliana

The Ear

The ears are vestibulocochlear organs. Each ear comprises three portions: external, middle and internal. External and middle ear function is for hearing process only. Internal ear function is for hearing and equilibrium.

The external ear (the external acoustic/auditory meatus) conducts sound toward the middle and internal components of the ear. It protects middle and internal ear from outside damage and acts as pressure amplifier. It is about 25mm in length, extends from the concha to the tympanic membrane. External ear is composed of auricle (pinna), which collect sound and external acoustic meatus (canal), which conducts sound to the tympanic membrane. The lateral part is largely cartilaginous and slightly concave anteriorly. Skin of auricle continuously lines the meatus tightly. In cartilaginous part of auricle, there are hair follicles, sebaceous and ceruminous glands. The sensory innervations of external ear is derived from the auricular nerve (5th _{cranial nerve), the cervical plexus, and 7}th _{cranial nerve.}

Glossopharyngeal nerve (9th _{cranial nerve) and vagus nerve (10}th _{cranial nerve) innervate} concha region. The blood supply mainly from the posterior auricular and superficial temporal arteries (of the external carotid).

The Tympanic Membrane/Ear Drum is about 1 cm in diameter, faces laterally, forward and downward. It is divided into tense part and flaccid part. Tense part is the larger portion and attached to the tympanic plate of the temporal bone. Flaccid part is thinner in the anteriorsuperior portion and is limited by anterior and posterior mallear fold. Its lateral surface is concave and the center is called the umbo. The tympanic membrane is innervated by 5th _{and 10}th _{cranial nerves for its lateral surface and 9}th _{cranial nerve for} medial surface.

The Middle Ear consists of tympanic cavity and auditory ossicles.

The tympanic cavity communicates with (1) the mastoid air cells and the mastoid antrum by means of the auditus, and (2) the nasopharynx by means of the auditory tube (phrayngotympanic tube). Auditory tube acts as equalizer for both ears. The cavity is divided into 3 portions (1) the affic or epitympanic recess situated above the level of the tympanic membrane. Its contains the head of the malleus and the body and short crus of the incus. This recess communicate with the aditus. (2) mesotympanum, the main portion, and (3) the lowest portion, the hypotympanic recess. The tympanic cavity is bounded laterally by tympanic membrane. The roof of the cavity is formed by tegmen tympani, a portion of the petrous temporal.

Auditory ossicles are three small bones: malleus (hammer), incus (anvil), and stapes (stirrup). They joint as incudomallear and incudo stapedial joints in type of synovial joint. The chain of the auditory ossicles act as a system of levers. The handle and the lateral process of the malleus are embedded in the fibrous layer of the tympanic membrane. So the motion of the membrane by the sound waves are converted into intensified movements of the stapes.

Two important muscles are tensor tympani and stapedius muscles. Tensor tympani muscle arises from cartilaginous part of the auditory tube and inserted on the handle of the malleus. It draws the handle medially, thereby tightening the tympanic membrane. The muscle supplied by the mandibular nerve and tympanic plexus. The stapedius muscle draws the stapes laterally and perhaps rotate the incus. The muscle is supplied by the 7th _cranial nerve.

The chief blood supply to the middle ear is from the external carotid (stylomastoid artery from posterior auricular artery) and the maxillary (anterior tympanic artery).

The internal ear is located within the petrous part of the temporal bone. It consists of the membranous and bony labyrinth. Membranous labyrinth is located within bony/osseous labyrinth. The bony labyrinth is a series of cavities composed of three parts: cochlea, vestibule and semicircular canals. The membranous labyrinth consists of three parts: (1) utricle and saccule, two small communicating sac in the vestibule; (2) three semicircular ducts in the semicircular canals and (3) cochlear duct in the cochlea that contains the organ of hearing. Its chief divisions are the cochlear labyrinth and the vestibular labyrinth. The utricle and saccule have specialized area of sensory epithelium, the maculae. The macula of the utricle is in the floor of the utricle; the macula of the saccule is vertically placed on the medial wall of the saccule. The hair cells in the macula are innervated by the vestibulocochlear nerve and the cell bodies are in the vestibular ganglion, which is in the internal acoustic meatus. The roof of the cochlear duct is formed by the vestibular membrane and the floor by the basilar membrane plus the outer adge of the osseous spiral lamina. The spiral organ (of Corti) contain hair cells situated on the basilar membrane. The tips of cells are embedded in the gelatinous tectorial membrane. The vibration of the base of stapes ascend to the apex by one cannel, the scala vestibule; then the pressure waves pass through the helicotrema and descend back to the basal turn by the other channel, the scala tympani.

Arijana / Ratnayanti

The functions of the ear are for hearing and equilibrium. Ears consisted of three major parts, namely external ear which received sound wave, middle ear which transmitted from air to fluid via a set of small bone and internal ear which transform fluid movement to nerve impulses. External ear has auricle, external acoustic meatus, ceruminous glands and tympanic membrane. Middle ear has tympanic cavity, Eustachian tube, oval window, round window, and auditory ossicles (malleus, incus and stapes). Internal ear has bony labyrinth and membranous labyrinth. Membranous labyrinth has vestibular labyrinth (equilibrium system) and cochlear labyrinth (hearing system). Vestibular labyrinth has utricle, saccule and semicircular ducts. For equilibrium the receptors are located in 2 maculae (utricular macula and saccular macula) and 3 cristae ampullaris (in each semicircular duct). For hearing the receptors are located in spiral organ of Corti in cochlear duct. The receptors are mechanoreceptors called hair cells which convert sound wave into electrical impulses in nerve. All regions of bony labyrinth are filled with perilymph and membranous labyrinth is filled with endolymph.

Day 13

Lecture 15 : Physiology of Hearing systems

Krisna Dinata

Audition, the sense of hearing, involves the transduction of sound waves into electrical energy, which then can be transmitted in the nervous system. Most sounds are mixtures of pure tones. The human ear is sensitive to tones with frequencies between 20 and 20,000 Hz and is most sensitive between 2000 and 5000 Hz. The usual range of frequencies in human speech is between 300 and 3500 Hz, and the sound intensity is about 65 dB. Sound intensities greater than 100 dB can damage the auditory apparatus, and those greater than 120 dB can cause pain.

Sound waves are directed toward the tympanic membrane, and, as the tympanic membrane vibrates, it causes the ossicles to vibrate and the stapes to be pushed into the oval window. This movement displaces fluid in the cochlea and cause vibration of the organ of Corti. Thus, vibration of the organ of Corti causes bending of cilia on the hair cells by a shearing force as the cilia push against the tectorial membrane. Bending of the cilia produces a change in K+ conductance of the hair cell membrane. Thus, oscillating depolarizing and hyperpolarizing receptor potentials in the hair cells cause intermittent release of glutamate, which produces intermittent firing of afferent cochlear nerves.

Information is transmitted from the hair cells of the organ of Corti to the afferent cochlear nerves. The cochlear nerves synapse on neurons of the dorsal and ventral cochlear nuclei of the medulla, which send out axons that ascend in the CNS.

Lecture 16. Otic Drug

Alit Widhiartini

Middle and inner ear disorder often requires oral systemic or topical medications. Treatment of external ear however depend on topical otic drugs instilled directly into the external meatus of the ear for local action to prevent or treat disorders. These drugs include antibiotics, antiinfectives, anti-inflammatory, anesthetics, drying and cerumen softener solvents. Many otic drugs are consist of single or combination of 2 or more drugs these are used to treat external ear infections, inflammation, and pain, and removing excessive or impacted cerumen.

Day 14

Ear is one off indera wich have important function. The ear caught sound and then processed at the hearing cortex area at cerebri. This connect us with others. That’s why we must take good care of our ear. Ear divided into three part wich are outer, middle and inner ear. Outer ear diseases include perichondritis, foreign bodies, bulous myringitis. Wax or cerumen in normal production have protective function

Day 15

Lecture 18. Membrane tymphani perforation, OMS, Labirinitis,

Paresis N.Facialis

Andi Dwi Saputra

Infections of the middle ear space and their sequelae have plagued mankind from the beginning of time. First described by Hippocrates in 450 BC, this universally observed process continues to present one of the most perplexing medical problems of infancy and childhood, while being the leading cause of hearing loss in this age group.

Complications of acute and chronic otitis media can cause grave morbidity and even mortality. Eventhough the incidence and prevalence of these complications have dramatically declined, their potential gravity requires physicians to have a thorough understanding of the diagnosis and management of each one.

Labyrinthitis could be part of otitis media when the infections spread into inner ear.

Acute facial palsy is a common diagnostic problem encountered by the otolaryngologist, but its presentation often provokes consternation on the physician's part. This reaction stems from our limited knowledge of facial nerve pathology, from the shortcomings of currently popular electrophysiologic tests in defining nerve injury, and from the controversy surrounding the management of facial palsy.

Day 16

Lecture 19. Ear trauma/othematoma, Barotrauma, Motion Sickness, PGPKT

Eka Putra

Trauma of the ear can cause damage to the ear structures such as Othematum, external ear canal, middle ear canal and tympanic membrane rupture as a change inpressure in the middle ear, and dinner ear damage. The journey traveled either by air, sea and land can lead to complaints of motion sickness, with symptoms: nausea, vomiting, pallor, sweating, so it should be anticipated. Broadly speaking the causes of hearing loss and deafness are: wax obsturan, OMSK, Noisy, Presbicus is and Congenital deaf, because the Ministry of Health and its staff enough trouble to his ministry then formed an independent forum that is the National Committee for Prevention Hearing Loss and Deafness (PGPKT).

Lecture 20. Hearing loss, noise induced hearing loss

Wiranadha

There are two major categories of hearing loss that are key concepts for the clinician to understand. The first, conductive hearing loss, is due to an outer or middle ear problem— a problem “conducting” sound waves through the ear canal to the eardrum and then through the middle ear apparatus toward the inner ear. Causes of conductive loss might include obstruction of the ear canal by cerumen (wax), impairment of middle ear function by fluid, or fixation of the middle ear ossicles by disease. With conductive loss, sounds coming from within, such as one’s own voice, are perceived as louder because of reduced competing ambient noise. Plug your right ear with your finger, creating a conductive loss, and note how your own voice sounds louder on this side. This phenomenon is known as autophony. A

patient with a conductive loss often feels like he or she is talking “in a barrel,” or “under water.”

Sensorineural hearing loss is due to a malfunction somewhere in the inner ear, from the cochlea inward through the auditory nerve. This is often termed “nerve deafness” and with this type of loss even one’s own voice does not sound loud. The distinction between these two types of loss is obviously important for determining the cause of a patient’s hearing complaint. Both conductive and sensorineural loss in the same ear. This would be referred to as a mixed loss. Tuning-fork evaluation can differentiate between the two hearing loss. The 512-Hz tuning fork is themost accepted frequency for assessing hearing using the Weber and Rinne tests. Audiometry is the precise method of hearing assessment.

Noise refers to unwanted, undesirable, or excessively loud sound experienced by an individual. The effects of noise depend on various characteristics of the sound: intensity, spectrum, cumulative lifetime exposure, and pattern. NIHL results from trauma to the sensory epithelium of the cochlea.

Patients with NIHL frequently complain of a gradual, insidious deterioration in hearing. The most common complaint is difficulty in comprehending speech, especially in the presence of competing background noise. NIHL is frequently accompanied by tinnitus. The diagnosis of NIHL characterized by “4000 Hz notch”. Evoked otoacoustic emissions (OAE) may be useful in detecting early NIHL in persons with normal audiograms. No medical or surgical treatments are available to reverse the effects of NIHL. In patients with NIHL, hearing generally stabilizes if the patient is removed from the noxious stimulus. NIHL does not progress after the worker is removed from the source of the hazardous noise.

LEARNING TASKS

Day 1

Functional Structure of the skin and its appendices

Vignette 1

A baby boy present with erythroderma and severe blisters blister at his feet. The doctor diagnosed him with epidermolytic hyperkeratosis.

1. In which stratum of epidermis the disorder occurs? 2. What type of keratins involved in this disorders? Vignette 2

A male 18 years old present with chief complaint with odor secretion in his armpit. 1. Why these situation could be happen ?

2. Please describe the microscopic structure involved ! Self assesment

1. Describe the differences between ecrine and apocrine sweat gland 2. Describe the hair growth cycles

3. Describe the anatomical structure of the thin and thick skin 4. List and describe the sensory receptor of the skin

5. Describe the hair growth cycles

6. Describe the morphology of 4 type cells that located in epidermis

Day 2 : BCS and Practicum 1 (see BCS schedule)

Day 3

Common pathological bases of skin disorders

Learning task

List and describe the Descriptive term of microscopic features in dermatopathology bellow: 1. Hyperkeratosis

2. Parakeratosis 3. Hypergranulosis 4. Acanthosis 5. Papillomatosis 6. Dyskeratosis 7. Acantholysis 8. Spongiosis 9. Hydropic swelling 10. Exocytosis 11. Erosion 12. Ulceration 13. Vacuolization 14. Lentigenous Self assesment

KETRAMPILAN KLINIS

~ CURRICULUM MAP ~

Smstr

Program or curriculum blocks

10

Senior Clerkship

9

Senior Clerkship

8

Senior clerksh

ip

7

Medical Emergency (3 weeks) BCS (1 weeks)

Special Topic: -Travel medicine (2 weeks)

Elective Study III (6 weeks)

Clinic Orientation (Clerkship) (6 weeks) 6 The Respiratory System and Disorders (4 weeks) BCS (1 weeks)

The

Cardiovascular System and Disorders (4 weeks) BCS (1 weeks)

The Urinary System and Disorders (3 weeks) BCS (1 weeks)

The Reproductive System and Disorders (3 weeks) BCS (1 weeks)

5 Elective Study II (1 weeks) Alimentary & hepato-biliary systems & disorders (4 Weeks) BCS (1 weeks)

The Endocrine System, Metabolism and Disorders (4 weeks) BCS (1 weeks)

Clinical Nutrition and Disorders (2 weeks) BCS (1 weeks)

Special Topic : - Palliative medicine -Compleme ntary & Alternative Medicine - Forensic (3 weeks) Elective Study II (1 weeks) 4 Musculoskeletal system & connective tissue disorders (4 weeks) BCS (1 weeks)

Neuroscience and

neurological disorders (4 weeks) BCS (1 weeks)

Behavior Change and disorders (4 weeks) BCS(1 weeks) The Visual system & disorders (2 weeks) BCS (1 weeks) 3 Hematologic system & disor-ders & clinical oncology (4 weeks) BCS (1 weeks)

Immune system & disorders (2 weeks) BCS(1 weeks) Infection & infectious diseases (5 weeks) BCS (1 weeks)

The skin & hearing system & disorders (3 weeks) BCS(1 weeks) 2 Medical Professionalism (2 weeks) BCS (1 weeks)

Evidence-based Medical Practice (2 weeks) Health System-based Practice (3 weeks) BCS (1 weeks)

Community-based practice (4 weeks) Special Topic - Ergonomi - Geriatri (2 weeks) Elective Study I (2 weeks) Studium Generale and Humaniora (3 weeks) Medical communication (3 weeks) BCS (1 weeks)

The cell as bioche-mical machinery (3 weeks) BCS(1 weeks) Growth & development (4 weeks) BCS: (1 weeks) Pendidikan Pancasila & Kewarganegaraan (3 weeks)