Study Guide Blok Urinary Semester 6 tayang 8 mei 2015

~ CURRICULUM ~

Aims:

1. Comprehend the biologic function of urogenital system to pathological process of urinary system disorders.

2. Apply and interpret special studies in diagnosis urogenital system disorders, including laboratory and imaging examination.

3. Diagnose and manage patient with common urogenital system disorders 4. Diagnose and refer special patient with urogenital system disorders

5. Plan patient, family, and community education about urogenital system disorders Learning Outcome

1. Describe the functional structure of urigenital system and its general clinical implications. 2. Comprehend the pathological basis underlying the symptoms and signs of urogenital

system disorders.

3. Recognize the potential uses of common diagnostic and therapeutic procedure in urogenital system disorders.

4. Manage urogenital system disorders:

1. Diagnose and manage independently uncomplicated urinary tract infection, including uncomplicated pyelonephritis.

2. Diagnose and manage independently phymosis and paraphymosis.

3. Diagnose, give initial treatment, and refer some urogenital system disorders such as acute and chronic glomerulonephritis, renal colic, kidney rupture, bladder rupture, urethra rupture, acute kidney injury, chronic kidney disease, acute tubular necrosis, prostatitis, and priapismus.

4. Diagnose and refer some urogenital system disorders such as, horse shoe kidney, kidney tumor, nephrotic syndrome, symptomatic polycystic kidney, epydidimitis, urothelial carcinoma, benign prostate hyperplasia, and prostate cancer, common penile tumor, hipospadia, and epispadia.

5. Manage secondary hypertension

Diagnose and refer secondary hypertension, especially renal hypertension 6. Implement patient education in the prevention and early detection of common urinary

system disorders. Curriculum content

1. Functional structure of urogenital system

2. Pathological basis of urogenital system disorders 3. Symptom and sign of urogenital system disorders

4. Physical examination, laboratory investigation and imaging studies in urogenital system disorders

5. Interpret and utilize results of Physical examination, laboratory investigation and imaging studies

6. Rational drug use in urogenital system disorders 7. Management of urogenital system disorders 8. Clinical procedure in urogenital system disorders

9. Communicate and apply basic principle in the prevention, and rehabilitation of urogenital system disorders

~ PLANNERS TEAM ~

N

O NAME DEPARTMENT

1 DR. dr. A A Gde Oka, Sp.U _{(Coordinator)} Urology 2 dr. I Wayan Juli Sumadi, Sp.PA _(Secretary) Pathology

3 Prof. dr. K. Tirtayasa, MS, AIF Physiology

4 dr. I A Ika Wahyuniari, M.Kes Histology

5 Prof. DR. dr. Mangku Karmaya, _M.Repro Anatomy 6 Prof. DR. dr. K. Suwitra, SpPD (KGH) Internal Medicine

7 dr. Made Adi Tarini, Sp.MK Microbiology

8 DR. dr. Wiradewi Lestari, Sp.PK Clinical Pathology

9 dr. IGAP Nilawati, Sp.A(K) Pediatric

10 dr. I Gst Ayu Artini, M.Sc Pharmacology

11 dr. Gede Wirya Kusuma Duarsa, Sp.U Urology

12 dr. Sri Laksminingsih, Sp.Rad Radiology

~ LECTURERS ~

NO NAME DEPARTMENT

1 Prof. DR. dr. K. Suwitra, SpPD (KGH) Internal Medicine

2 Prof. dr. K. Tirtayasa, MS, AIF _Physiology

3 dr. I A Putri Wirawati, Sp.PK _{Clinical Pathology}

4 dr. G A P Nilawati, Sp.A _Pediatric

5 Prof. DR. dr. N. Mangku Karmaya, M.Repro

Anatomy

6 dr. A A Gde Oka, Sp.U Urology

7 dr. Jodhi Sidarta L, SpPD (KGH) Internal Medicine

8 dr. Ni Wayan Winarti, Sp.PA Pathology Anatomy

9 dr. G. Wirya K Duarsa, SpU, M.Kes Urology

10 dr. I Wayan Sugiritama, M.Kes Histology

11 dr. I Gst Ayu Artini, M.Sc Pharmacology

12 dr. A A Wiradewi Lestari, Sp.PK Clinical Pathology

13 dr. Sri Laksminingsih, Sp.Rad Radiology

~ FACILITATORS ~

Regular Class (Class A)

No Name Group Departement Phone ₍₂Venue rd _floor)

1

dr. Ida Bagus Wirakusuma,

MOH A1

Public Health 08124696647 2nd

floor: R.2.09 2

dr. Kadek Agus Heryana,

Sp.An A2

Anasthesi 081338568883 2nd

floor: R.2.11 3

dr. Ketut Agus Somia,

Sp.PD-KPTI A3

Interna 08123989353 2nd

floor: R.2.12 4

dr. Ketut Rai Purnami, Sp.PD

A4

Interna 0818350703 2nd

floor: R.2.13 5

dr. Komang Andi Dwi Saputra

, Sp.THT-KL A5

ENT 081338701828/

081338701878

2nd floor: R.2.14 6

dr. I Kadek Swastika , M Kes

A6

Parasitology 08124649002 2nd

floor: R.2.15 7

dr. Kumara Tini, Sp.S

A7

Neurology 081238701081 2nd

floor: R.2.16 8

dr. Made Agus Hendrayana ,

M.Ked A8

Microbiology 081339158241 2nd

floor: R.2.20 9

dr. Luh Putu Ratna Sundari,

M.Biomed A9

Fisiology 0361-7860532 2nd

floor: R.2.21 10

dr. I Gusti Ayu Artini , M.Sc

A10

Pharmacology 08123650481 2nd

floor: R.2.22 English Class (Class B)

No Name Group Departement Phone Venue

(2rd _floor) 1 dr. I Dewa Ayu Inten Dwi

Primayanti, M.Biomed B1

Fisiology 081337761299 2nd floor: R.2.09 2 dr. Made Ratna Saraswati, _{Sp.PD-KEMD-FINASIM} B2 Interna 08123814688 2nd floor:_R.2.11 3 dr. Made Sudarmaja, M.Kes B3 Parasitology 08123953945 2nd floor:_R.2.12 4 dr. Made Widhi Asih, Sp.Rad B4 Radiology 081916442626 2nd floor:_R.2.13 5 dr. I G A Sri Darmayani, _Sp.OG B5 DME 081338644411 2nd floor:_R.2.14 6 dr. Putu Ayu Asri Damayanti ,_{M Kes} B6 Parasitology 085338565783 2nd floor:_R.2.15

7 dr. Ni Kadek Mulyantari , _{Sp PK} B7 _PathologyClinical 08123647413 2nd floor:_R.2.16 8 dr. I Wayan Niryana, Sp.BS, _{M. Kes.} B8 Surgery 08179201958 2nd floor:_R.2.20 9 dr. Ni Luh Putu Ratih _{Vibriyanti Karna, Sp.KK} B9 Dermatology 081337808844 2nd floor:_R.2.21 10 dr. Ni Made Adi Tarini, Sp.MK B10 Microbiology 081338675344 2nd floor:_R.2.22

~ TIME TABLE ~

REGULAR CLASS

DAY/DATE TIME ACTIVITY VENUE PIC

I 08-05-2015

08.00-09.00 Macroscopic Anatomy of The Urinary System

3.02 Mangku

Karmaya

08.00-10.00 Individual Learning -

-10.00-11.00 Practical Session (Anatomy): Group A1-A5

Anatomy Lab

Mangku Karmaya

11.00-12.30 SGD 1 Discussio

n room Facilitators

12.30-13.00 Break -

-13.00-14.00 Practical Session (Anatomy): Group A6-A10

Anatomy Lab

Mangku Karmaya

14.00-15.00 Plenary 3.02 Mangku

Karmaya II

11-05-2015

08.00-09.00 Microscopic Anatomy of The Urinary System

3.02 Sugiritama

09.00-10.00 Individual Learning -

-10.00-11.00 Practical Session (Histology): Group A1-A5

Histology Lab

Sugiritama

11.00-12.30 SGD 2 Discussio

n room

Facilitators

12.30-13.00 Break -

-13.00-14.00 Practical Session (Anatomy): Group A6-A10

Histology Lab

Sugiritama

14.00-15.00 Plenary 3.02 Sugiritama

III 12-05-2015

08.00-09.00 The function of the urinary system:

7. Urine formation 8. Urine micturition

3.02 Tirtayasa

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 3 Discussio

n Room

Facilitators

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Tirtayasa

IV 13-05-2015

08.00-09.00 The kidney as water, electrolyte and acid-base balance controller

3.02 Tirtayasa

09.00-10.30 Individual Learning -

n Room

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Tirtayasa

V 18-05-2015

08.00-09.00 Pathogenesis of Glomerular and Tubulointerstitial Injury

3.02 Winarti

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 5 Discussio

n Room

Facilitators

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Winarti

VI 19-05-2015

08.00-09.00 Urinary System Disorders in Children:

- Nephrotic syndrome

- PSAGN

- UTI in Children

3.02 Nilawati

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 6 Discussio

n Room

Facilitators

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Nilawati

VII 20-05-2015

08.00-09.00 Uncomplicated and complicated Urinary tract infection

3.02 Suwitra and Team

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 7 Discussio

n Room Facilitators

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Suwitra and

Team VIII

21-05-2015

08.00-09.00 Urolithiasis (with and without colic); Urethral Stricture

3.02 AA Gde Oka

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 8 Discussio

n Room

Facilitators

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 AA Gde Oka

IX 23-05-2015

08.00-09.00 Common Neoplasm in Urinary System: Renal tumors, bladder tumors.

3.02 AA Gde Oka

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 9 Discussio

n Room

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 AA Gde Oka

X 25-05-2015

08.00-09.00 Urinary tract trauma (rupture of the kidney and urinary tract)

3.02 AA Gde Oka

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 10 Discussio

n Room

Facilitators 12.00-13.00 Student Project Presentation

1 (Horse Shoe Kidney)

3.02 AA Gde Oka

13.00-15.00 Break -

-14.00-15.00 Plenary 3.02 AA Gde Oka

XI 26-05-2015

08.00-09.00 Acute Kidney Injury 3.02 Suwitra and

Team

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 11 Discussio

n Room

Facilitators 12.00-13.00 Student Project Presentation

2 (Symptomatic Polycystic Kidney)

3.02 Suwitra and Team

13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Suwitra and

Team XII

27-05-2015

08.00-09.00 Chronic Kidney Disease 3.02 Suwitra and

Team

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 12 Discussio

n Room

Facilitators 12.00-13.00 Student Project Presentation

3 (Hemodialysis)

3.02 Suwitra and Team

13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Suwitra and

Team XIII

28-05-2015

08.00-09.00 Renal hypertension 3.02 Jodi SL

09.00-10.30 Individual Learning -

-10.30-11.30 Drug Use in Renal Disorders:

Diuretics; Urinary Antiseptic 3.02 Artini

11.30-13.00 SGD 13 Discussio

n Room

Facilitators

13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Jodi SL, Artini

XIV 29-05-2015

08.00-09.00 Common Prostate Disorders: Prostatitis, BPH, Prostate Cancer

3.02 G. Wirya K. Duarsa

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 14 Discussio

n Room

12.00-13.00 Student Project Presentation 4 (Urodinamic examination and Uroflowmetry)

3.02 AA Gde Oka

13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 Artini

XV 01-06-2015

08.00-09.00 Common penile disorders: Epispadia, hypospadia, phimosis, paraphimosis, epididimitis, prostatitis, priapismus and Common tumor of the penis

G. Wirya K. Duarsa

09.00-10.30 Individual Learning -

-10.30-12.00 SGD 14 Discussio

n Room

Facilitators 12.00-13.00 Student Project Presentation

5 (Micturating Cystigraphy)

3.02 G. Wirya K. Duarsa

13.00-14.00 Break -

-14.00-15.00 Plenary session 3.02 G. Wirya K.

Duarsa XVI

03-06-2015

08.00-09.00 Anamnesis and Physical Examination in Urinary System Disorders (Lecture & Demonstration)

3.02 Suwitra and Team

09.00-10.00 Individual Learning -

-10.00-11.00 Urethral catheterization, Clear intermittent

catheterization, suprapubic punctie (Lecture &

Demonstration)

3.02 AA Gde Oka

11.00-12.00 Break

-12.00-14.00 Skills Training Skills Lab

2nd _Floor

Facilitators

14.00-15.00 Free Training Skills Lab

2nd _Floor

-XVII

04-06-2015

08.00-09.00 Urinalysis 3.02 Wirawati/Wirade

wi

09.00-10.00 Individual Learning -

-10.00-11.00 Urethral Swab, Urine Culture and Sensitivity Test

3.02 Adi Tarini

11.00-12.00 Break

-12.00-14.00 Skills Training Skills Lab

2nd _Floor Facilitators

14.00-15.00 Free Training Skills Lab

2nd _Floor

-XVIII

05-06-2015

08.00-09.00 Circumcision, Prostate Palpation, Bulbocavernosus reflex (Lecture and

Demonstration)

3.02 G. Wirya K. Duarsa

09.00-10.00 Individual Learning -

-10.00-11.00 Student Project Presentation 6 (Urine Cytology)

3.02 Juli Sumadi

-12.00-14.00 Skills Training Skills Lab

2nd _Floor Facilitators

14.00-15.00 Free Training Skills Lab

2nd _Floor

-XIX

08-06-2015

08.00-09.00 BNO and IVP 3.02 Laksminingsih

09.00-10.00 Individual Learning -

-10.00-11.00 Student Project Presentation 7 (Pathological aspect of BPH and Prostate Cancer)

3.02 Winarti

11.00-12.00 Break -

-12.00-14.00 Skills Training Skills Lab

2nd _Floor Facilitators

14.00-15.00 Free Training Skills Lab

2nd _Floor

-XX

09-06-2015

08.00-09.00 Student Project Presentation 8 (The role of USG in

diagnosis Urinary system disorders)

3.02 Laksminingsih

09.00-10.00 Student Project Presentation 9 (The role of CT Scan in diagnosis Urinary system disorders)

3.02 Laksminingsih

10.00-11.00 Individual Learning -

-11.00-12.00 Break -

-12.00-13.00 Student Project Presentation 10 (Renal Funtion Test (BUN, SC))

3.02 Wirawati/Wirade wi

13.00-15.00 Free Training Skills Lab

2nd _Floor

-XXI

11-06-2015 Preparation Day

XXII 12-06-2015

10.00-11.40 Final Examination Computer

Room

Team

ENGLISH CLASS

DAY/DATE TIME ACTIVITY VENUE PIC

I 08-05-2015

09.00-10.00

Macroscopic Anatomy of The Urinary System

3.02 Mangku Karmaya

10.00-11.00

Individual Learning -

- 11.00-12.00

Practical Session

(Anatomy): Group B1-B5

Anatomy Lab

Mangku Karmaya

12.00-13.00

Practical Session

(Anatomy): Group B6-B10

Anatomy Lab

Mangku Karmaya

13.00-14.30

SGD 1 Discussion

room

14.30-15.00

Break -

- 15.00-16.00

Plenary 3.02 Mangku Karmaya

II 11-05-2015

09.00-10.00

Microscopic Anatomy of The Urinary System

3.02 Sugiritama

10.00-11.00

Individual Learning -

- 11.00-12.00

Practical Session

(Histology): Group B1-B5

Histology Lab

Sugiritama

12.00-13.00

Practical Session

(Histology): Group B6-B10

Histology Lab

Sugiritama

13.00-14.30

SGD 2 Discussion

room

Facilitators

14.30-15.00

Break -

- 15.00-16.00

Plenary 3.02 Sugiritama

III 12-05-2015

09.00-10.00

The function of the urinary system:

Urine formation Urine micturition

3.02 Tirtayasa

10.00-11.30

Individual Learning -

- 11.30-12.30

Break -

- 12.30-14.00

SGD 3 Discussion

Room

Facilitators

14.00-15.00

Student Project -

- 15.00-16.00

Plenary session 3.02 Tirtayasa

IV 13-05-2015

09.00-10.00

The kidney as water, electrolyte and acid-base balance controller

3.02 Tirtayasa

10.00-11.30

Individual Learning -

- 11.30-12.30

Break -

- 12.30-14.00

SGD 4 Discussion

Room

Facilitators

14.00-15.00

Student Project -

- 15.00-16.00

V 18-05-2015

09.00-10.00

Pathogenesis of Glomerular and Tubulointerstitial Injury

3.02 Winarti

10.00-11.30

Individual Learning -

- 11.30-12.30

Break -

- 12.30-14.00

SGD 5 Discussion

Room

Facilitators

14.00-15.00

Student Project -

- 15.00-16.00

Plenary session 3.02 Winarti

VI 19-05-2015

09.00-10.00

Urinary System Disorders in Children:

- Nephrotic syndrome

- PSAGN

- UTI in children

3.02 Nilawati

10.00-11.30

Individual Learning -

- 11.30-12.30

Break -

- 12.30-14.00

SGD 6 Discussion

Room

Facilitators

14.00-15.00

Student Project -

- 15.00-16.00

Plenary session 3.02 Suarta/Nilawati

VII 20-05-2015

09.00-10.00

Uncomplicated and complicated Urinary tract infection

3.02 Suwitra and team

10.00-11.30

Individual Learning -

- 11.30-12.30

Break -

- 12.30-14.00

SGD 7 Discussion

Room

Facilitators

14.00-15.00

Student Project -

- 15.00-16.00

Plenary session 3.02 Suwitra/AA Gde

Oka VIII

21-05-2015

09.00-10.00

Urolithiasis (with and without colic), urethral stricture

3.02 AA Gde Oka

10.00-11.30

Individual Learning -

- 11.30-12.30

Break -

- 12.30-14.00

SGD 8 Discussion

Room

Facilitators

14.00-15.00

Student Project -

16.00 IX

23-05-2015

09.00-10.00

Common Tumors in Urinary System: Renal cancer, bladder cancer

3.02 AA Gde Oka

10.00-11.30

Individual Learning -

-

11.30-12.30 Break -

- 12.30-14.00

SGD 9 Discussion

Room

Facilitators

14.00-15.00

Student Project -

- 15.00-16.00

Plenary session 3.02 AA Gde Oka

X

25-05-2015 09.00-10.00 Urinary tract trauma (ruptureof the kidney and urinary tract)

3.02 AA Gde Oka

10.00-11.00

Student Project Presentation 1 (Horse Shoe Kidney)

3.02 AA Gde Oka

11.00-12.30

Individual Learning -

- 12.30-14.00

SGD 10 Discussion

Room

Facilitators

14.00-15.00

Break -

- 15.00-16.00

Plenary session 3.02 AA Gde Oka

XI 26-05-2015

09.00-10.00

Acute Kidney Injury 3.02 Suwitra and team

10.00-11.00 Student Project Presentation2 (Symptomatic Polycystic Kidney)

3.02 Suwitra and Team

11.00-12.30

Individual Learning -

- 12.30-14.00

SGD 11 Discussion

Room

Facilitators

14.00-15.00

Break -

- 15.00-16.00

Plenary session 3.02 Suwitra and team

XII 27-05-2015

09.00-10.00

Chronic Kidney Disease 3.02 Suwitra and team

10.00-11.00

Student Project Presentation 3 (Hemoadialysis)

3.02 Suwitra and Team

11.00-12.30

Individual Learning -

- 12.30-14.00

SGD 12 Discussion

Room

Facilitators

14.00-15.00

Break -

- 15.00-16.00

XIII 28-05-2015

09.00-10.00

Renal Hypertension 3.02 Jodi SL

10.00-11.00

Individual Learning -

- 11.00-12.30

Drug Use in Urinary System Disorders: Diuretics; Urinary Antiseptic

- Artini

12.30-14.00

SGD 13 Discussion

Room

Facilitators

14.00-15.00

Break -

- 15.00-16.00

Plenary session 3.02 Jodi SL, Artini

XIV 29-05-2015

09.00-10.00

Common prostate disorders: Prostatitis, BPH, Prostate Cancer

3.02 G. Wirya K. Duarsa

10.00-11.00

Student Project Presentation 4 (Urodinamic examination and Uroflowmetry)

3.02 AA Gde Oka

11.00-12.30

Individual Learning -

- 12.30-14.00

SGD 14 Discussion

Room

Facilitators

14.00-15.00

Break -

- 15.00-16.00

Plenary session 3.02 G. Wirya K.

Duarsa XV

01-06-2015

09.00-10.00

Common penile disorders: Epispadia, hypospadia, phimosis, paraphimosis, epididimitis, prostatitis, priapismus and Common tumor of the penis

G. Wirya K. Duarsa

10.00-11.00

Student Project Presentation 5 (Micturating Cystigraphy)

3.02 G. Wirya K. Duarsa

11.00-12.30

Individual Learning -

- 12.30-14.00

SGD 14 Discussion

Room

Facilitators

14.00-15.00

Break -

- 15.00-16.00

Plenary session 3.02 G. Wirya K.

Duarsa XVI

03-06-2015

09.00-10.00

Anamnesis and Physical Examination in Urinary System Disorders (Lecture & Demonstration)

3.02 Suwitra and Team

10.00-11.00

Individual Learning -

- 11.00-12.00

Urethral catheterization, Clear intermittent

catheterization, suprapubic

punctie (Lecture & Demonstration) 12.00-13.00 Break - 13.00-15.00

Skills Training Skills Lab

2nd _Floor

Facilitators

15.00-16.00

Free Training Skills Lab

2nd _Floor

-XVII 04-06-2015

09.00-10.00

Urinalysis 3.02 Wirawati/Wiradew

i

10.00-11.00

Individual Learning -

- 11.00-12.00

Urethral Swab, Urine Culture and Sensitivity Test

3.02 Adi Tarini

12.00-13.00

Break

- 13.00-15.00

Skills Training Skills Lab

2nd _Floor

Facilitators

15.00-16.00

Free Training Skills Lab

2nd _Floor

-XVIII 05-06-2015 09.00-10.00 Circumcision, Prostate Palpation, Bulbocavernosus reflex (Lecture and

Demonstration)

3.02 G. Wirya K. Duarsa

10.00-11.00

Individual Learning -

- 11.00-12.00

Student Project Presentation 6 (Urine Cytology)

3.02 Juli Sumadi

12.00-13.00

Break

- 13.00-15.00

Skills Training Skills Lab

2nd _Floor

Facilitators

15.00-16.00

Free Training Skills Lab

2nd _Floor

-XIX

08-06-2015

09.00-10.00

BNO and IVP 3.02 Laksminingsih

10.00-11.00

Individual Learning -

- 11.00-12.00

Student Project Presentation 7 (Pathological aspect of BPH and Prostate Cancer)

3.02 Winarti

12.00-13.00

Break -

- 13.00-15.00

Skills Training Skills Lab

2nd _Floor Facilitators

15.00-16.00

Free Training Skills Lab

2nd _Floor

-XX

09-06-2015

09.00-10.00

Individual Learning -

- 10.00-11.00

Student Project Presentation 8 (The role of USG in diagnosis Urinary system disorders)

3.02 Laksminingsih

12.00 9 (The role of CT Scan in diagnosis Urinary system disorders)

12.00-13.00

Break -

- 13.00-14.00

Student Project Presentation 10 (Renal Funtion Test (BUN, SC))

3.02 Wirawati/Wiradew i

14.00-16.00

Free Training Skills Lab

2nd _Floor

-XXII 11-06-2015

PREPARATION DAY XXI

12-06-2015

FINAL EXAMINATION

~ STUDENT PROJECT ~

No Group Topic PIC

1 A1, B1 Horse Shoe Kidney AA Gde Oka

2 A2, B2 Symptomatic Polycystic Kidney Suwitra and Team

3 A3, B3 Hemodialysis Suwitra and Team

4 A4, B4 Urodinamic examination and Uroflowmetry AA GdeOka

5 A5, B5 Micturating cystigraphy AA GdeOka

6 A6, B6 Urine Cytology Juli Sumadi

7 A7, B7 Pathological aspect of BPH and Prostatic Carcinoma

Winarti 8 A8, B8 The role of USG in diagnosis Urinary system

disorders

Sri Laksminingsih 9 A9, B9 The role of CT Scan in diagnosis Urinary system

disorders

Sri Laksminingsih 10 A10,

B10

Renal Function Test (BUN, SC) Wirawati/Wiradewi

~ ASSESSMENT METHOD ~

Assessment will be carried out on June 12, 2014. There will be 100 questions consisting mostly of Multiple Choice Questions (MCQ) and some other types of questions. The minimal passing score for the assessment is 70. Other than the examination score, your performance and attitude during group discussions and your study project will be considered in the calculation of your average final score.

ABSTRACTS

The urinary system (urinary tract) consists of two kidneys, two ureters, a urinary bladder, and the urethra. The kidney is subdivided into cortex and medulla. The kidney is made up by subunits called uriniferous tubule. The uriniferous tubule consists of the nephron and the collecting tubule that is functional unit of the kidney. It modifies the fluid passing through it to form urine. Beside its’ excretion function, kidney also involve in controlling blood pressure. This function is provided by juxtaglomerular apparatus, which consists of juxtaglomerular cell, extraglomerular mesangial cell and macula densa cell. This complex secretes hormones and contains receptors that can modify vasoconstriction and vasodilatation of blood vessels. Urine enters the renal pelvis, a structure that connects the kidney with ureter. The ureters that consist of mucosa, muscular coat, and fibrous outer coat deliver urine from the kidneys to urinary bladder. The urinary bladder is an essentially organ for storing urine until it is ready to be voided. It’s wall consists of mucosa, lined by transitional epithelium that is thin in full bladder, but thicker when contracted. Urine will be excreted from urinary bladder through the urethra. The urethra of male and female have different structure. In male the urethra is divided into three parts, urethra pars prostatica, urethra pars membranasea and urethra pars cavernosa. In female, the urethra is shorter and covered by transitional epithelium and stratified squamous epithelium.

SGD 1

Macroscopic Anatomy of Urinary System Trigger Case

A 30 years old man came to the doctor with flank pain since 2 days. One week before he fell while he was riding a bike and he didn’t feel any flank pain. His friends suggested that he have to see the doctor, they afraid there is something wrong in his kidney. His friends also suggest drinking much water. After drinking much water, the frequency of urination is increasing and he has very clear urine. He never feels any pain when urinate. On physical examination, the doctor didn’t find any disturbance either on his kidney or urinary tract. The patient asks the doctor to explain about: where is the kidney taking place, why the frequency of urination and urine volume increasing if we drink much water? If you as a doctor, please explain to the patient.

Learning Task:

1. Explain the location of urinary system in the abdominal region and its vasculature and innervations!

2. Draw the anatomical structure of urinary tract!

3. Draw the vasculature and innervations of urinary tract!

SGD 2

Lecture 1 - 2:

Macroscopic and Microscopic Structure the

Urinary System

Microscopic Anatomy of Urinary System Trigger Case 1

A male patient came to the doctor with complaint of generalized swelling, especially around his eyes, feet, and hands. From examination there were albuminuria and

hipoalbunemia. After complete examination, the doctor diagnosed the patient with nephrotic syndrome which damage glomeruli.

Learning Task

1. Differentiate the microscopic structure of cortex and medulla of the kidney!

2. Explain the structure of the functional unit of the kidney! Explain about the structures that participate in filtrating process!

3. Explain the microscopic structure of the juxtaglomerular apparatus and its function! 4. Why in the case above, albumin is present in the urine?

Trigger case 2

A 60 years old man complained with abdominal colic and uncontinuous flow of urination. From abdominal ultrasonography (USG), the doctor found stone in urinary bladder. After urinalysis, there are bloods in urine (hematuria).

Learning task

1. Explain the microscopic structure of ureter! Which structure is mainly involved in passing down urine from kidney to urinary bladder? Why urine could not regurgitate from the bladder back into ureters?

2. Explain the microscopic structure of urinary bladder! Why urine does not pass into the underlying lamina propria?

The kidneys perform their most important functions by filtering the plasma and removing substances from the filtrate at variable rate, depending on the need of the body. Ultimately, the kidneys “clear” unwanted substances from the filtrate (and therefore from the blood) by excreting them in the urine while returning substances that are needed back to the blood. All process in urine formation takes place in the nephrons as the functional unit of the kidneys. A nephron consists of glomerulus, Bowman’s capsule, proximal tubule, loop of Henle descending limb, loop of Henle ascending limb, distal tubule. Some distal tubules of nephrons empty their product into cortical and medullary collecting tubules and then to collecting duct and all collecting ducts empty into to renal pelvis. Each kidney in the human contain about 1 million nephrons, each of it capable to forming urine.

The glomerular filtrates (water, ion, nitrogen waste and organic solute) along the proximal tubule are reabsorbed into the interstitial space and blood. The components of reabsorbed filtrate are water, glucose and protein.

In the loop of Henle descending limb, the filtrate is less dilute due to high permeability of tubule cell to water. So the water reabsorbed more in this part of tubule. Meanwhile the filtrate is more diluted due to more NaCl and no water is reabsorbed at ascending limb of loop of Henle. Concentrated filtrate is also resulted from the counter-current exchange of vasa recta in the renal medulla.

Lecture 3-4:

Along the distal tubule, the filtrate is more concentrated due to more reabsorption than secretion process. It is also influenced by anti diuretic hormone (ADH) and aldosteron hormone. The rate of reabsorption or secretion at distal tubule depends upon the body internal environment to maintain homeostasis.

Urine as the last result of all process of filtrate (through filtration, reabsorption and secretion) along the renal tubules, then empty into renal pelvis. Through the right and left ureter the urine is collected in the bladder. Muscle contraction of the bladder push out the urine through the urethra.

The glomerular filtrates (water, ion, nitrogen waste and organic solute) along the proximal tubule are reabsorbed into the interstitial space and blood. The components of reabsorbed filtrate are water, glucose and protein.

In the loop of Henle descending limb, the filtrate is less dilute due to high permeability of tubule cell to water. So the water reabsorbed more in this part of tubule. Meanwhile the filtrate is more diluted due to more NaCl and no water is reabsorbed at ascending limb of loop of Henle. Concentrated filtrate is also resulted from the counter-current exchange of vasa recta in the renal medulla.

Along the distal tubule, the filtrate is more concentrated due to more reabsorption than secretion process. It is also influenced by anti diuretic hormone (ADH) and aldosteron hormone. The rate of reabsorption or secretion at distal tubule depends upon the body internal environment to maintain homeostasis.

The result of all process is urine. Through the right and left ureter the urine is collected in the bladder. Muscle contraction of the bladder push out the urine through the urethra.

Learning Task: SGD 3

The function of urinary system: urine formation and micturition process Learning Tasks:

1. Explain that the glomerular filtration rate (GFR) of kidneys depend on the variability of some forces

2. Explain how the autoregulation of glomerular filtration rate and renal blood flow 3. Explain the process and related substances such as water and electrolytes that take

place along the proximal tubule of nephron

4. Explain the process and related substances such as water and electrolytes that take place along the loop of Henle of nephron

5. Explain the process and related substances such as water and electrolytes that take place along the distal tubule of nephron

6. Explain the process and related substances such as water and electrolytes that take place along the collective tubule of nephron

7. Normally the urine cannot backflow from bladder to ureter. Please describe the rule of muscles of ureter in urine flow

8. What nerves are involved in micturition and describe the mechanism and rule of bladder muscles, sphincter and nerves that involved in urination process.

SDG 4

The Kidneys as water, electrolyte and acid-base balance controller Learning Tasks

1. Explain the concept of countercurrent multiplier system and countercurrent exchange 2. Explain the osmoreceptor- anti diuretic hormone feedback system

3. Explain the process in kidneys to conserve the fluid osmolarity and sodium concentration of body fluid

4. Explain the potassium excretion and potassium concentration in the extracellular fluid that is controlled by kidneys

5. What are the causes of acidity of body fluid?

6. What can you define the body in acidosis or alkalosis condition 7. Explain some buffers system in the body and what are their function 8. Explain the renal correction of acidosis condition and alkalosis condition.

Pathogenesis of Glomerular Injury

Glomerular diseases constitute some of the major problems in nephrology. The glomeruli may be injured by a variety of facilitatorstors and in the course of a number of systemic diseases. Some systemic diseases often affect glomeruli and causing glomerulopathy, termed secondary glomerulonephritis. It’s different with primary glomerulonephritis in which the kidney is the predominant organ involved.

Although we know little of etiologic agent and triggering events, it is clear that immune mechanisms, both humoral and cell-mediated immune reactions, underlie most forms of primary glomerulonephritis and many of the secondary glomerular disorders.

Two form of antibody-associated injury have been established: 1). Injury by antibodies reacting in situ within the glomerulus, either with insoluble fixed (intrinsic) glomerular antigens or with molecules planted within the glomerulus, and 2). Injury results from deposition of circulating antigen-antibody complexes in the glomerulus. In addition, there is experimental evidence that cytotoxic antibodies directed against glomerular cell components may cause glomerular injury. These pathways are not mutually exclusive and all may contribute to injury.

Injuries induced by these immune responses will lead the activation of many cells and mediators, resulting in functional and structural alteration of the glomeruli, followed by alteration of tubulointerstitial components.

Pathogenesis of Tubular/Interstitial Injury

Most forms of tubular injury also involve the interstitium; therefore, diseases affecting these two components are discussed together. Two major forms of this process are: 1). Ischemic or toxic tubular injury, leading to Acute Tubular Necrosis (ATN) and acute renal failure, and 2). Tubulointerstitial nephritis. In this lecture, we stress on ATN and certain tubulointerstitial nephritides.

ATN is a clinicopathologic entity characterized morphologically by destruction of tubular epithelial cells and clinically by acute diminution or loss of renal function. It can be caused by a variety of conditions, including ischemia, toxin, acute tubulointerstitial nephritis, urinary obstruction, etc. Based on its etiopathogenesis, the ATN can be grouped into two patterns, i.e. ischemic ATN and nephrotoxic ATN.

Tubulointerstitial nephritis characterized histologically by inflammation of tubules and interstitium. Pyelonephritis is the most common type of tubulointerstitial nephritis, commonly

Lecture 5:

Pathogenesis of Glomerular and

Tubulo-Interstitial Injury

caused by infection. Toxins and drugs are other important causes. It can produce renal injury in at least three ways: 1). Trigger an interstitial immunologic reaction, exemplified by the acute hypersensitivity nephritis induced by such drugs as methicillin, 2). Those may also cause acute renal failure, and 3). Cause subtle but cumulative injury to tubules that take years to become manifest, resulting in chronic renal insufficiency.

SGD 5

Pathogenesis of glomerular and tubulo/interstitial injury Trigger Case 1

A 50 year old man has suffered from nephrotic syndrome since 3 months ago. Renal biopsy revealed diffuse capillary wall thickening by light microscopy. Immunoflurescence examination showed diffuse granular IgG and C3 deposits, located subepithelium (electron microscopy). No evidence of underlying systemic disease. This patient was diagnosed getting membranous glomerulopathy.

Learning Task

1. Mention classification of primary glomerular diseases!

2. Mention some diseases commonly induce glomerular injury (secondary glomerulopathy)! 3. Explain the pathogenesis of human membranous glomerulopathy!

4. Explain the differences between in situ immune complex deposition and circulating immune complex deposition!

5. Mention one best known type of glomerular disease which induced by circulating immune complex deposition!

6. Describe four major tissue reactions found in glomerulopathy! Trigger Case 2

A 60 year old man suffers from cardiac infarction and has been admitted since a week ago. Yesterday the nurse noted his urine production decreased, 250mL/24 hours. This oligouria is continuing until this day. Laboratory examination revealed increase of serum urea nitrogen and creatinin.

Learning Task

1. Discuss the mechanism responsible for oligouric state in this patient! 2. Explain about pathogenesis of acute kidney injury (AKI)!

3. What is the difference between AKI and tubulo-interstitial nephritis? 4. Mention some causes of tubule-interstitial nephritis!

Post Streptoccocal Acute Glomerulonephritis

Hematuria defined as the excretion in urine of abnormal amounts of red blood cells (RBCs). The presence of at least 5 RBCs in the urine was considered abnormal. It occurs with a prevalence of 0.5-2.0% among school aged children.

The child who exhibits gross hematuria needs prompt evaluation. The urinalysis should be repeated in the child who has the combination of microscopic hematuria, without proteinuria, normal blood pressure, and normal renal function. If the hematuria persist, further evaluation is appropriate.

Acute glomerulonephritis (AGN) is a syndrome characterized by the abrupt onset of macroscopic hematuria and edema. The majority of instances of AGN appear to be postinfectious, and a number of bacterial and viral infections have been etiologically incriminated. The most common recognized clinical picture follows group A, -hemolytic streptococcus infections. So the term used in this report is poststreptococcal acute glomerulonephritis (PSAGN).

Only certain nephritogenic strains of streptococci have been associated with PSAGN. The more common sporadic variety of PSAGN usually follows type 12 streptococcal infection of the pharynx. Epidemics of the disorder have been linked to several strains causing either throat or skin infections.

PSAGN predominantly affects children between the ages of 2 and 10 years, with a slight predominance of males. Typically, children with PSAGN present with sudden onset of painless gross hematuria, and some edema is usually present. Hypertension is a common feature of PSAGN and may lead to hypertensive encephalopathy. The laboratory findings of PSAGN include increased of ASTO titre and decreased serum complement C3. Urinalysis in most scenarios shows hematuria, proteinuria, and abnormal sediment including erythrocyte cast.

In adult from 15% to 30% of patients with PSAGN had been reported to progress to a chronic state while estimation in children have generally ranged from approximately 5% to 10%. The chronicity of PSAGN can be predicted if the microscopic hematuria, proteinuria, and a low serum complement C3 level are present for a period exceeding than six months after initial onset of illness. It is prudent to follow the patients with PSAGN until the proteinuria normalizes and microhematuria has disappeared in the urinalysis.

Nephrotic Syndrome

Nephrotic syndrome is primarily a pediatric disorder and is 15 times more common in children than adults. The incidence is 2-3/100,000 children per year, and the vast majority of affected children will have steroid sensitive with minimal change disease. The characteristic features of nephritic syndrome are heavy proteinuria (> 40 mg/m2_{/hour in children),}

hypoalbuminemia (< 2.5 g/dL), edema, and hyperlipidemia.

Most children (90 %) with nephrotic syndrome have a form of the idiopathic nephritic syndrome. The causes of idiopathic nephritic syndrome include minimal change disease (85%), mesangial proliferation (5%), and focal segmental glomerulosclerosis (10%). The

Lecture 6:

Common Kidney Diseases in Children

(Acute Poststreptococcal Glomerulonephritis and

remaining 10% of children with nephrotic syndrome have secondary nephritic syndrome related to glomerular diseases such as membranous nephropathy or membranoproliferative glomerulonephritis.

The underlying abnormality in nephritic syndrome is an increase permeability of the glomerular capillary wall, which leads to massive proteinurioa and hypoalbuminemia. The cause of the increase permeability is not yet fully understood.

Although the mechanism of edema formation in nephrotic syndrome is incompletely understood, it seems likely that, in most instances, urinary protein loss lead to hypoalbuminemia, which lead to decrease in the plasma oncotic pressure and transudation of fluid from the intravascular compartment to the interstitial space.

The diagnoses of nephrotic syndrome based on clinical manifestation that usually present with edema which initially noted around the eyes and in the lower extremities. With the time, the edema became generalized with the development of ascites, pleural effusions, and genital edema. Anorexia, irritability, abdominal pain, and diarrhea are common; hypertension and gross hematuria are uncommon.

The urinalysis reveals 3+ or 4+ proteinuria; microscpic hematuria may be present in 20% of children. Urinary protein exceeds > 40 mg/m2_{/hour in children. The serum albumin}

level is generally less than 2.5 g/dL and the serum cholesterol and triglyceride levels are elevated. C3 and C4 levels are normal.

Treatment of children with the first episode of nephrotic syndrome and mild to moderate edema may be managed as outpatient. Children with onset of nephrotic syndrome between 1 and 8 year of age are likely to have steroid responsive minimal change disease; therefore, steroid therapy may be initiated without renal biopsy. The majority of children with steroid-responsive nephritic syndrome have repeated relapses, which generally decreased in frequency as the child grows older.

SGD 6

Common Kidney Diseases in Children Trigger Case 1

Three years old boy was admitted to the outpatient clinic with swollen on both eyelids and followed on both legs. No symptom like this previously. Urination was decreased with cloudy yellow color since swelling was begun. Make the diagnosis, treatment and education for this patient.

Learning Task:

1. What are the diagnosis and differential diagnosis for this case? 2. Explain the characteristic features of Nephrotic syndrome? 3. Explain edema mechanism for this case?

4. Describe the laboratory investigation to diagnosed Nephrotic Syndrome? 5. Explain techniques of proteinuria examination

6. Provide initial management of nephrotic syndrome 7. Comprehend the complication of nephrotic syndrome Trigger Case 2

A 12-year-old female present with three days history of the red urine and puffiness of her face. The patient was having fever and sore throat in previous 2 week. Examination reveals minimal puffiness with pitting edema of the lower limbs. Her blood pressure is140/100 mmHg with pulse 88 bpm. Chest, cardiovascular and abdominal examination are normal.

1. Diagnosis and differential diagnosis for this case? 2. Describe characteristic features of PSAGN

3. Describe the laboratory investigation to diagnose PSAGN

4. Explain the mechanism of hypertension in PSAGN and it complication? 5. Provide initial management for this case

6. List the complication of PSAGN

Urinary tract infection (UTI):a documented episode of significant bacteriuria (i.e. an infection with a colony count of > 100,000 organisms per ml) that may affect the upper urinary tract (pyelonephritis, renal abscess) or lower urinary tract (cystitis), or both. UTI is a very common condition in general practice (usually E. coli). Ascending infection (most UTI) is caused in this way (bacteria from gastrointestinal tract colonize lower urinary tract). Haematogenous spread is an infrequent cause of UTI (seen in intravenous drug users, bacterial endocarditis and tuberculosis).

Clinical features of Upper urinary tract infection are fever, rigors/chill, flank pain, malaise, anorexia, costovertebral angle and abdominal tenderness; and lower urinary tract infection are dysuria, frequency, urgency, suprapubic pain, haematuria, scrotal pain (epididymo-orchitis) or perineal pain (prostates).

Principles of management are to treat the infection with an appropriate antibiotic based on urine culture results and deal with any underlying cause (e.g. relieve obstruction). High fluid intake should be encouraged and potassium citrate may relieve dysuria. Upper-tract UTIs, epididymo-orchitis and prostatitis require intravenous antibiotic therapy. Agents commonly used: gentamicin, cephalosporin or co-trimoxazole. Cystitis and uncomplicated lower UTIs can be managed with oral antibiotics. Agents commonly used are trimethroprim, ampicillin, nitrofurantoin, and cephalosporin. An abscess will require drainage either radiologically or surgically. If there is a poor response to treatment, consider unusual urinary infections: tuberculosis (sterile pyuria), candiduria, schistosomiasis, C. trachomatis, N. gonorrhoeae.

The complications of urinary tract infection are bacteraemia and septic shock, chronic and xanthogranulomatous pyelonephritis, renal and perinephric abscesses.

Learning task 7 Case 1

Seventy years old man referred from primary health care with recurrent lower urinary tract symptoms (LUTS) since 5 years. He had history of antibiotic treatment, and passed urethral stone 10 years ago. Urinalysis revealed Leucocyturia, erythrocyturia, and bacteriuria.

Task

Lecture 7:

Urinary Tract Infection:

Uncomplicated and Complicated

If you a doctor in small city (in Indonesia, type B hospital) and not so far from top referral hospital (type A Hospital):

1. What is the need to be complete diagnosed? 2. What is the proper medical treatment

3. When should you refer the patient to referred hospital (type A hospital)? Case 2

A 40 years-old man has been suffering current lower abdominal pain during urination since 1 year. Cloudy urine and sometime the urine colours were red. On digital rectal examination (DRE) do not fine any pathology. The result of laboratory test are: BUN and SC in normal limit (10.0 mg%, and 0.5 mg%), urinalysis revealed erythrocyturia, leucocyturia, and bacteriuria with significant urine culture (E. Coli count 100, 000 cfu/ml). Plain abdominal photo (BNO/BOF) result saw radio opaque picture 20 mm in size at pelvic cavity.

1. What is possible diagnosis?

2. Give some example treatment, if you are a doctor in primary health care practice! 3. What are possible treatments to do at referred hospital?

Urolithiasis is a frequent clinical problem. The calculi may be form at any level in the urinary tract, can be bilateral, but frequently unilateral. The favored sites for their formation are within the renal calyces and pelvis, and in the bladder.

There are four main types of calculi: (1) Calcium containing calculi, (2) Struvite calculi, (3) Uric acid stone, and (4) Cystine stone. An organic matrix of mucoprotein is present in all calculi.

Although there are many causes for initiation and propagation of stone, the most important determinant is an increased urinary concentration of the stone constituents, such that it exceeds their solubility in urine (supersaturation). A low urine volume in some metabolically normal patients may also favor supersaturation.

Clinical features of urolithiasis: calyceal stones may be asymptomatic; staghorn calculi present with loin pain and upper tract UTI; ureteric colic: severe colicky pain radiating from the loin to title groin and into the testes or labia associated with gross or microscopic haematuria; bladder calculi present with sudden interruption of urinary stream, perineal pain and pain at the tip of the penis. The management including pain relief for ureteric colic; pethidine, Voltarol, high fluid intake, 80% of ureteric stones pass spontaneously: stones < 4 mm in diameter almost always pass; stones > 6 mm almost never. Indications for intervention: kidney stones: symptomatic, obstruction, staghorn; ureteric stones: failure to pass, large stone, obstruction, infection; bladder: all stones.

Learning Task 8

Lecture 8:

Case 1

A 50 years-old woman has been getting colicky pain since 2 hours. On the physical examination he has right flank mass and pain full during palpation and percussion. Leucocyturia, erythrocyturia and bacteriuria in urin analysis.

Learning Task

If you a doctor in small city (in Indonesia, type B hospital) and not so far from general hospital (type A hospital):

1. What are differential diagnoses of this case?

2. Whatare the radiologic examination need to definitive diagnose? 3. Whatare the initial management of this case?

4. When are you going to referral a patient to referred hospital (RS type A)? Case 2

Forty years old man referred from primary health care with lower urinary tract symptoms (LUTS) since 5 years. He had history of antibiotic treatment, and passed urethral stone 10 years ago. Urinalysis revealed leucocyturia, erythrocyturia and bacteriuria.

Learning Task

If you a doctor in small city (in Indonesia, type B hospital) and not so far from general hospital (type A hospital):

1. What are differential diagnoses of this case?

2. Whatare the radiologic examination need to definitive diagnose? 3. Whatare the initial management of this case?

4. When are you going to referral a patient to referred hospital (RS type A)? Case 3

Twenty years old man referred from primary health care with lower urinary tract symptoms (LUTS) since 2 years. He had history straddle/saddle injury 3 years ago.

Learning Task

If you a doctor in small (in Indonesia, type B hospital) and not so far from general hospital (type A hospital):

1. What are differential diagnoses of this case?

2. Whatare the radiologic examination need to definitive diagnose?

3. When are you going to referral a patient to referred hospital (RS type A)?

Because of the diverse connotations of the term, it is necessary to define BPH as microscopic BPH, macroscopic BPH, or clinical BPH. Microscopic BPH represents histologic evidence of cellular proliferation of the prostate. Macroscopic BPH refers to enlargement of the prostate resulting from microscopic BPH. Clinical BPH represents the LUTS, bladder dysfunction, hematuria, and urinary tract infection (UTI) resulting from macroscopic BPH. Abrams (1994) has suggested using the more clinically descriptive terms benign prostatic enlargement (BPE), BOO, and LUTS to replace BPH.

Lecture 9:

Common Neoplasm in Urinary System: Renal

tumors, bladder tumors.

The histologic diagnosis of prostate cancer is made, in the majority of cases, by prostate needle biopsy. Prostate cancer rarely causes symptoms until it is advanced. Thus, suspicion of prostate cancer resulting in a recommendation for pros-tatic biopsy is most often raised by abnormalities found on digital rectal examination (DRE) or by serum prostate-specific antigen (PSA) elevations. Although there is controversy regarding the benefits of early diagnosis, it has been demonstrated that an early diagnosis of prostate cancer is best achieved using a combination of DRE and PSA. Transrectal ultrasound (TRUS)-guided, systematic needle biopsy is the most reliable method, at present, to ensure accurate sampling of prostatic tissue in men considered at high risk for harboring prostatic cancer on the basis of DRE and PSA findings.

Both benign and malignant tumors occur in the kidney. The benign tumors rarely cause clinical problems while malignant tumors are of great importance clinically and deserve considerable emphasis.

The common malignant tumors of the kidney are Renal Cell Carcinoma (RCC), Wilm tumor and urothelial carcinoma of renal pelvis. RCC occurs most often in older individual, usually in the sixth and seventh decade of life. Morphologically, RCC is divided into four major types, i.e. clear cell carcinoma, papillary carcinoma, chromophobe renal carcinoma and Bellini duct carcinoma. Wilmtumor usually occur in children. Urothelial carcinoma originates from urothelium of the pelvis, and it often clinically apparent within a relatively short time because they lie between the pelvis and by fragmentation produce noticeable hematuria

Learning Task 9 Case 1

Seventy years old man was referred from primary health care with left flank mass since 2 years. He had no history of haematuria, and febrile. Urinalysis revealed leucocyturia, erythrocyturia and bacteriuria.

Learning Task

If you a doctor in small (in Indonesia, type B hospital) and not so far from general hospital (type A hospital):

1. What are differential diagnoses of this case?

2. Whatare the radiologic examination need to definitive diagnose?

3. When are you going to referral a patient to referred hospital (RS type A)? Case 2

Seven years old boy was reffered from primary health care with left flank mass since 1 year. He had no history haematuria, and febrile. Urinalysis revealed leucocyturia, erythrocyturia and bacteriuria.

Learning Task

If you a doctor in small (in Indonesia, type B hospital) and not so far from general hospital (type A hospital):

1. What are differential diagnoses of this case?

2. Whatare the radiologic examination need to definitive diagnose?

3. When are you going to referral a patient to referred hospital (RS type A)? Case 3

Sixty years old man was referred from primary health care with painless gross haematuria since 2 years. He had history of antibiotic treatment, and did not found any stone on plain abdominal X ray and ultrasound examination.

Learning Task

If you a doctor in small (in Indonesia, type B hospital) and not so far from general hospital (type A hospital):

1. What are differential diagnoses of this case?

2. Whatare the radiologic examination need to definitive diagnose?

3. When are you going to referral a patient to referred hospital (RS type A)?

Of all injuries to the genitourinary system, injuries to the kidney from external trauma are the most common. It is essential to obtain as many details of the injury as possible; for example, depending on whether the cause is blunt or penetrating trauma, the approach to evaluation and management is quite different.

Blunt renal injuries most often come from motor vehicle accidents, falls from heights, and assaults. Perhaps the most important information to obtain in the history of the injury is the extent of deceleration involved. Rapid deceleration can cause vascular damage to the renal vessels, resulting in renal artery thrombosis, renal vein disruption, or renal pedicle avulsion. In high-velocity-impact trauma, multiple-organ injury is likely to be associated.

Penetrating renal injuries most often come from gunshot and stab wounds. The gunshot to the upper abdomen or lower chest should alert the physician to renal injury; of all patients sustaining renal trauma in a large reported series, renal gunshot wounds occurred in approximately 4.0% (McAninch et al, 1993 ). Important factors in assessing a gunshot wound initially are weapon characteristics and bullet ballistics.

Ureteral injuries after external violence are rare, occurring in less than 4% of cases of penetrating trauma and less than 1% of cases of blunt trauma. During wartime in the past century, 3% to 15% of urologic injuries have involved the ureter, with an average of 5% over reports from World War II up to modern conflicts. In the nonmilitary setting, a similar incidence of ureteral injuries is caused by civilian gunshot injuries. These patients often have significant associated injuries and a devastating degree of mortality that approaches one third. Associated visceral injury is common, predominantly small (39% to 65%) and large (28% to 33%) bowel perforation. Significant percentages (10% to 28%) of patients with ureteral injuries also have associated renal injuries. A smaller percentage (5%) has associated bladder injuries.

Ureteral injuries can occur after a multitude of surgical procedures but largely result from surgeries in the pelvis (such as hysterectomy) and retroperitoneum (such as major vascular replacement). One report, which reviewed 13 previously published studies, concluded that hysterectomy was responsible for the majority (54%) of surgical ureteral injuries. Next most common was colorectal surgery (14%), followed by pelvic surgery such as ovarian tumor removal and transabdominal urethropexy (8%), and followed lastly by abdominal vascular surgery (6%). One series reported that repeat cesarean section can also result in a large number of ureteral injuries, in this case up to 23% of the reported ureteral injuries at one hospital (Ghali et al, 1999 ). The total incidence of ureteral injury after gynecologic surgery is reported to be between 0.5% and 1.5%, and after abdominoperineal colon resection it ranges from 0.3% to 5.7%. Open urologic procedures, because they often occur in proximity to the ureters, were also responsible for a significant number (21%) of reported ureteral injuries in one series.

Lecture 10:

Urinary tract trauma

The urinary bladder is generally protected from external trauma because of its deep location in the bony pelvis. Most blunt bladder injuries are the result of rapid-deceleration motor vehicle crashes, but they also occur with falls, crush injuries, assault, and blows to the lower abdomen. Whereas disruption of the bony pelvis tends to tear the bladder at its fascial attachments, bone fragments can also directly lacerate the organ. Bladder laceration may also arise from penetrating trauma or various iatrogenic surgical complications and may occur spontaneously in patients with altered sensorium, such as those who are intoxicated or have neuropathic disease.

Learning task 11 Case 1

Twenty years old man reffered from primary health care with gross haematuria and history of fall from manggo tree 5 meters in high, 4 hours before hospitalize. Bruise and palpable pain on left side flank.

Learning Task

If you a doctor in small (in Indonesia, type B hospital) and not so far from general hospital (type A hospital)

1. What are differential diagnoses of this case?

2. What are the radiologic examinations need to definitive diagnose? 3. What is the initial management of this case?

4. When are you going to referral a patient to referred hospital (RS type A)? Case 2

A 22 years-old man has been suffering from urethral bloody discharge and pain on lower abdominal region since he had motor cycle accident 5 hours ago. On physical examination found that he has bruising and mass lower abdominal region area.

Learning Task

If you a doctor in small (in Indonesia, type B hospital) and not so far from general hospital (type A hospital)What are differential diagnosis of this case?

5. What are the radiologic examinations need to definitive diagnose? 6. What is the initial management of this case?

7. When are you going to referral a patient to referred hospital (RS type A)?

The syndrome of acute renal failure (ARF) is defined as a reduction of glomerular filtration rate (GFR) that is often reversible. The syndrome may occur in three clinical settings: (1) as an adaptive response to severe volume depletion and hypotensiuon with structurally ang functionally intact nephrons, (2) in response to cytotoxic insults to the kidney when both renal structure and function are abnormal, and (3) when the passage of urine is blocked. Thus ARF may be classified as prerenal, intrinsic, or postrenal.

Chronic kidney disease (CKD) is characterized by a progressive course with ongoing loss of kidney function. Once the glomerulous filtration rate (GFR) falls below about half of normal, kidney function tends to decline even if the initial insult of kidney has been

Lecture 11 & 12:

eliminated. This phenomenon has been defined as progression of CKD and typically moves through phases from initial diminution of renal reserve to mild, moderate, and severe reduction of GFR, then kidney failure ultimately requiring renal replacement therapy (end stage renal disease).

Learning Task 11 Case 1

36 year old man is admitted for an increased serum creatinine level. He has been taking intravenous antibiotics at home for the past 2 weeks for osteomyelitis caused by Staphylococcus aureus. He reports no change in his urine output. On physical examination, his blood pressure was 124/76 mmHg and his pulse was 82 beats per minute while he was supine and 126/74 mmHg 86 beats per minute while he was standing. He has a diffuse red maculopapular rash on his trunk and limbs. The remainder of the examination is normal. His serum creatinine level is 2,4 mg/dl today and it was 1,0 mg/dl a week ago. Other blood laboratory findings include the following: WBC count 11.000/ml; sodium 142 mmol/L; potassium 4,2 mmol/L; and blood urea nitrogen 34 mg/dl. His urine showed a sodium level of 54 mmol/L and creatinine level of 39 mg/dl. The urinalysis with dipstick testing showed +1 protein; the microscopic analysis showed 5-10 leucocytes/HPF(high power field). And an occasional leucocytes cast. Kidney ultrasound showed no hydronephrosis.

Learning Task

1. What is the most likely diagnosis for this patient’s AKI? Give your reason! a. AKI (acute kidney injury) as a result of acute interstitial nephritis b. Chronic kidney diseases as a result of diabetes

c. AKI as a result of acute tubular necrosis (ATN) d. AKI as a result of prostate diseases

Explain your answer! What kind of abnormality findings was found in the patient supports your conclusion?

2. Explain the pathophysiology!

3. Explain the management for this patient! Case 2

79 year old white man comes to emergency unit with the symptom: not being able to urinate this day. He recently saw his primary care physician for an upper respiratory infection, and began taking diphenhydramine (anti-histamine) for relief the nasal congestion. He reports a history that is significant for benign prostatic hyperplasia (BPH) and hypertension. A Foley catheter was placed, with the return of 1200 ml of urine. Urinalysis was within normal limit. His blood urea nitrogen (BUN) level was 21 mg/dl and his creatinine level was 1,5 mg/dl (base line creatinine level, 1.0 mg/dl).

Learning Task

1. What is the most likely diagnosis for this patient? a. Pre renal as a result of hypovolemia b. Intra renal as a result of ATN

c. Intra renal as a result of acute interstitial nephritis d. Post renal as a result of obstruction

Explain your answer! What kind of abnormality findings was found in the patient supports your conclusion?

2. Explain the pathophysiology!

Learning task 12 Trigger Case

A 63-year-old African-American woman with type 2 diabetes mellitus and hypertension for last 17 years is seen in the clinic for worsening feet edema. Her history reveals that she underwent laser surgery for diabetic retinopathy. Her medications include metoprolol (50 mg twice daily), hydrochlorothiazide (25 mg daily), and insulin. On physical examination her blood pressure is 148/88 mmHg, and pulse rate is 85 beats/min. She has (+) 2 pedal edema. Laboratory tests show a serum creatinine level of 0,7 mg/dl and BUN level of 32 mg/dl. The glycosylated hemoglobin level is 7,5 %. Urine testing shows +4 proteins by dipstick.

Learning Task

1. Describe the classification of chronic kidney disease! 2. Which of the following statements is true?

a. This patient does not have CKD (chronic kidney disease) b. This patient has stage 1 CKD

c. This patient has stage 2 CKD d. This patient has stage 3 CKD

Explain your answer! What kind of abnormality findings was found in the patient that supports your conclusion?

3. Explain the pathophysiology!

4. Which of the following facilitatorstors is not likely to increase the progression of CKD for this patient?

a. Female gender b. (+) 4 proteinuria

c. Blood pressure of 144/88 mmHg

d. Glycosylated hemoglobin level of 7.5 %. Explain your answer!

5. Describe the management of chronic kidney disease according to the class/stage! 6. Explain the rational management for the patient above!

Renovascular hypertension is the most common cause of secondary hypertension in the United States. Renovascular hypertension is an elevation of blood pressure due to activation of the renin-angiotensin system in the setting of renal artery occlusive diseases. The diagnosis of renovascular hypertension can be made only if blood pressure improves following intervention, thereby making renovascular hypertension a retrospective diagnosis. The presence of anatomic renal artery stenosis is not synonymous with renovascular hypertension. Progressive and occlusive renovascular disease may lead to impaired kidney function, termed “ischemic nephropathy”.

Learning Task 13:

1. Describe the pathophysiology of Renovascular hypertension 2. Explain the type of endocrine hypertension

3. Describe the principle management for the patient with secondary hypertension

Lecture 13:

Renal Hypertension

Kidney performs a number of essential functions in the body including clearance of waste product, drug or other substances, control of volume status, maintenance of electrolyte and acid base balance. Renal impairment (disorders) frequently alters the pharmacokinetic and pharmacodynamic of certain drugs. Absorption, bioavailability, protein binding, distribution volume and clearance (metabolism) of several drugs can be affected, as well as pharmacodynamic processes. Alterations in pharmacokinetic and pharmacodynamic of drugs in renal disorders (diseases) potentially cause increased risk of adverse drug reaction. In addition, multiple medical problems in patient with kidney disease frequently result in polypharmacy and consequently increased drug interaction.

Careful attention should also be taken for drug use in renal disease. Many drugs potentially cause drug-induced renal disease, thus their uses in renal impairment should be avoided or the dosage should be adjusted. Drug-induced renal disease may result from immunological or non immunological process, and may affect pre renal, renal or post renal. Dosage adjustment in renal disorders commonly required for drugs which eliminated mainly by renal excretion or drugs with narrow safety margin.

Diuretic is group of drugs that increase the secretion of urine (water, electrolytes and waste products) by the kidney. Diuretics inhibit renal sodium reabsorption by several mechanisms. Each type of diuretic acts upon a single anatomic segment of the nephron, which has a distinctive transport function. There are several types of diuretics available recently, carbonic anhydrase inhibitors, loop diuretics, thiazides, potassium sparing diuretics, and osmotic diuretics.

Urinary antiseptics are oral drugs that are rapidly excreted into the urine and act there to suppress bacteriuria. Types of urinary antiseptic available are nitrofurantoin, nalidixic acid and methenamine.

SELF-DIRECTED LEARNING Basic knowledge must be known:

1. The role of kidney on drug disposition

2. The pharmacokinetic and pharmacodynamic changes of drugs in renal disorders 3. Types of drug-induced renal disease and the pathophysiological mechanism 4. Drug dosage adjustment in renal disorders

5. Mechanism of action, clinical indication, adverse effects of several types of diuretics 6. Types of urinary antiseptics, the mechanism of action and adverse effects

Learning Task 14 SCENARIO 1

A 38 years old man was admitted to emergency unit due to bloody urine and flank pain since last week. Patient had history of hypertension since 4 years. Physical examination revealed BP=180/100 mmHg, edema (+) in both lower extremities, anemia (+), t =38˚C. Laboratory result revealed WBC= 13.0; Hb= 8.5; BUN= 201; SC= 16.4. Doctor decided to give several drugs to manage patient’s disease. One of the medications planned to be given was antibiotic.

Lecture 14:

Drug use in renal disorders

Diuretics

TASK 1

1. From the scenario above, what is the most appropriate antibiotic for this patient? Explain the reason.

2. What are the principal factors should be considered before giving antibiotic treatment for patient with chronic kidney disease?

3. If patient required any analgesic medication, what analgesic would be the safest one? 4. Mention types of antibiotic and analgesic that potentially induced renal injury/disease

and the type of renal injury/disease might be resulted from it.

5. Mention the basic concepts of drug dosage adjustment in chronic kidney disease SCENARIO 2

A 40 years old man was admitted to emergency unit due to swelling on both legs since 2 weeks before. After complete physical and laboratory examination patient was diagnosed as having chronic kidney disease. Doctor decided to give furosemide for relieving the oedema. After several days of furosemide treatment, patient was suffered from hypokalemia.

TASK 2

1. How does furosemide exert its action?

2. When used chronically, what adverse effects would possibly occur?

3. How was the possible mechanism of hypokalemia result from furosemide treatment? 4. What is the effect of concurrent NSAID treatment in patient receiving furosemide?

Disorder of male genital system include penis (malformation, inflammation, neoplasm), scrotum, testis (cryptorchidism, inflammation, neoplasma), epididymis, prostate (prostatitis, BPH, carcinoma) and sexual transmitted diseases.

Malformations of the penis are hypospadia, epispadia, priapism, peyronie disease. Hypospadia is more common than epispadia. These malformations may result in lower urinary tract problem and failure to impregnate women.

Inflammatory condition of the penis that unrelated to STDs is called balanitis and posthitis. In phimosis, where prepuce cannot be retracted, smegma is deposited between glans penis and prepuce. Therefore most cases of phimosis accompanied by balanoosthitis. When phimosis is forcibly retracted it may result in paraphimosis. In this condition, the circulation to the glans penis may be strangulated by the stenotic prepuce. This may cause congestion, swelling and pain. In severe case, urinary retention may occur.

Carcinoma of the penis is the most neoplasm occurs in the penis. Some predisposition factors are pimosis, BXO and chronic irritation. It is believed that smegma and infection of HPV (type 16 & 18) have an important role in the occurrence of carcinoma of the penis. Microscopically carcinoma of the penis is squamous cell carcinoma.

Learning Task 15

Man 68 years old come with lower abdominal pain and unable to void since one day ago. He suffered from Lower urinary tract symptoms since 6 months ago.

1. What is the possible diagnosis of this patient?

2. What are the anamnesis, signs, symptoms and examination to support the diagnosis? 3. What is your planning to complete the diagnosis?

4. What is your planning treatment of this patient?

Lecture 15&16

Learning Task 16

A 34- years- old man, came with complaint of unable to void since 2 days ago. He also complains of weak urinary flow and terminal dribbling since last 2 months. He had history of urethral discharge due to sexual transmitted diseases. No complaint on erectile capability. He has a good general condition, composmentis, normal blood pressure 120/80, pulse 88x/minutes, uncircumcised, narrow MUE. Normal scrotal finding, right testicle normal. Questions:

1. What is the possible diagnosis of this patient?

2. What are the anamnesis, signs, symptoms and examination to support the diagnosis? 3. What is your planning to complete the diagnosis?

4. What is your planning treatment of this patient? Questions:

5. What is the most possible diagnose of your patients?

6. If you are in doubt, the best diagnostic tool that you propose? 7. What is the treatment of your patient?

SELF ASSESSMENT SELF ASSESSMENT 1

(Macroscopic structure of the Urinary system) 1. Drawing and describe the topography of kidneys 2. Drawing and describe the vascularisations of kidneys 3. Drawing and describe the innervations of kidneys 4. Drawing the profile of uriniferous tubules

5. Drawing the anatomical structure of urinary tract

6. Drawing the vasculature and innervations of urinary tract SELF ASSESSMENT 2

(Microscopic structure of the urinary system)

1. Explain the kidney disorders in relation with it’s microscopic structure! 2. How is the relation between Bowman’s capsule and glomerulus? 3. Differentiate afferent and efferent glomerular arteriole!

4. Explain the epithelium of proximal tubule, Henle’s loop, and distal tubule! 5. What is filtration barrier in renal corpuscle!

6. Explain about podocyte, mesangial cells and its function!

7. Explain about two types of nephron and cell types composing the thin limbs of Henle’s loop?

8. Explain three regions of collecting tubules! 9. What is renal interstitium?

10. Explain the urinary tract disorders in relation with it’s microscopic structure!

11. The structure that separates transitional epithelial from underlying lamina propria is…. 12. The structure of fibrous outer coat of ureter at its proximal and distal terminal is… 13. The function of plaque regions of the transitional epithelial cell plasmalemma is….. 14. What is the microscopic structure of the triangular region of the bladder?

15. Explain the two layers of lamina propria of the bladder! 16. What is gland of Littre?

SELF ASSESSMENT 3

1. Explain the pressures that involved in filtration process 2. Describe the myogenic response in autoregulation of GFR

3. Describe the tubulo-glomerular feedback in autoregulation of GFR 4. Describe the hormonal and autonomic nerve factor in autoregulation

5. Describe the process of water, electrolyte and other solute along the proximal, loop of Henle, distal and collective tubules of nephrons

6. Describe the rule of muscles of ureter in urine flow

7. Describe the rule of muscles of bladder and sphincter internal and external of urethrae

8. Describe the nerve that involved in micturition process

9. Describe the counter-current concept in relation to maintain the difference of tissues osmolarity between cortex and medulla of kidneys

10. Explain the rule of anti diuretic hormone (ADH) in kidneys to maintain the body fluid balance

11. Explain the aldosterone hormone to maintain the electrolytes balance

12. Explain the mechanism of water and electrolytes excretion that influenced by diuretic drug

13. Describe the mechanism for producing concentrated and dilute urine excretion 14. Describe what is the meaning of acidosis condition and alkalosis condition 15. Describe the buffers and their function in the body

16. Describe the renal correction in acidosis and alkalosis condition SELF ASSESSMENT 5

(Pathogenesis of the glomerular and tubulointerstitial injury) State whether the statement is true or false!

1. Goodpasture syndrome is characterized by membranous glomerulonephritis induced by circulating antigen-antibody complex deposition within glomeruli.

2. Glomerular disease associated with immune response to streptococcal infection is commonly showed acute diffuse glomerulonephritis.

3. Podocytes alteration in minimal change disease can be detected by histomorphology examination.

4. The distribution of tubular necrosis in ischemic ATN and nephrotoxic ATN is similar. 5. Acute hypersensitivity nephritis induced by methicillin usually associated by subtle

and cumulative injury to tubules. SELF ASSESSMENT 6

Common kidney diseases in children 1. Assessment for proteinuria

2. Describe the term of remission, relapse, steroid dependent and steroid resistant in nephrotic syndrome

3. What is the most form of Nephrotic syndrome in children?

4. Explain the monitoring for the hospitalized patient with Nephrotic Syndrome?

5. Is it possible to give furosemide for edema in Nephrotic Syndrome? Explain your answer.

6. Explain the time and percentage of response for steroid therapy in Nephrotic Syndrome?

7. Describe differentiation of glomerular and extra glomerular hematuria. 8. List the source of infection and bacterial strain in PSAGN

9. Pathophysiology of APSGN 10. Monitoring for inpatient PSAGN 11. Follow up for outpatient PSAGN 12. Clinical and laboratory evaluation

13. When is the symptom and laboratory resolves 14. Prognosis of PSAGN?

 Tindakan asepsis & drapping duk steril berlubang

 Tindakan Anestesi

 Membuka preputium perlahan-lahan dan bersihkan penis dari smegma menggunakan kasa betadin sampai corona glandis terlihat

 Kembalikan preputium pada posisi semula

 Klem preputium pada jam 11, 1 dan jam 6

 Gunting preputium pada jam 12 sampai corona gland

 Lakukan jahit kendali mukosa – kulit pada jam 12

 Gunting preputium secara melingkar kanan dan kiri dengan menyisakan frenulum pada klem jam 6

 Observasi perdarahan (bila ada perdarahan, klem arteri/vena, ligasi dengan jahitan melingkar)

 Jahit angka 8 pada frenulum.

 Lakukan pemotongan frenulum di distal jahitan

 Kontrol luka dan jahitan, oleskan salep antibiotik di sekeliling luka jahitan

 Balut luka dengan kasa steril

 Buka duk dan handscoen, cek alat dan rapikan kembali semua peralatan

 Pemberian obat dan edukasi pasien

~ CURRICULUM MAP ~

Smstr

Program or curriculum blocks

10 Senior Clerkship

9 Senior Clerkship

8 Senior clerkship

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) 1 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)

REFERENCES

1. Moore KL, Agur AMR: Essential Clinical Anatomy, 2 nd _{ed. Philadelphia, Lippincott} Williams & Wilkins, 2002.

2. Gartner LP, Hiatt JL. Color Textbook of Histology, International edition. Elsevier. 2007 3. Fawcett DW, Jenish RP : Bloom and Fawcett’s Concise Histology, 2nd ed. London,

Arnold, 2002.

4. Guyton A. C and Jhon E. Hall: Textbook of Medical Physiology, 10th _{ed. Philadelpia,} WB Saunders Company, 2000

5. Silverthorn DU. Human Physiology an integrated approach, 2nd _{edition, Prentice Hall.} 2001

6. Mitchell RN, Kumar V, Abbas K, Fausto N. Robbins & Cotran, Pathologic Basis of Disease, 8th _{edition. New York. , W.B. Sounders Company, 2010}

7. Fischbach FT, Dunning MB: A Manual of Laboratory and Diagnostic Tests, 7th _ed. Philadelphia, Lippincott Williams & Wilkins, 2004.

8. Behrman RE, Kliegman RM, Jenson HB: Nelson Textbook of Pediatrics, 17th _{ed. New} York, W.B. Sounders Company, 2004

9. Macfarlane MT, et al. : Urology, 4th _{ed. Lippincott Williams & Wilkins, 2006}

10. Friedman AL. Nephrology: Fluids and electrolytes. In: Behrman RE, Kliegman RM, editors. Nelson Essentials of pediatrics. 4th edition. Philadelphia: WB Saunders Co, 2001.

11. Davis ID, Avner ED. Nephrology. In: Behrman RE, Kliegman RM, Jenson HB, editors. Nelson textbook of pediatrics. 17th edition Philadelphia: WB Saunders Co, 2004. 12. Smiths general Urology, 17th ed, 2008

INTRODUCTION

The curriculum block on Urinary System and Disorder is developed collectively by the academic staff from various departments: Anatomy, Histology, Physiology, Pharmacology, Pathology, Clinical Pathology, Nephrology, Urology, and Pediatric.

The number of Urinary System credits is three. This book consists of general information on the learning schedule, block members, facilitatorsilitators, and the core curriculum, such as learning outcomes, learning situation, learning task and self-evaluation.

Lecture is only given to emphasize crucial things or objectives of material and to guide the students before discussion. During discussion, students also have to evaluate their learning progress independently (self evaluation). For difficult concepts in discussion and self evaluation, the students are also being asked to discuss several example of scenario. More than half of the learning material should be learned independently and in small group discussion.

Curriculum content, study load and teaching-learning are specified in curriculum and study guide, student assessment is carried out mainly by objective test at the end of theme course, and the minimum passing level is set at 70 (70%). A remedial is provided for those who failed, and later they have to re-sit a second summative test.

Since the integrated curriculum at Facilitatorsulty of Medicine Udayana University is still in progress, this guide book will also still have some changes in the future. Regarding that, we invite readers to give any positive comments for its development.

Planners

Udayana University Faculty of Medicine, DME 54 | P a g e

CONTENTS

Introduction ………..………. i

Table of contents ……….. ………. ii

Curriculum Block Urinary System and Disorders………...……… 1

Planners Team ………..………...2

Lecturers ……….………... 2

Facilitators ………... ………….. 3

Time Table Regular Class ……….………..…… 4

Time Table English Class ……….………..……. 8

Student Project ……….. 12

Assessment Method ……….13

Learning Program ………..…………..….. 14

1. Abstract and Learning task of Lectures ……… 14

2. Self assessment ………...………. 32

Basic Clinical Skills ……….. . 36

Curriculum Mapping ………..……….. 50

Block Mapping ……….. 51

Reference ………..……..52

Udayana University Faculty of Medicine, DME 55 | P a g e