Study Guide Blok Urinary Semester VI tayang 17 Mei 2016

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~ 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 urogenital 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 systemdisorders:

1. Diagnose and manage independentlyuncomplicated urinary tract infection, phymosis and paraphymosis

2. Diagnose and manage independentlyphymosis and paraphymosis.

3. Diagnose, give initial treatment, and refer some urogenital systemdisorders such as glomerulonephritis, renal colic, acute kidney injury including acute tubular necrosis, chronic kidney disease, prostatitis, priapismusand, torsio testis.

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, epispadia, varicocele, hydrocele, retractile testis, cryptorchidism, spermatocele, epydidimitis, and common testicular tumor (seminoma and teratoma).

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 urogenitalsystem disorders 3. Symptom and sign of urogenitalsystem disorders

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

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

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

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~ PLANNERS TEAM ~

NO NAME DEPARTMENT

1 Dr. dr. A A Gde Oka, Sp.U _{(Coordinator)} Urology

2 dr. I Wayan Juli Sumadi, Sp.PA _(Secretary) Pathology Anatomy

3 Prof. dr. K. Tirtayasa, MS, AIF Physiology 4 dr. I Wayan Sugiritama, M.Kes Histology 5 Prof. Dr. dr. Mangku Karmaya,M.Repro Anatomy 6 dr. Jodi Sidartha L, Sp.PD (KGH) Internal Medicine 7 dr. Dwi Fatmawati, Sp.MK, Ph.D 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. Ketut Suarta, Sp.A (K) _Pediatric

4 dr. G A P Nilawati, Sp.A (K) _Pediatric 5 Prof. Dr. dr. N. Mangku Karmaya,

M.Repro

Anatomy

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

7 dr. Jodhi Sidartha L, SpPD (KGH) Internal Medicine 8 dr. I Wayan Juli Sumadi, 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. dr. A A Wiradewi Lestari, Sp.PK Clinical Pathology 13 dr. Sri Laksminingsih, Sp.Rad Radiology 14 dr. Dwi Fatmawati, Sp.MK, Ph.D Microbiology 15 Dr. dr. I Wayan Sudhana, Sp.PD (KGH) Internal Medicine 16 Dr. dr. Yeni Kandarini, Sp.PD (KGH) Internal Medicine 17 Prof. Dr. dr. Raka Widiana, Sp.PD (KGH) Internal Medicine

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~ FACILITATORS ~

Regular Class (Class A)

No Name Group Departement Phone (2Venuerd floor)

1 dr. Ni Nyoman Metriani Nesa,

M.Sc., Sp.A A1

Pediatric 081337072141 2nd floor: R.2.09

2 dr. Yuliana, M.Biomed A2 Anatomy 085792652363 2nd floor:_R.2.10

3 dr. I Made Dharmadi , MPH A3 Public Health 08123804985 2nd floor:_R.2.11

4 dr. I Gusti Ayu Sri Darmayani,_Sp.OG A4 DME 081338644411 2nd floor:_R.2.12

5 dr. I G Kamasan Nyoman _{Arijana, M.Si, Med} A5 Histology 08124665966 2nd floor:_R.2.13

6 dr. I Nyoman Wiryawan, _Sp.JP A6 Cardiology 081289053234 2nd floor:_R.2.14

7 dr. I Wayan Gede _{Sutadarma, M Gizi} A7 Biochemistry 082144071268 2nd floor:_R.2.15

8 dr. I Gusti Ngurah _{Pramesemara , M.Biomed} A8 Andrology 081338605087 2nd floor:_R.2.16

9 Dr.dr. Ni Made Linawati, M.Si A9 Histology 081337222567 2nd floor:_R.2.23

10 Dr. dr. I Dewa Made _{Sukrama, MSi, Sp.MK(K)} A10 Microbiology 081338291965 3nd floor:_R.3.21

11

dr.A.A. Ayu Dwi Adelia Yasmin, M.Biomed, Sp.JP,FIHA

A11

Cardiology 087861402169 3nd floor: R.3.22

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English Class (Class B)

No Name Group Departement Phone Venue

(2rd_floor)

1 dr. I Made Oka Negara, FIAS B1 Andrology 085935054964 2nd floor:_R.2.09

2 dr. A.A. Gde Yuda Asmara, _Sp.OT B2 Orthopaedi 081337870347 2nd floor:_R.2.10

3 dr. Ida Ayu Dewi Wiryanthini, _{M Biomed} B3 Biochemistry 081239990399 2nd floor:_R.2.11

4 Dr.dr. Susy Purnawati, MKK B4 Fisiology 08123989891 2nd floor:_R.2.12

5 dr. Ketut Rai Purnami, Sp.PD B5 Interna 0818350703 2nd floor:_R.2.13

6 dr. Ni Nengah Dwi Fatmawati_{, Sp.MK, Ph.D} B6 Microbiology 087862200814 2nd floor:_R.2.14

7 Prof.Dr.dr.I Putu Gede _{Adiatmika, M.Kes} B7 Fisiology 08123811019 2nd floor:_R.2.15

8 dr. I Kadek Swastika , M Kes B8 Parasitology 08124649002 2nd floor:_R.2.16

9 Dr.dr. Anak Agung Wiradewi _{Lestari, Sp.PK} B9 _PathologyClinical 08155237937 2nd floor:_R.2.23

10 dr. I Nyoman Budi Hartawan,

M.Sc., Sp.A (K) B10

Pediatric 081353027973 3nd floor: R.3.21 11 dr. Made Agus Hendrayana ,_M.Ked B11 Microbiology 08123921590 3nd floor:_R.3.22

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TIME TABLE

CLASS A

DAY/DATE TIME ACTIVITY VENUE PIC

I

17-5-2016

08.00-09.00 Macroscopic Anatomy of The Urinary System and Male Genitalia

4.01 Mangku Karmaya

09.00-10.00 Practical Session (Anatomy): Group A1-A5

Anatomy Lab

Mangku Karmaya

10.00-10.30

Break

-

-10.30-12.00 SGD 1 Discussion

room Facilitators

12.30-13.00 Individual Learning -

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

Anatomy Lab

Mangku Karmaya

14.00-15.00 Plenary 4.01 Mangku

Karmaya II

18-5-2016

08.00-09.00 Microscopic Anatomy of The Urinary System

4.01 Sugiritama

09.00-10.00 Practical Session (Histology): Group A1-A5

Histology Lab

Sugiritama

10.00-10.30 Break -

room

Facilitators

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

Histology Lab

Sugiritama

14.00-15.00 Plenary 4.01 Sugiritama

III

19-5-2016

08.00-09.00 The function of the urinary system:

- Urine formation - Urine micturition

4.01 Tirtayasa

Room

Facilitators

12.00-13.00 Student Project -

-13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 Tirtayasa IV

20-5-2016

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

4.01 Tirtayasa

Room

Facilitators

-13.00-14.00 Break -

(6)

V

23-5-2016

08.00-09.00 Pathogenesis of Glomerular and Tubulointerstitial Injury

4.01 Winarti/Juli Sumadi

Room

Facilitators

-13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 Winarti/Juli Sumadi VI

24-5-2016

08.00-09.00 Urinary System Disorders in Children:

- Nephrotic syndrome - PSAGN

- UTI in Children

4.01 Suarta/Nilawati

Room

Facilitators

-13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 Suarta/Nilawati VII

25-5-2016

08.00-09.00 Uncomplicated and Complicated Urinary tract infection

4.01 I Wayan Sudana

Room

Facilitators

-13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 I Wayan Sudana VIII

26-5-2016

08.00-09.00 Urolithiasis (with and without colic)

4.01 AA Gde Oka

Room

Facilitators

-13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 AA Gde Oka

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

4.01 AA Gde Oka

27-5-2016

Room

Facilitators

-13.00-14.00 Break -

(7)

X

30-5-2016

08.00-09.00 Acute Kidney Injury 4.01 Yeni Kandarini

Room

Facilitators

12.00-13.00 Student Project Presentation 1 (Horse Shoe Kidney)

4.01 AA Gde Oka

13.00-15.00 Break -

-14.00-15.00 Plenary 4.01 Yeni Kandarini

XI

31-5-2016

08.00-09.00 Chronic Kidney Disease 4.01 Raka Widiana

Room

Facilitators

12.00-13.00 Student Project Presentation 2 (Symptomatic Polycystic Kidney)

4.01 Yeni Kandarini

13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 Raka Widiana XII

1-6-2016

08.00-09.00 Secondary hypertension 4.01 Jodi Sidharta L

Room

Facilitators

12.00-13.00 Student Project Presentation 3 (Hemodialysis)

4.01 Wayan Sudana

13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 Jodi Sidharta L XIII

2-6-2016

08.00-09.00 Diuretics and Urinary Antiseptic

4.01 Artini

Room

Facilitators

12.00-13.00 Common testicular disorders: Hydrocele, Varicocele, undencensus testis, torsio testis, tumor

4.01 G. Wirya K. Duarsa

13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 G. Wirya K. Duarsa, Artini XIV

3-6-2016

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

Room

Facilitators

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

(8)

13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 Artini

XV

6-6-2016

08.00-09.00 Common Prostate Disorders (Prostatitis, BPH, Prostate Cancer), Urethral Stricture and Hydronephrosis in children

Room

Facilitators

12.00-13.00 Student Project Presentation

5 (MicturatingCystigraphy) 4.01 G. Wirya K. Duarsa

13.00-14.00 Break -

-14.00-15.00 Plenary session 4.01 G. Wirya K. Duarsa XVI

7-6-2016

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

4.01 Raka Widiana

-10.00-11.00 Urethral catheterization, Clear intermittent catheterization,

suprapubicpunctie (Lecture & Demonstration)

4.01 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

8-6-2016

08.00-09.00 Urinalysis 4.01 Wiradewi

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

4.01 Dwi Fatmawati

11.00-12.00 Break

-12.00-14.00 Skills Training Skills Lab 2nd_Floor

Facilitators

-XVIII

9-6-2016

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

Demonstration)

4.01 Wayan Yudiana

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

4.01 JuliSumadi

11.00-12.00 Break

Facilitators

(9)

-XIX

10-6-2016

08.00-09.00 BNO and IVP 4.01 Laksminingsih

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

11.00-12.00 Break -

Facilitators

-XX

13-6-2016

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

diagnosis Urinary system disorders)

4.01 Laksminingsih

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

4.01 Laksminingsih

-11.00-12.00 Break -

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

4.01 Wiradewi

-XXI

14-6-2016

Preparation Day

XXII

15-6-2016

10.00-11.40 Final Examination Computer Room

Team

CLASS B

(10)

I

17-5-2016

-10.00-11.00 Macroscopic Anatomy of The Urinary System

4.01 Mangku Karmaya

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 Break -

room

Facilitators

15.00-16.00 Plenary 4.01 Mangku Karmaya

II

18-5-2016

-10.00-11.00 Microscopic Anatomy of The Urinary System

4.01 Sugiritama

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 Break -

room

Facilitators

15.00-16.00 Plenary 4.01 Sugiritama

III

19-5-2016

09.00-10.00 The function of the urinary system:

Urine formation Urine micturition

4.01 Tirtayasa

-11.30-12.00 Break -

-12.00-13.30

Independent Learning

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 Tirtayasa IV

20-5-2016

09.00-10.00 The kidney as water, electrolyte and acid-base balance controller

4.01 Tirtayasa

-11.30-12.00 Break -

-12.00-13.30

Independent Learning

-

Room

(11)

15.00-16.00 Plenary session 4.01 Tirtayasa V

23-5-2016

09.00-10.00 Pathogenesis of Glomerular and Tubulointerstitial Injury

-11.30-12.00 Break -

-12.00-13.30

Independent Learning

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 Winarti/Juli Sumadi VI

24-5-2016

09.00-10.00 Urinary System Disorders in Children:

- Nephrotic syndrome - PSAGN

- UTI in children

4.01 Suarta/Nilawati

-11.30-12.00 Break -

-12.00-13.30

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 Suarta/Nilawati VII

25-5-2016

09.00-10.00 Uncomplicated and Complicated Urinary tract infection

4.01 I Wayan Sudana

-11.30-12.00 Break -

-12.00-13.30

Independent Learning

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 I Wayan Sudana VIII

26-5-2016

09.00-10.00 Urolithiasis (with and without colic)

4.01 AA Gde Oka

-11.30-12.00 Break -

-12.00-13.30

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 AA Gde Oka

IX

27-5-2016

09.00-10.00 Common Neoplasm in Urinary System: Renal tumors, bladder tumors.

4.01 AA Gde Oka

(12)

-12.00-13.30

Independent Learning

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 AA Gde Oka X

30-5-2016

09.00-10.00 Acute Kidney Injury 4.01 Yeni Kandarini 10.00-11.30 Student Project Presentation

1 (Horse Shoe Kidney)

4.01 AA Gde Oka

11.30-12.00 Break -

-12.00-13.30

-

Room

Facilitators

15.00-16.00 Plenary 4.01 Yeni Kandarini

XI

31-5-2016

09.00-10.00 Chronic Kidney Disease 4.01 Raka Widiana 10.00-11.30 Student Project Presentation

2 (Symptomatic Polycystic Kidney)

4.01 Yeni Kandarini

11.30-12.00 Break -

-12.00-13.30

Independent Learning

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 Raka Widiana XII

1-6-2016

09.00-10.00 Secondary Hypertension 4.01 Jodi Sidharta L 10.00-11.30 Student Project Presentation

3 (Hemoadialysis)

4.01 Wayan Sudana

11.30-12.00 Break -

-12.00-13.30

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 Jodi Sidharta L XIII

2-6-2016

09.00-10.00 Diuretics and Urinary Antiseptic

4.01 Artini

10.00-11.00 Common testicular disorders: Hydrocele, Varicocele, undencensus testis, torsio testis, tumor

11.00-12.00 Break -

-12.00-13.30

Independent Learning

-

Room

Facilitators

(13)

XIV

3-6-2016

09.00-10.00 Common penile disorders: Epispadia, hypospadia, phimosis, paraphimosis, epididimitis, and common tumor of the penis

10.00-11.30 Student Project Presentation 4 (Urodinamic examination and Uroflowmetry)

4.01 AA Gde Oka

11.30-12.00 Break -

-12.00-13.30

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 G. Wirya K. Duarsa XV

6-6-2016

09.00-10.00 Common Prostate Disorders (Prostatitis, BPH, Prostate Cancer), Urethral Stricture and Hydronephrosis in children

G. Wirya K. Duarsa

10.00-11.30 Student Project Presentation

5 (Micturating Cystigraphy) 4.01 G. Wirya K. Duarsa

11.30-12.00 Break -

-12.00-13.30

Independent Learning

-

Room

Facilitators

15.00-16.00 Plenary session 4.01 G. Wirya K. Duarsa XVI

7-6-2016

09.00-10.00 Anamnesis and Physical Examination in Urinary System Disorders (Lecture & Demonstration)

4.01 Raka Widiana

-11.00-12.00 Urethral catheterization, Clear intermittent

catheterization, suprapubic punctie (Lecture &

Demonstration)

4.01 AA Gde Oka

12.00-13.00 Break

-13.00-15.00 Skills Training Skills Lab

3rd_Floor Facilitators

15.00-16.00 Free Training Skills Lab 3rd_Floor

-XVII

8-6-2016

09.00-10.00 Urinalysis 4.01 Wiradewi

-11.00-12.00 Urethral Swab, Urine Culture and Sensitivity Test

4.01 Dwi Fatmawati

12.00-13.00 Break

-13.00-15.00 Skills Training Skills Lab 3rd_Floor

Facilitators

(14)

-3rd_Floor

XVIII

9-6-2016

09.00-10.00 Circumcision, Prostate Palpation, Bulbocavernosus reflex (Lecture and

Demonstration)

4.01 Wayan Yudiana

-11.00-12.00 Student Project Presentation 6 (Urine Cytology)

4.01 Juli Sumadi

12.00-13.00 Break

Facilitators

-XIX

10-6-2016

09.00-10.00 BNO and IVP 4.01 Laksminingsih

-11.00-12.00 Student Project Presentation 7 (Pathological aspect of Prostate Cancer)

12.00-13.00 Break -

Facilitators

-XX

13-6-2016

-10.00-11.00 Student Project Presentation 8 (The role of USG in

diagnosis Urinary system disorders)

4.01 Laksminingsih

11.00-12.00 Student Project Presentation 9 (The role of CT Scan in diagnosis Urinary system disorders)

4.01 Laksminingsih

12.00-13.00 Break -

-13.00-14.00 Student Project Presentation 10 (Renal Funtion Test (BUN, SC))

4.01 Wiradewi

-XXI

14-6-2016

PREPARATION DAY

XXII

15-6-2016

FINAL EXAMINATION

(15)

Format

1. Cover:

 Title

Article Review writed at top left corner Udayana Symbol

Name

Student Registration Number

Udayana University, School of Medicine, 2016 2. Introduction

3. Content: From Definition to treatment (disease) or Definition to complication (procedure) 4. Summary

5. Reference (minimal 6 references)  Vancouver style

Note:

1.5 space, Time New Roman 12, page at right bottom.

Facilitator Score with 60% qualification, while Evaluator Score the Presentation with 40% qualification.

Topic

No Group Topic PIC

1 A1, B1 Horse Shoe Kidney AA Gde Oka

2 A2, B2 Symptomatic Polycystic Kidney Yeni Kandarini

3 A3, B3 Hemodialysis Wayan Sudhana

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 Prostatic Carcinoma Winarti/Juli Sumadi 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) Wiradewi Lestari

Student Project Assessments Form

(16)

Name :………..

Student Reg. Number :………..

Facilitator :………..

Title :………..

Time Table of Consultation

No Point of Discussion Date Facilitators Sign 1 Outline of Paper

2 Final Discussion

No

Item Assessment

Range Score (%) Score

1 Ability to find the literature 0-20 2 Communication/attitude/presentation 0-30

3 Quality of material (SOAP) 0-40

4 Student interest and motivation 0-10

TOTAL 100

Facilitator,

(………) NIP

No

Item Assessment

Range Score (%) Score

1 Quality of material 0-60

2 Capability of Information Searching 0-10

3 Critical Thinking 0-30

TOTAL 100

Evaluator/Supervisor,

(………)

NIP

(17)

Assessment will be carried out on June15, 2016. 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.

~ LEARNING PROGRAMS ~

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:

Lecture 1 -2:

(18)

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

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.

Lecture 3-4:

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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.

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.

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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,

Lecture 5:

Pathogenesis of Glomerular

and

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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 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?

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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 Nephrotic

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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.

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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:

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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 diagnosis? 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 urinationsince 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 Case 1

Lecture 8:

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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):

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

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):

2. Whatare the radiologic examination need to definitive diagnose?

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. Wilm’s tumor usually occur in children. Urothelial carcinoma originates from

Lecture 9:

Common Neoplasm in Urinary

System: Renal tumors, bladder

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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

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

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

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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 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 10 Case1

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.

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!

Case2

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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).

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?

3. Explain the management for this patient!

Learning task 11 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.

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?

4. Which of the following 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!

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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 12:

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

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.

Lecture 13:

Drug use in renal disorders

(Diuretics,

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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 13a 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.

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?

Varicocel, Hydrocele,

- Comprehend the definition, epidemiology and etiology of varicocele, and hydrocele - Apply basic principles of special investigation of varicocele, hydrocele

- Recognize clinically, provide initial management and refer patients with varicocele, and hydrocele

Testicle Tortion

- Comprehend the definition, epidemiology and etiology of testicle torsion - Apply basic principles of special investigation of testicle torsion

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Epididymitis

- Comprehend the definition, epidemiology and etiology of epididymitis - Apply basic principles of special investigation epididymitis

- Recognize clinically, provide initial management and refer patients with epididymitis

Cryptorchidism

- Comprehend the definition, epidemiology and etiology of cryptorchidism - Apply basic principles of special investigation Cryptorchidism

- Recognize clinically, provide initial management and refer patients with Cryptorchidism

Testicle tumors

- Comprehend the definition, epidemiology and aetiology testcile tumors - Apply basic principles of special investigation testicle tumors

- Recognize clinically, provide initial and refer patients with testicle tumors

LEARNING TASK 13b

1. Man 34 years old, came with complaint of secondary infertile. His first child was born 6 years ago. He also complaint of intermittent left scrotal pain. No complaint on erectile capability. He has a good general condition, composmentis, normal blood pressure 120/80, pulse 88x/minutes. Normal scrotal finding, right testicle normal, left testicle a little bit smaller than right one. Both of epydidimis are normal. Small, cystic, worm like mass was felt during valsava maneuver.

Questions:

What is the differential diagnosis of this patient?

What are the anamnesis, signs, symptoms and examination to establish the diagnosis? How is the management of this patient?

2. Eight year old boy crying for left scrotal pain for the last 6 hours. No history of trauma nor mumps. Left scrotal is redness, swollen so that very difficult to differentiate testicles to epididymis. Phren sign is doubtfull

Question:

The possible diagnosis are?

What kind of test is needed to establish the diagnoses If no radiologist are available, what is your decision?

3. Two years old boy came with complaint of left scrotal enlargement since he was born. The enlargement is cystic form and trans illuminated. No scrotal pain. No complaint on erectile capability. He has a good general condition, composmentis, and normal blood pressure 120/80, pulse 88x/minutes. Normal right and left testicles. Both of epydidimis are normal. Questions:

What is the diagnosis of this patient?

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

What is your planning treatment of this patient?

Lecture 14 &15

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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 14

1.

Man 34 years old, 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, unsircumsized, narrow MUE. Normal scrotal finding, right testicle normal.

Questions:

What is the possible diagnosis of this patient?

2. 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.

What is the possible diagnosis of this patient?

Learning Task 15

1. Man 34 years old, came with complain 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, unc