Diagnose and manage independentlyuncomplicated urinary tract infection, Diagnose and refer some urogenital system disorders such as, horse shoe

~ 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 9. Communicate and apply basic principle in the prevention, and rehabilitation of urogenitalsystem disorders Udayana University Faculty of Medicine, DME 1 | P a g e ~ 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.AK 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 18 dr. I Wayan Yudiana, Sp.U Urology Udayana University Faculty of Medicine, DME 2 | P a g e ~ FACILITATORS ~ Regular Class Class A No Name Group Departement Phone Venue 2 rd 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.MKK 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 12 dr. I Wayan Subawa, Sp.OT A12 Orthopaedi 081337096388 3nd floor: R.3.23 Udayana University Faculty of Medicine, DME 3 | P a g e English Class Class B No Name Group Departement Phone Venue 2 rd 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 Clinical Pathology 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 12 dr. Putu Budhiastra, Sp.MK B12 Opthalmology 085238238999 3nd floor: R.3.23 Udayana University Faculty of Medicine, DME 4 | P a g e TIME TABLE CLASS A DAYDATE 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 - - 10.30-12.00 SGD 2 Discussion room Facilitators 12.00-13.00 Individual Learning - - 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 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 3 Discussion 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 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 4 Discussion Room Facilitators 12.00-13.00 Student Project - - 13.00-14.00 Break - - 14.00-15.00 Plenary session 4.01 Tirtayasa Udayana University Faculty of Medicine, DME 5 | P a g e V 23-5-2016 08.00-09.00 Pathogenesis of Glomerular and Tubulointerstitial Injury 4.01 WinartiJuli Sumadi 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 5 Discussion Room Facilitators 12.00-13.00 Student Project - - 13.00-14.00 Break - - 14.00-15.00 Plenary session 4.01 WinartiJuli Sumadi VI 24-5-2016 08.00-09.00 Urinary System Disorders in Children: - Nephrotic syndrome - PSAGN - UTI in Children 4.01 SuartaNilawati 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 6 Discussion Room Facilitators 12.00-13.00 Student Project - - 13.00-14.00 Break - - 14.00-15.00 Plenary session 4.01 SuartaNilawati VII 25-5-2016 08.00-09.00 Uncomplicated and Complicated Urinary tract infection 4.01 I Wayan Sudana 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 7 Discussion Room Facilitators 12.00-13.00 Student Project - - 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 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 8 Discussion Room Facilitators 12.00-13.00 Student Project - - 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 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 9 Discussion Room Facilitators 12.00-13.00 Student Project - - 13.00-14.00 Break - - 14.00-15.00 Plenary session 4.01 AA Gde Oka Udayana University Faculty of Medicine, DME 6 | P a g e X 30-5-2016 08.00-09.00 Acute Kidney Injury 4.01 Yeni Kandarini 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 10 Discussion 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 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 11 Discussion 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 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 12 Discussion 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 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 13 Discussion 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 4.01 G. Wirya K. Duarsa 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 14 Discussion Room Facilitators 12.00-13.00 Student Project Presentation 4 Urodinamic examination and Uroflowmetry 4.01 AA Gde Oka Udayana University Faculty of Medicine, DME 7 | P a g e 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 4.01 G. Wirya K. Duarsa 09.00-10.30 Individual Learning - - 10.30-12.00 SGD 14 Discussion 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 09.00-10.00 Individual Learning - - 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 2 nd Floor Facilitators 14.00-15.00 Free Training Skills Lab 2 nd Floor - XVII 8-6-2016 08.00-09.00 Urinalysis 4.01 Wiradewi 09.00-10.00 Individual Learning - - 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 2 nd Floor Facilitators 14.00-15.00 Free Training Skills Lab 2 nd Floor - XVIII 9-6-2016 08.00-09.00 Circumcision, Prostate Palpation, Bulbocavernosus reflex Lecture and Demonstration 4.01 Wayan Yudiana 09.00-10.00 Individual Learning - - 10.00-11.00 Student Project Presentation 6 Urine Cytology 4.01 JuliSumadi 11.00-12.00 Break - 12.00-14.00 Skills Training Skills Lab 2 nd Floor Facilitators 14.00-15.00 Free Training Skills Lab 2 nd Floor - Udayana University Faculty of Medicine, DME 8 | P a g e XIX 10-6-2016 08.00-09.00 BNO and IVP 4.01 Laksminingsih 09.00-10.00 Individual Learning - - 10.00-11.00 Student Project Presentation 7 Pathological aspect of Prostate Cancer 4.01 WinartiJuli Sumadi 11.00-12.00 Break - - 12.00-14.00 Skills Training Skills Lab 2 nd Floor Facilitators 14.00-15.00 Free Training Skills Lab 2 nd Floor - 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 10.00-11.00 Individual Learning - - 11.00-12.00 Break - - 12.00-13.00 Student Project Presentation 10 Renal Funtion Test BUN, SC 4.01 Wiradewi 13.00-15.00 Free Training Skills Lab 2 nd Floor - XXI 14-6-2016 Preparation Day XXII 15-6-2016 10.00-11.40 Final Examination Computer Room Team CLASS B DAYDATE TIME ACTIVITY VENUE PIC Udayana University Faculty of Medicine, DME 9 | P a g e I 17-5-2016 09.00-10.00 Individual Learning - - 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 - - 14.30-15.00 SGD 1 Discussion room Facilitators 15.00-16.00 Plenary 4.01 Mangku Karmaya II 18-5-2016 09.00-10.00 Individual Learning - - 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 - - 14.30-15.00 SGD 2 Discussion 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 10.00-11.30 Student Project - - 11.30-12.00 Break - - 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 3 Discussion 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 10.00-11.30 Student Project - - 11.30-12.00 Break - - 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 4 Discussion Room Facilitators Udayana University Faculty of Medicine, DME 10 | P a g e 15.00-16.00 Plenary session 4.01 Tirtayasa V 23-5-2016 09.00-10.00 Pathogenesis of Glomerular and Tubulointerstitial Injury 4.01 WinartiJuli Sumadi 10.00-11.30 Student Project - - 11.30-12.00 Break - - 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 5 Discussion Room Facilitators 15.00-16.00 Plenary session 4.01 WinartiJuli Sumadi VI 24-5-2016 09.00-10.00 Urinary System Disorders in Children: - Nephrotic syndrome - PSAGN - UTI in children 4.01 SuartaNilawati 10.00-11.30 Student Project - - 11.30-12.00 Break - - 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 6 Discussion Room Facilitators 15.00-16.00 Plenary session 4.01 SuartaNilawati VII 25-5-2016 09.00-10.00 Uncomplicated and Complicated Urinary tract infection 4.01 I Wayan Sudana 10.00-11.30 Student Project - - 11.30-12.00 Break - - 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 7 Discussion 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 10.00-11.30 Student Project - - 11.30-12.00 Break - - 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 8 Discussion 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 10.00-11.30 Student Project - - 11.30-12.00 Break - - Udayana University Faculty of Medicine, DME 11 | P a g e 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 9 Discussion 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 Independent Learning - - 13.30-15.00 SGD 10 Discussion 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 - - 13.30-15.00 SGD 11 Discussion 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 Independent Learning - - 13.30-15.00 SGD 12 Discussion 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 4.01 G. Wirya K. Duarsa 11.00-12.00 Break - - 12.00-13.30 Independent Learning - - 13.30-15.00 SGD 13 Discussion Room Facilitators 15.00-16.00 Plenary session 4.01 G. Wirya K. Duarsa, Artini Udayana University Faculty of Medicine, DME 12 | P a g e XIV 3-6-2016 09.00-10.00 Common penile disorders: Epispadia, hypospadia, phimosis, paraphimosis, epididimitis, and common tumor of the penis 4.01 G. Wirya K. Duarsa 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 Independent Learning - - 13.30-15.00 SGD 14 Discussion 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 - - 13.30-15.00 SGD 15 Discussion 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 10.00-11.00 Individual Learning - - 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 3 rd Floor Facilitators 15.00-16.00 Free Training Skills Lab 3 rd Floor - XVII 8-6-2016 09.00-10.00 Urinalysis 4.01 Wiradewi 10.00-11.00 Individual Learning - - 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 3 rd Floor Facilitators 15.00-16.00 Free Training Skills Lab - Udayana University Faculty of Medicine, DME 13 | P a g e 3 rd Floor XVIII 9-6-2016 09.00-10.00 Circumcision, Prostate Palpation, Bulbocavernosus reflex Lecture and Demonstration 4.01 Wayan Yudiana 10.00-11.00 Individual Learning - - 11.00-12.00 Student Project Presentation 6 Urine Cytology 4.01 Juli Sumadi 12.00-13.00 Break - 13.00-15.00 Skills Training Skills Lab 3 rd Floor Facilitators 15.00-16.00 Free Training Skills Lab 3 rd Floor - XIX 10-6-2016 09.00-10.00 BNO and IVP 4.01 Laksminingsih 10.00-11.00 Individual Learning - - 11.00-12.00 Student Project Presentation 7 Pathological aspect of Prostate Cancer 4.01 WinartiJuli Sumadi 12.00-13.00 Break - - 13.00-15.00 Skills Training Skills Lab 3 rd Floor Facilitators 15.00-16.00 Free Training Skills Lab 3 rd Floor - XX 13-6-2016 09.00-10.00 Individual Learning - - 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 14.00-16.00 Free Training Skills Lab 3 rd Floor - XXI 14-6-2016 PREPARATION DAY XXII 15-6-2016 FINAL EXAMINATION ~ STUDENT PROJECT ~ Udayana University Faculty of Medicine, DME 14 | P a g e 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 WinartiJuli 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 Block of Urinary and Male Genital System disorders Udayana University Faculty of Medicine, DME 15 | P a g e 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 Communicationattitudepresentation 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 EvaluatorSupervisor, ……………………………………… NIP ~ ASSESSMENT METHOD ~ Udayana University Faculty of Medicine, DME 16 | P a g e 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: Udayana University Faculty of Medicine, DME 17 | P a g e Lecture 1 -2: Macroscopic and Microscopic Structure the Urinary System 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. Udayana University Faculty of Medicine, DME 18 | P a g e Lecture 3-4: The Function of Urinary System 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. SDG 4 Udayana University Faculty of Medicine, DME 19 | P a g e 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 TubularInterstitial 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, Udayana University Faculty of Medicine, DME 20 | P a g e Lecture 5: Pathogenesis of Glomerular and Tubulo-Interstitial Injury 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 tubulointerstitial 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, 250mL24 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 Udayana University Faculty of Medicine, DME 21 | P a g e 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 2-3100,000 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 mgm 2 hour in children, hypoalbuminemia 2.5 gdL, 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 Udayana University Faculty of Medicine, DME 22 | P a g e Lecture 6: Common Kidney Diseases in Children Acute Poststreptococcal Glomerulonephritis and Nephrotic Syndrome, UTI in Children 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 mgm 2 hour in children. The serum albumin level is generally less than 2.5 gdL 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 is140100 mmHg with pulse 88 bpm. Chest, cardiovascular and abdominal examination are normal. Learning Task: Udayana University Faculty of Medicine, DME 23 | P a g e 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, rigorschill, 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 Udayana University Faculty of Medicine, DME 24 | P a g e 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 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 cfuml. Plain abdominal photo BNOBOF 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 Udayana University Faculty of Medicine, DME 25 | P a g e Lecture 8: Urinary Calculi Urolithiasis and Urethral Stricture 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 straddlesaddle 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? 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 Udayana University Faculty of Medicine, DME 26 | P a g e Lecture 9: Common Neoplasm in Urinary System: Renal tumors, bladder tumors. 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? Udayana University Faculty of Medicine, DME 27 | P a g e Lecture 1011: Acute Kidney Injury Chronic Kidney Diseases 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 12476 mmHg and his pulse was 82 beats per minute while he was supine and 12674 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 mgdl today and it was 1,0 mgdl a week ago. Other blood laboratory findings include the following: WBC count 11.000ml; sodium 142 mmolL; potassium 4,2 mmolL; and blood urea nitrogen 34 mgdl. His urine showed a sodium level of 54 mmolL and creatinine level of 39 mgdl. The urinalysis with dipstick testing showed +1 protein; the microscopic analysis showed 5-10 leucocytesHPFhigh 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 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. Udayana University Faculty of Medicine, DME 28 | P a g e His blood urea nitrogen BUN level was 21 mgdl and his creatinine level was 1,5 mgdl base line creatinine level, 1.0 mgdl. 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 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 14888 mmHg, and pulse rate is 85 beatsmin. She has + 2 pedal edema. Laboratory tests show a serum creatinine level of 0,7 mgdl and BUN level of 32 mgdl. 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? 3. Explain the pathophysiology 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 14488 mmHg d. Glycosylated hemoglobin level of 7.5 . Explain your answer 5. Describe the management of chronic kidney disease according to the classstage 6. Explain the rational management for the patient above Udayana University Faculty of Medicine, DME 29 | P a g e Lecture 12: Secondary Renal Hypertension 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. Udayana University Faculty of Medicine, DME 30 | P a g e Lecture 13: Drug use in renal disorders Diuretics, Urinary antiseptics Common Testicular Disorders 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=180100 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 injurydisease and the type of renal injurydisease 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 - Recognize clinically, provide initial management and refer patients with testicle torsion Udayana University Faculty of Medicine, DME 31 | P a g e 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 12080, pulse 88xminutes. 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 12080, pulse 88xminutes. 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? Udayana University Faculty of Medicine, DME 32 | P a g e Lecture 14 15 Common Penile Prostate Disorders 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 12080, pulse 88xminutes, unsircumsized, narrow MUE. Normal scrotal finding, right testicle normal. Questions: What is the possible 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? 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? 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? 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 12080, pulse 88xminutes, uncircumcised, narrow MUE. Normal scrotal finding and right testicle normal. Questions: What is the possible 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? 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. Question: What is the possible diagnosis of this patient? What are the anamnesis, signs, symptoms and examination to support the diagnosis? Udayana University Faculty of Medicine, DME 33 | P a g e What is your planning to complete the diagnosis? What is your planning treatment of this patient? 3. A fifty two years old male, came to your clinic due to burning sensation in pie. He is sexually active man. DRE revealed 35 gram prostate enlargement. Normal finding in USG Question Were there any other history taking or physical examination needed? What is your treatment plan? 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 The function of the urinary system 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 Udayana University Faculty of Medicine, DME 34 | P a g e 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? SELF ASSESSMENT 7 Complicated and Uncomplicated Urinary tract infection 1. How to do a complete anamnesis history talking by fundamental four and secrete seven in complicated UTI? Udayana University Faculty of Medicine, DME 35 | P a g e 2. How to do a complete diagnosis primary, scondary and complication by history talking, physical, X ray and ultrasound in complicated UTI? 3. How to do the proper medical management in complicated UTI? 4. How to do the education in complicated UTI, if a patien is going to reffered hospital and surgical management? SELF ASSESSMENT 8 Urolithiasis and urethral stricture Self Assessment Urolithiasis 1. How to do a complete anamnesis history talking by fundamental four and secrete seven in renal, ureteral, bladder and urethral stone? 2. How to do a complete diagnosis primary, secondary and complication by history talking, physical, X ray and ultrasound examination in renal, ureteral, bladder and urethral stone? 3. How to do initial management in renal, ureteral, bladder and urethral stone? 4. How to do education in renal, ureteral, bladder and urethral stone, if a patient going to do to referred hospital and surgical management? Self Assessment Urethral stricture 1. How to do a complete anamnesis history talking by fundamental four and secrete seven in urethral stricture? 2. How to do a complete diagnosis primary, secondary and complication by history talking, physical, X ray examinations in urethral stricture? 3. How to do education in urethral stricture, if a patient going to do to referred hospital and surgical management? SELF ASSESSMENT 9 Common neoplasm of the urinary tract and related structure 1. How to do a complete anamnesis history talking by fundamental four and secrete seven in kidney and bladder neoplasma? 2. How to do a complete diagnosis primary, secondary and complication by history talking, physical, X ray examinations in kidney and bladder neoplasma? 3. How to do education in kidney and bladder neoplasma, if a patient going to do to referred hospital and surgical management? SELF ASSESSMENT 10 Acute kidney injury 1. Explain about acute kidney disease and its classification 2. Explain about the RIFLE criteria 3. Explain the pathophysiology of acute kidney disease due to gastroenteritis with dehidration? 4. Explain the management of acute kidney disease? 5. Can you describe the compication of acute kidney injury? SELF ASSESSMENT 11 Chronic kidney disease 1. Describe the classification of Chronic Kidney disease 2. Explain the pathophysiology of hypertension in cronic kidney disease? 3. Explain the pathophysiology of anemia in cronic kidney disease? 4. Describe the management of Chronic Kidney disease according to the classification SELF ASSESSMENT 12 Secondary hypertension Udayana University Faculty of Medicine, DME 36 | P a g e Secondary Hypertension 1. In a patient with bilateral renal artery stenosis, drugs that inhibit ACE inhibitors or that block angiotensin receptors can have a negative impact of renal function. Which renal function can be made worse? A. The ability to secrete renin B. The ability to concentrate urine C. Glucose-reabsorbing ability D. Glomerular filtration 2. Which of the following clinical symptoms and signs is not seen in patient with primary hyperaldosterinism A. Edema of the angkles B. Weakness of the muscle C. Systolic blood pressure of more than 180 mmHg D. Muscle cramps 3. A physician is practicing in a third world region with no radiology or nuclear medicine support and a laboratory that can only measure blood counts, electrolytes and simple blood chemistries. A young patient with hypertension who has no family history of hypertension presents to the clinic. Which of the following tests would the physician request to investigate the possibility that the patient has primary hyperaldosteronism? A. Serum sodium concentration B. Serum and 24-hour urine potassium C. 24-hour urine sodium and creatinine D. Urine sodium concentration and pH SELF ASSESSMENT 13a 1. Mention several drugs that potentially induce renal disease 2. Mention the possible mechanisms of drug-induced renal disease 3. Mention pharmacokinetic and pharmacodynamic changes possibly occur in renal disease. 4. What are the basic concepts of dosage adjustment in patient with renal disease? 5. How is the mechanism of action for each type of diuretics? 6. What is the effect of each class of diuretics in acid base balance and serum potassium level? 7. Why spironolactone would not cause potassium wasting? 8. What other adverse effects might occur in diuretic treatment? 9. Mention some clinical indications of diuretics. 10. Mention types of urinary antiseptics. 11. How is the mechanism of urinary antiseptic action? 12. What are the adverse effects of each type of urinary antiseptic? SELF ASSESSMENT 13b 1. What are the most common symptoms of Varicocele? 2. When does the varicocele need an operation? 3. What is the differential diagnostic of scrotal testicle enlargement? 4. What is the difference between cryptorchidism and retractile testicle? 5. What is the caused of testicle undecensus? What is the complication of cryptorchidism? How is the management of this condition? 6. How are the diagnostic and treatment management of testicle torsion? 7. What is the differential diagnostic of scrotal testicle enlargement? Udayana University Faculty of Medicine, DME 37 | P a g e 8. Explain the type and tumor marker of testicle tumors. SELF ASSESSMENT 14 1. What is the definition of phimosis and paraphimosis, priapismus and peyronie disease? 2. What is the definition and the management of urethral stricture? 3. What is the complication of the long term phimosis and poor hygiene of the male external genital? 4. What is the definition and aetiology of hypospadia? 5. What is the caused and complication than can be caused by balanopostitis? 6. What is the correlation between phymosis and penile cancer? 7. How is the management of penile cancer? SELF ASSESSMENT 15 1. What is the symptom and sign of Prostatitis, BPH and prostate cancer? 2. What is the definition and the management of urethral stricture? 3. What is the differential diagnosis of right or left flank mass neonatal? 4. Explain the division of posterior urethral valve 5. How is the management of benign prostate enlargement? BASIC CLINICAL SKILLS In general, patients with kidney diseases usually come with non specific symptom. They usually come with hematuria, foamy urine, abnormality of the urine volume poliuria, oligouria, anuria, or disturbance in micturition process. Another symptom also not infrequently, such as edema, fatigue, pale, nausea and vomiting. Edema starts from face and spread to all of the body. They also come with flank pain renal colic and ureter colic. The patient with severe kidney destruction may come with shortness of the breath as the result of lung edema or acidosis. Udayana University Faculty of Medicine, DME 38 | P a g e Sign that frequently seen in kidney diseases including anemia, hypertension, and edema. If a patient come to seek the treatment with nausea, vomiting, fatigue, hypertension and edema always think that the most possibility is chronic kidney diseases. Renal colic is a severe pain at right or left lumbal region and referred to genital region. Also accompanied by percussion pain at costovertebral angle. Test for kidney patient include routine laboratory test, imaging, and biopsy. Laboratory test, including, routine hematology, urinalysis, ureumBUN, creatinine, electrolyte K,Na, uric acid serum, urine volume, in special scenario, blood gas analysis, total protein and albumin, calsium, anorganik phosphate maybe required. Another examination should be done based on their indication. Clearence creatinine test is important in measuring glomerular filtration rate.Imaging examination including BNO, IVP, Ultrasonography, CT Scan and, retrograde pielography. Urine cytology and renal biopsy can be done based on indication. One of the necessary laboratory examination is the examination of the microbiology laboratory. To be able to produce accurate data from the microbiological examination, the specimen quality is a factor that must be considered. A good quality specimen is needed to assist in establishing a reliable diagnosis. Improper management of specimens, both in terms of collection, storage, or transportation, can lead to failure in finding the cause of microorganisms. Interpretation of result culture and susceptibility testing must be tailored according to the patient at risk and the specimen type submitted. There are three things that should be considered in cases of urinary tract infections are the colony count of microorganisms growing in culture, measurement of pyuria and presence or absence of symptoms dysuria and frequency. Knowledge of the normal flora in the area genetalia are also required similarly with microorganisms that are often the causes of urinary tract infections are very helpful in determining the culture of an agent causing the infection or merely contamination only. Anamnesis and Physical Examination in Urinary System and Male Genital System Disorders Learning task Title : Anamnesis and physical examination in lower urinary tract disorders Objective : Student can do structured anamnesis and physical examination in lower urinary tract disorders Competency bold letter :

1. Anamnesis skill