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Modul Practicum Guidelines Laboratory Skills Guidelines BLOCKS OF ENDOCRINE FACULTY OF MEDICINE

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Page 1: Buku Modul Endokrin 2010

Modul Practicum Guidelines Laboratory Skills Guidelines

BLOCKS OF ENDOCRINE

FACULTY OF MEDICINEMUHAMMADIYAH UNIVERSITY OF YOGYAKARTA

2010

Page 2: Buku Modul Endokrin 2010

MODULEBLOCK OF ENDOCRINE

Editordr. Sri Sundari M.Kes

dr. Agus Widyatmoko, MKes, SpPDdr. Alfaina Wahyuni, MKes

Person In Charge:dr. Sri Sundari, MKes

Departments Involved:

Internal MedicinePhysiology

Obstetry and gynaecologyAnatomy

Anatomical Pathology Clinical Pathology Surgery Pharmacology

Center for Islamic Medicine Studies (PSKI)Center for Family Medicine Studies (PSKK)

FACULTY OF MEDICINEMUHAMMADIYAH UNIVERSITY OF YOGYAKARTA

2008

Page 3: Buku Modul Endokrin 2010

OVERVIEWBLOCK OF ENDOCRINE

Block of endocrine is the fourteenth block of 24 blocks of medical curriculum in

preclinical stage. The topics of this block range from preclinical, clinical, community and

family medicine in which the integration of EBM and family medicine. In this block there

are some learning activities consists of small group discussion or tutorial, lecture, clinical

skills and practical in laboratory.

Generally, this block consist of disease or disorder of endocrine system,

patophysiology, diagnosis, and management Finishing this module, students are expected

to be able to understand the basic concept of the process on how endocrine diseases and

disorders occur and students are also expected to understand the management

.

Page 4: Buku Modul Endokrin 2010

TOPIC TREE

BLOCK OF ENDOCRINE

Page 5: Buku Modul Endokrin 2010

COMPETENCE AREABLOCK OF ENDOCRINE

Competence area of Competence Standard for Medical Doctor (SKD) that will be

achieved on this block i.e:

1. Area 1 : Efffective comunication

2. Area 2 : Clinical skills

3. Area 3 : Basic Science of medicine

4. Area 4 : Management of Health disorder

5. Area 5 : Management of information

TEACHING LEARNING PLAN

BLOCK COMPETENCIES

At the end of this block students are expected to be able to understand the basic

concept of the process on how endocrine diseases and disorders occur and students are also

A. Characteristic of the students

The students attending the block of Endocrine are those who have learned 13

blocks, it means that they sitting in semester 5 or in year 3. They are supposed to have been

familiar with the basics of medical science and been introduced to clinical science. The

students are expected to develop clinical thinking and clinical reasoning as well as

maintaining their independent and in depth learnig process, particularly when they deal

with the endocrine.

B. Learning outcome

At the end of this Endocrine block, the students will be able to:

1. Utilize well developed communication skills to facilitate effective patient care and

productive collaboration with patients and their families and communities who have

endocrine disorder (Area 1)

2. Will be able to collect and record accurate and important information about the

patient and his/her family and also can conduct endocrine disorder (Area 2)

3. Apply the concepts and principles of biomedical, clinical, and behavioural science,

and public health about the endocrine disorder, appropriate to the delivery of

primary health care, can summarize an appropriate interpretation of the history and

endocrine examination of endocrine disorder and then evaluate the effectiveness of

patient management.(Area 3)

4. After the student can make diagnosis endocrine disorder, they can manage the

patient’s disorder and problem in the context of the whole person, as a part of a

Page 6: Buku Modul Endokrin 2010

family and a community, conduct prevention and health education of endocrine

disorder in order to promote health and to prevent endocrine disorder and also use a

family medicine approach to manage cases of endocrine disorder (Area 4)

5. Use the information of technology and communication to diagnose, therapy,

prevention and promotion, and control of the state of patient who have endocrine

disease or disorder. (Area 5)

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C.Learning of Competence

Level of expected ability

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D. Topics

Competence Area

Core Competency(SKD)

StrategyLecture, Practical,

Clinical Skills, Tutorial

Topics

AREA 1

Able to explore and exchange information verbally and non verbally with patients of any age, family members, communities, collegues and other professionals.

Clinical skills

Patient education of DMDiit DM dan exercise (leg exercise)

AREA 2 Conduct clinical procedures based on the patient’s problem and needs, and the doctor’s accreditation

Lecture

Pathology of Thyroid and other glandsPathology of thyroid, parathyroid, hipofisis and adrenal

PracticalPathology of thyroid, parathyroid, hipofisis and adrenal

Clinical skills Thyroid examinationTechnique in giving Insulin, examination of blood glucose

Tutorial Conduct clinical procedure (Scenario 1 – 4)

AREA 3 Identify, explain and plan a scientific approach to health problem solving, based on current medical and health science to get an optimal result.

Lecture

Endocrine system Physiology Endocrine Reproduction

Hormone Biochemical

Endocrine System

feminine reproduction SystemWomen’s and men’s InfertilityDemography and Family PlanningEndocrine diseases and complicationsDM Juvenile disease, ThyroidMenstrustion disorder

Bormone biochemical

Sexualities

Azoosperm

Tutorial Physiology and pathophysiology of the disease (scenario 1 – 4)

AREA 4 Manage health problems in a person, family or Lecture

Pharmacotherapy disorders or Hormonal diseases

Page 9: Buku Modul Endokrin 2010

community comprehensively, holistically, sustainably, coordinatedly, and collaboratively in the context of a primary health care service.

ACTH

Management of endocrine disease and treatment

Treatment of hormone disorder diseases

Tutorial Management of endcocrine disease and disorder (scenario 1 – 4)

AREA 5 Acces, care, critical analize of the information to solve the problem or desicion making in the context of a primary health care service.

Tutorial Evidence Based Medicine of Doagnose, Managemen and therapy of endocrine disease and disorder.

E. Pre-assessment

Block of endocrine is the 14th block in UMY curriculum which give the students to

the basic concept of the process on how endocrine diseases and disorders occur and

students are also expected to understand the management

Learning activities must be followed by the students as the requirements to do final

examination. Minimal attendance of the learning activity :

1. Lecture : 75%

2. Tutorial : 75%

3. Clinical Skill : 100%

4. Practical in laboratory: 100%

Page 10: Buku Modul Endokrin 2010

F. Teaching strategy and learning experience

Week 1Topics Strategy Department Duration

Endocrine system Physiology Lecture 5Endocrine System Lecture 1Endocrine System Lecture 1Endocrine disease 1 Lecture Internal

Medicine 2

Pathology of Thyroid and other glands Lecture 2Scenario 1 Tutorial 2 x 2Thyroid examination Clinical skills 2

Week 2Topics Strategy Department Duration

Hormone Biochemical Lecture 3Pathology of Thyroid and other glands Lecture 2Pathology of thyroid, parathyroid, hipofisis and adrenal

Lecture 3

Endocrine disease 2 Lecture 2Treatment of hormone disorder diseases Lecture 2Scenario 2 Tutorial 2 x 2Pathology of thyroid, parathyroid, hipofisis and adrenal

Practical 2,5

Technique in giving Insulin , examination of blood glucose, treatment of hypoglycemic.

Clinical skills 2

Week 3Topics Strategy Department Duration

Endocrine disease 3 and 4 Lecture Internal Medicine

4

DM Juvenile disease, Thyroid Lecture 2Pharmacotherapy disorders or Hormonal diseases

Lecture 2

Scenario 3 Tutorial 2 x 2Diit DM dan exercise (leg exercise) Clinical skills 2

Week 4Topics Strategy Department Duration

Endocrine Reproduction Lecture 2Endocrine disease 5 Lecture Internal

Medicine 2

ACTH Lecture 1Feminine reproduction System Lecture 2Women’s and men’s Infertility Lecture 4Demography and Family Planning Lecture 2Menstruation Disorders Lecture 3Sexualities Lecture 2Azoosperm Lecture 2Scenario 4 Tutorial 2 x 2Patient education of DM Clinical

skills

Page 11: Buku Modul Endokrin 2010

Week 5

Topics Strategy Department DurationEndocrine disease 6 Lecture Internal

Medicine 2

Menstruation and the disorder of menstruation

Lecture 1

Human behavior: Emotion and self-control Lecture 1Scenario 5 (in English) Tutorial 2Plenary Discussion 2-3Practical ExamClinical Skills Exam 2 x 4

Week 6

Topics Strategy Department Duration

Block Exam

G. Facilities

Medical faculty of UMY has some facilities to support teaching learning activities.

The facilities consists of :

a. 3 Amphitheatre for lecturing completed with computer/notebook & LCD

projector, audio recorder, internet

b. 15 tutorial room for small group discussion with capacity 12-15

sudents/room completed with TV, DVD media player, CCTV, internet

c. 2 clinical skills laboratory rooms

d. 6 laboratoties for practical work

e. 1 Faculty’s Library

f. 1 Laboratory of Information Technology

g. hot-spot area

H. Evaluation

Assessment is conducted using formative and summative assessment. Formative

assessment by assessing daily activities using check list, written report, kuiz, etc.

summative assessment using written examination (MCQ) and OSCE. The final score of

block will be determined by

50% of MCQ

30 % of Tutorial

20 % of OSCE and Practical in laboratory.

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The students pass Learning skills block if fulfill all of these criteria below :

the minimum score of MCQ is 60

the minimum score of OSCE is 60

the minimum of the final score is 60

I. Learning Resources

a. Text Book

1. Ganong W.P., 1995. Review Medical Physiology. 17th ed, Prentice Hall International, Englewood, New Jersey.2. Gilman, A.G., rall, T.W., Nies, A.S., and Taylor, P., 1990. Goodman and Gilman’s

the Pharmacological Basis of Therapeutics, 8 th ed, Pergamonn Press, New York.3. Granner, D.K., Mayer, D.A., Rodwell V.W., Harper’s Biochemistry, Lange

Medical Book , 18th ed.4. Guyton, A.C., & Hall, J.E., 1996. Textbook of Medical Physiology. W.B Saunders

Company, USA.5. Harrison’s, Principles of Internal Medicine (Wilson et al).6. Kanagasuntheram, R., Sivanandasingham, P, Krisnamurti, A., 1987. Anatomy

Regional, Functional & Clinical. P&G Publishing. Singapore.7. Katzung, B.G (editor). 1998. Basic and Clinical Pharmacology. 7th ed. Appleton &

Lange, Conneticut.8. Lynch’s. 1993. Medical Laboratory Technology. 4th ed.9. Markum. 1991. Buku ajar Ilmu Kesehatan Anak FK UI, Jakarta.10. Nelson’s. 1996. Textbook of Pediatric, 16th ed,11. Omar Hasan Kasule. 2000. Lectures Islamic Medicine, International Islamic

University Malaysia.12. Robbin, Pathologic Basic disease.13. Sabiston , Texbook of Surgery.14. Sarwono, Ilmu Kebidanan.15. Shahid Athar. 2000. Islamic Medicine. Indiana Univ. School of Medicine,

Inidianapolis, Indiana.16. Staf Pengajar IKA_UI. 1986. Buku Kuliah Ilmu Kesehatan Anak, Jakarta.17. Widmann’s. 1991. Clinical Interpretation of laboratory Test. 10th ed, 18. Williams, P.I., 1995. Gray’s Anatomy The Anatomical Basics of Medicine and

Surgery. ELBS with Churchil Livingstone, great Briatin.19. Spheroff L & Fitz M.A. 2005. Clinical Gynecology Endocrinology and

Infertility,7th ed. Lippincot Williams & Wilkins

a. Journal

1. BMJ

2. NEJM

3. PubMed

b. Expert

1. Prof. Dr. Sri Kadarsih Soejono, MSc, PhD

2. dr. Luthfan Budi Nugroho, SpPD

3. dr. Zain Alkaf, SpOG

Page 13: Buku Modul Endokrin 2010

LECTURE TOPICS (ENDOCRINE MODULE)

NO TOPICS DEPARTMENT LENGTH (HOURS)

1 Endocrine system Physiology Physiology 5 hours2 Endocrine Reproduction 2 hours3 Hormone Biochemical Biochemistry 3 hours4 Endocrine System Histology 1 hours5 Endocrine System Anatomy 1 hours6 Pathology of Thyroid and other

glandsClinical

Pathology 4 hours

7 Pathology of thyroid, parathyroid, hipofisis and adrenal

Pathology Anatomy

3 hours

8 feminine reproduction System Obsgyn 2 hours9 Women’s and men’s Infertility 4 hours10 Demography and Family Planning 2 hours11 Menstruation Disorders 3 hours12 Sexualities 2 hours13 Endocrine diseases, complications

and treatmentsIPD 12 hours

14 DM Juvenile disease, Thyroid IKA 2 hours15 Pharmacotherapy disorders or

Hormonal diseasesPharmacology 2 hours

16 ACTH 1 hours17 Treatment of hormone disorder

diseases Surgery science 2 hours

18 Azoosperm 2 hours19 Human behavior: Emotion and self-

controlPSKI 1 hours

PRACTICUM TOPICS (ENDOCRINE MODULE)

NO TOPICS DEPARTMENT LENGTH (HOURS)

1 Pathology of thyroid, parathyroid, hipofisis and adrenal

Pathology Anatomy 2,5 jam

SKILLS LAB TOPICS/FIELD (ENDOCRINE MODULE)

NO TOPIK DEPARTEMEN DURASI (JAM)1 Thyroid examination.

Skills Lab.

2 jam2 Technique in giving Insulin ,

examination of blood glucose, treatment of hypoglycemic.

2 jam

3 Patient education of DM 2,5 jam4 Diit DM dan exercise (leg exercise)

Page 14: Buku Modul Endokrin 2010

SUPPLEMENTS OF

BLOCK OF ENDOCRINE

Page 15: Buku Modul Endokrin 2010

GUIDANCE OF TUTORIAL

BLOCK OF ENDOCRINE

Page 16: Buku Modul Endokrin 2010

TECHNICAL GUIDELINES OF TUTORIALSEVEN JUMPS

Tutorial process in problem based learning (PBL) will use seven jumps as guidance for tutor and students to discus problem from scenario. There are seven steps in Seven jumps i.e. :

1. Clarifying unfamiliar terms2. Problem definitions3. Brainstorm4. Analyzing the problem5. Formulating learning issues6. Self study 7. Reporting

1. Clarifying unfamiliar termsUnclear terms and concepts in a problem description are clarified, so that every group member understands the information that is given

2. Problem definitionsThe problem is defined in the form of one or more questions. The group has to agree upon the phenomena that need to be explained

3. Brainstorm

The preexisting knowledge of group members is activated and determined. This process entails the generation of as many explanations and hypotheses as possible. The ideas of all the group members are collected, without critical analysis

4. Analyzing the problemExplanations and hypotheses of the group members are discussed in depth and are systematically analyzed. Ideas from the brainstorm are ordered and related to each other

5. Formulating learning issues

Based on obscurities and contradictions from the problem analysis, questions are formulated that form the foundation for the study activities of the group members. In short, it is determined what knowledge the group lacks and learning issues are formulated on these topics

6. Self studyGroup members search relevant literature that can answer the questions in their learning issues. After studying this literature the group members prepare themselves for reporting that they have found to the tutorial group

7. Reporting After reporting what sources group members have used in their self study activities, a discussion of the learning issues takes place based on the studied literature. Group members try to synthesize what they have found in different sources

Step 1 to 5 will be conduct in the first meeting, after that the students will conduct self study to search the explanation to answer the learning issues. The 7 step will be conduct in the second meeting.

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Overview of student skills in PBL

Preliminary discussion

Step Description Chair Scribe1. Clarifying unfamiliar terms

Unfamiliar terms in the problem text are clarified

Invites group members to read the problem

Checks if everyone has read the problem

Checks if there are unfamiliar terms in the problem

Concludes and proceeds to the next phase

Divides the blackboard into three parts

Notes down the unfamiliar terms

2. Problem definition

The tutorial group defines the problem in a set of questions

Ask the group for possible problem definitions

Paraphrases contributions of group members

Checks if everyone is satisfied with the problem definitions

Concludes and proceeds to the next phase

Notes down the problem definitions

3. Brainstorm

Preexisting knowledge is activated and determined, hypotheses are generated

Allows all group members to contribute one by one

Summarizes contributions of group members

Stimulates all group members to contribute

Summarizes at the end of the brainstorm

Makes sure that a critical analysis of all contributions is postponed until step four

Makes brief and clear summaries of contributions

Distinguishes between main points and side issues

4. Analyzing the problem

Explanation and hypotheses are discussed in depth and are systematically analyzed and related to each other

Makes sure that all points from the brainstorm are discussed

Summarizes contributions of group members

Asks questions, promotes depth in the discussion

Makes sure the group does not stray from the subject

Stimulates group members to find relations between topics

Stimulates all group members to contribute

Makes brief and clear summaries of contributions

Indicates relations between topics, makes schemata

5. Formulating learning issues

It is determined what knowledge the group lacks, and learning issues are formulated on these topics

Asks for possible learning issues Paraphrases contributions of group

members Checks if everyone is satisfied with

the learning issues Checks if all obscurities and

contradictions from the problem analysis have been converted into learning issues

Notes down the learning issues

Page 18: Buku Modul Endokrin 2010

Reporting phase

Step Description Chair Scribe7. Reporting

Findings from the literature are reported and answers to the learning issues are discussed

Prepares the structure of the reporting phase

Makes an inventory of what sources have been used

Repeats every learning issue and asks what has been found

Summarizes contributions of group members

Asks questions, promotes depth in the discussion

Stimulates group members to find relations between topics

Stimulates all group members to contribute

Concludes the discussion of each learning issue with a summary

Makes brief and clear summaries of contributions

Indicates relations between topics, makes schemata

Distinguishes between main points and side issues

Page 19: Buku Modul Endokrin 2010

CHECKLIST ON ASSESMENT TUTORIAL

Tutorial contributes 30% to the final score of the block, consisting of 15% average score of mini quiz and another 15 % of activities score of each tutorial meeting. The components to score in each tutorial are as follow:

Student’s name :Student’s number :BLOCK :

No CriteriaScore (meeting …………)

Unsatisfactory Satisfactory Good No judgmentDEALING WITH WORK

1 Preparation of task

2 Completeness in performing task

3 Brainstorming task

4 Active participation in a group

5 Report backDEALING WITH OTHERS

6 Working in a team

7 Listening to others

8 Performance as a chair of a group

9 Summarizing discussionDEALING WITH ONE SELF

10 Dealing with feedback

11 Giving feedback

12 The ability to reflect

13 Dealing with appointment

14 Being in time

Unsatisfactory : below the expected average level of the tutorial group. Item for improvement are clear and easy to mention. (score: <60)

Satisfactory : on the expected level of the tutorial group. Some issues for improvement rest. (score: 60-69,9)

Good : students perform better than expected average of the group (score: 70-80)

No Judgment : because student was absent to frequently. (score: 0)

Page 20: Buku Modul Endokrin 2010

ENDOCRINE MODULE SCENARIOS

SCENARIO 1

A 53-year old woman who lives in the area of Merbabu Mountain feels anxious because of

the bump in the front part of her neck. She has been feeling it for few months. Whenever

she does her activity, she feels her heart beats rapidly. She also feels that her hands are

shaking and her legs are swollen. The woman has two shildren. She looking for wood

everyday after her husband passed away 1 years ago. Because of anxious about her signs,

the woman goes to Primary Health care.

Discuss the case above using seven jumps!

Page 21: Buku Modul Endokrin 2010

SCENARIO 2

A Primary Health Care doctor found a 24 year old woman has a 120 cm hight and low IQ

when he had a job in Primary Health Care at Menoreh Mountain. The doctor got a part of

communities have a cretinism after he had got an epidemiology survey. A part of

communities who have a cretinism, they have thyroid enlargement grade III to. The doctor

looking for the cause of this disease, because the couple who has cretinism so they have a

cretinism child to.

Discuss the case above using seven jumps!

Page 22: Buku Modul Endokrin 2010

SCENARIO 3

References:

1. Dods, R.R., 1996. Diabetes Mellitus, in Clinical Chemistry Theory, Analysis, Correlation. Eds. Kapaln L.A, Pesce , J. eds. Mosby Inc, USA: 613-640

2. Sacks, D.B., 2001. Carbohydrats, In Tietz Fundamentals of Clinical Chemistry, eds. Burtis, C.A., Ashwood, E.R., 5th eds, W.B. Saunders Company, USA, 427-461

3. Foster, D.W., 2007. Diabetes Mellitus. In Harrison,s Principles of Internal Medicine, Eds, Fauci, Barunwald, Isselbacher et al, 14th ed, Mc. Graw Hill Companies, USA, 623-75

4. Hendromartono, 1998. Consensus on the Management of Diabetes Mellitus (Perkeni). In Surabaya Diabetes Update VI , Eds Tjokro[rawiro, A., Hendromartono, Sutjahjo, A., Tandra, H., Pranoto, A, 1-14

5. Kaplan, L.A., 1987. Laboratory Approaches. In Method’s in Clinical Chemistry, Eds Amadeo J., Kapaln, L.A., 94-96

Page 23: Buku Modul Endokrin 2010

SCENARIO 4

A married couple who has been married for 2 years goes to a family doctor because

the wife is not pregnant yet. The wife is anxious because since she was a young girl, her

period is irregular; sometimes she got her period once in three months. Her parents to push

aside her to take a baby as soon as. They don’t have brother or sister. A Family doctor gives

counseling for them.

Discuss the case above using seven jumps.

Page 24: Buku Modul Endokrin 2010

SCENARIO IN ENGLISH

A 35-year old woman presents to he physician for the first time at 10 weeks

gestational age. She is well and reports no problem. Her first child was delivered vaginally

without complications and weighted 4500 g.

Discuss the case above using seven jumps.

Page 25: Buku Modul Endokrin 2010

GUIDANCE OF

SKILL’S LABORATORY

BLOCK OF ENDOCRINE

Contributrs

dr. Tri Wahyuliati, MKes, SpS

dr. Denny Prakoso

dr. Agus Widyatmoko, MKes, SpPD

dr. Sri Sundari, MKes

Page 26: Buku Modul Endokrin 2010

PRACTICAL SIDES OF MANAGEMENT OF

DIABETES MELLITUS IN A FAMILY

General Objective:

Students understand the practical sides of Management of DM in a family covering

DM diet, leg treatment of DM sufferers, independent examination of blood glucose and,

injection techniques of insulin pen.

Specific Objectives:

1. Students are able to count calories needs of DM patients.

2. Students are able to write down need substitutes on DM leaflet.

3. Students are able to provide education on material substitutes with leaflet and meals

models.

4. Students are able to provide diet education in relation with the condition of normal

body organs.

5. Students are able to demonstrate legs exercise on DM sufferers.

6. Students are able to show any types of insulin and insulin injection tools.

7. Students are able to conduct and provide education on how to inject insulin pen.

8. Students are able to conduct and provide education on the importance, objectives

and ways of blood glucose examination.

DIABETES MELLITUS DIET

Objective: adjust the meals with body ability to use them, so that the sufferers reach

normal organs condition and are able to do daily activities like usual.

Requirements:

1. The amount of calories is determined by age, sex, body height and weight,

activities, body temperature, metabolic abnormality.

2. The amount of carbohydrates is in line with body ability to use it while pure sugar is

not permitted.

3. Proteins, minerals and vitamins are sufficient in food.

4. Food giving is in accordance with types of medicine given. if tablets or injection RI

3x a day are given, meals are given 3x a day; if given PZI, meals are given 4 x a day

in relatively same amount. Snacks at 10.00 and 21.00 o’clock are taken from the

portions of morning and afternoon meals.

Page 27: Buku Modul Endokrin 2010

Diet Types and Giving Indication

As a guideline, 8 diets of DM are applied:

Diet Type Calorie Protein Fat Carbohydrate

g g g

I 1100 50 30 160

II 1300 55 35 195

III 1500 60 40 225

IV 1700 65 45 260

V 1900 70 50 300

VI 2100 75 55 325

VII 2300 80 60 350

VIII 2500 85 65 390

Diet I to III are given to too fat sufferers.

Diet IV to V are given to the sufferers with normal body weight.

Diet VI to VIII are given to thin sufferers, juvenile diabetes) or diabetes with

complications.

KNOWING YOUR OWN CALORIE NEED

NAME : _______________________________________

DATA

Height : ………… cm → Ideal Body Weight = 90% (Height – 100) Kg = ……… Kg (a)

(Women → Height < 150 cm, Man → Height < 160 cm =

Ideal Body Weight = (Height (cm) – 100) Kg = ………. Kg

Actual Body Weight = …………… Kg → Overweight / Underweight / normal weight

Sex → Man / Woman

Basal Calorie = ……… Calorie (Man 30 cal/kg, Woman 25 cal/kg) (b)

Activity → Sedentary / Mild

Age = …………………… year

CALORIE COUNTING

Basal Calorie = a x b  = ……….. x …………  = ………… Calorie (c) 

Correction →

Page 28: Buku Modul Endokrin 2010

Age > 40 year → -5 % x (c)  = -5 % x ………….  = …………….. Calorie

Activity = Sedentary = + 20 % x (c) = + 20 % x ………….  = + ……………Calorie

Mild = + 30% x (c) = + 30 % x ………….  = + .………….. Calorie

Body Weight =

- Overweight = - 20 % x (c)  = - 20 % x ………….  = - .……….…. Calorie

- Underweight = + 20% x (c)  = + 20 % x …………  = + ….……….. Calorie

                                Total Requirement  = ……………. .Calorie

                                Diet → DM = …………….. Calorie

Page 29: Buku Modul Endokrin 2010

DIABETES DIET STANDARD (in Food Exchange)

ENERGY Time 1100 1300 1500 1700 1900 2100 2300 2500

Exchanges Breakfast                   Rice 1/2 1/2 1 1 1 1/2 1 1/2 1 1/2 2 Meat 1 1 1 1 1 1 1 1 Tempe     1/2 1/2 1/2 1 1 1 Vegetable                 A As you like B 1 1 1 1 1 1 1 1 Fruit 1 1 1 1 1 1 1 1 Fat 1 1 1 1 1 1 1 1                   10,00                                   Fruit 1 1 1 1 1 1 1 1 Milk                 Lunch                   Rice 1 1 1/2 2 2 2 1/2 3 3 3 Fish 1 1 1 1 1 1 1 1 Tempe 1 1 1 1 1 1 1 2 Vegetable                 -A As you like B 1 1 1 1 1 1 1 1 Fruit 1 1 1 1 1 1 1 1 Fat 1 1 1 1 2 3 3 3                   16,00                                   Fruit 1 1 1 1 1 1 1 1               1 1 Dinner                                   Rice 1 1 1 1/2 2 2 2 1/2 3 3 1/2 Fish 1 1 1 1 1 1 1 1 Tempe 1 1 1 1 1 1 1 2 Vegetables                 A As you like B 1 1 1 1 1 1 1 1 Fruit 1 1 1 1 1 1 1 1 Fat 1 2 2 2 3 3 3 3                 

Page 30: Buku Modul Endokrin 2010

EXCHANGE LISTS

For Meal Planning Dietary Department

And

Diabetes and Lipid Center

Dr. Cipto Mangunkusumo Hospital

Jakarta

What are exchange lists?

The 8 exchange lists help make your meal plan work. Foods are grouped together on a list because every food on a list has about the same amount of carbohydrate, protein, fat, and calories. In the amounts given, all the food on a list can be exchanged or traded for any other foods on the same list. Using the exchange lists and following your meal plan will provide you with a great variety of food choices and will control the distribution of calories, carbohydrate, protein and fat throughout the day.

Measurement of the food.

1 Tablespoon (Tbs.)  = 10 ml

1 Teaspoon (Tsp.) = 3 ml

1 Glass (Glass)  = 240 ml

1 Cup (C)  = 240 ml

*) HHM : House Hold Measurement

List 1 : STARCH / RICE

      Each item in this list contains approximately 40 grams of carbohydrate, 4 grams protein, a trace offat, and 175 calories.

FOOD HHM*) Gram     Biscuit

Bread (white)

Cassava

Cassava (flour)

Corn flour

Crackers

Elephant ear

Oat meal

Mung bean starch

4

3 slices

1 medium

8 Tbs.

10 Tbs.

5

1 medium

5 ½ Tbs.

10 Tbs.

40

70

120

50

50

50

125

45

50

Page 31: Buku Modul Endokrin 2010

Macaroni

Noodle (dry)

Noodle (cooked)

Potato

Rice (cooked)

Rice Noodle

Rice Grueal

Rice flour

Sago

Sweet Potato

Wheat flour

½ glass

1 glass

2 glasses

2 medium

¾ glass

½ cup

2 glasses

8 Tbs.

8 Tbs.

1 medium

5 Tbs.

50

50

200

210

100

50

400

50

50

135

50

List 2 : MEAT EXCHANGE

1. Low Fat

      Each item in this list contains approximately 7 gram of protein, 2 grams of fat, and 50 calories.

       FOOD HHM*) Gram     Blood cake

Buffalo no fat

Chicken no skin

Fish

Salted fish

Small fish

Tripe

1 piece

1 piece

1 piece

1 medium

1 small

1 Tbs.

1 piece

35

35

40

40

15

20

40

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1. Medium Fat

      Each item in this list contains approximately 7 grams of protein, 5 grams of fat and 75 calories.

       FOOD HHM*) Gram     Beef

Beef liver

Brain

Egg

Chicken livers

Duck egg

Intes

Goat meat

Meat balls

Shrimp

1 piece

1 piece

1 piece

1 medium

1 piece

1 medium

1 piece

1 piece

10 medium

5 medium

35

35

65

55

30

55

50

40

170

351. High Fat

      Each item in this list contains approximately 7 grams of protein, 13 grams of fat and 150 calories.

       FOOD HHM*) Gram     Chicken with skin

Egg yolk

Corned beef

Duck meat

Pork

Sausage

1 medium

4 medium

3 Tbs.

1 piece

1 piece

2 small pieces

55

45

45

45

50

50

list 3 : BEAN & NUTS

Page 33: Buku Modul Endokrin 2010

Each item in this list contains approximately 7 grams of carbohydrate, 5 grams of protein, 3 grams of fat and 75 calories.       FOOD HHM*) Gram     Cow peas

Mung bean

Fermented peanut cake

Peanuts

Peanut butter

Red Kidney beans

Soya bean

Soybean curd

Soy milk powder

Tempeh

2 Tbs.

2 Tbs.

2 small pieces

2 Tbs.

1 Tbs.

2 Tbs.

2 ½ Tbs.

1 piece

2 ½ Tbs.

2 pieces

20

20

40

15

15

20

25

110

185

50

List IV : VEGETABLES1. Vegetables A exchanges

Negligible Carbohydrate Protein, Fat and calories.

Calabash

Chinese radish

Cucumber

Lettuce

Mushroom

Ridge gourd

Tomatoes

Water crush

Wax gourd

1. Vegetables B exchanges

One exchange (1 cup cooked, drained) equal 5 grams of carbohydrate, 1 gram of protein and 25 calories.

Bamboo shoot

Beef

Bitter ground

Broccoli

Cabbages

Caisin

Goa bean

Mung bean sprouts

Inflorescence of banana

Yard long beans

Mustard greens

Papaya baby

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Carrot

Cauliflower

Chajola

Corn baby

Eggplant

Squash pumpkin

Swamp cabbages

Spinach

String beans

1. Vegetables C exchanges

One exchange (1 cup cooked, drained) equals 10 grams of carbohydrate, 3 grams of protein and 50 calories.

Belinjo

Belinjo leaves

Bread fruit

Cassava leaves

Elephants ear leaves

Garden peas

Papaya leaves

Red spinach

Soybean sprout

Young jack fruit

List V : FRUITS & SUGAR

Each item in this list contains approximately 12 grams of carbohydrate and 50 calories.

       FOOD HHM*) Gram     Apple

Banana

Carambola

Grapes

Guava

Honey

Jack fruit

Dates

Lanzon

Lychee

Malay rose apple

1 medium

1

1 big

20

1 big

1 Tbs.

3

3

16

10

1 small

85

50

140

165

100

15

45

15

80

75

110

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Mango

Rock Melon

Papaya

Peach

Pineapple

Rambootan

Soursop

Sapodillas

Spanish plum

Sweet orange

Sugar

Watermelon

Watery rose apple

¾

1 piece

1 piece

1 small

¼

8

½ glass

1

2

2

1 Tbs.

1

2 big

90

190

110

115

95

75

60

55

120

110

10

180

110

List VI : M I L K

Non-Fat Milk

    Each item in this list contains about 10 grams of carbohydrate, 7 grams of protein and 75 calories.

     FOOD HHM*) Gram     Skim milk (powder)

Skim milk

Yogurt non fat

4 Tbs.

1 cup

2/3 cup

20

200

1201. Low fat milk

    Each item in this list contains about 10 grams of carbohydrate, 6 grams of fat, 7 grams of protein, and 125 calories.

     FOOD HHM*) Gram     Cheese

Goat milk

1 small

¾ cup

35

165

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Cows milk

Unsweetened evaporated milk

Yogurt non fat

1 cup

½ cup

1 cup

200

100

200

1. High milk

    Each item in this list contains about 10 grams of carbohydrate, 10 grams of fat, 7 grams of protein and 150 calories.

     FOOD HHM*) Gram     Buffalo milk

Whole milk

½ cup

6 Tbs.

100

30       List VII : F A T S

      Each item in this list contains 5 grams of fat and 50 calories.

1. Unsaturated fat

       FOOD HHM*) Gram     Almond

Avocado

Corn margarine

Corn oil

Peanuts oil

Soy bean oil

Sun flower oil

Olive oil

7

½ big

1 Tsp.

1 Tsp.

1 Tsp.

1 Tsp.

1 Tsp.

1 Tsp.

25

60

5

5

5

5

5

52. Saturated fat

       FOOD HHM*) Gram     Butter

Coconut

1 Tbs.

1

15

15

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Coconut milk

Coconut oil

Coconut shredded

Palm oil

Bacon

1/3 cup

1 Tsp.

2 ½ Tbs.

1 Tsp.

1 Slice

40

5

15

5

5       List VIII : NEGLIGIBLE CALORIE FOODAlternative sugar: aspartame, saccharin Bouillon (Without fat) Coffee / Tea Gelatin

Mineral water Soybean sauce Vinegar spices

SCENARIO 1

A 50 –year-old man with body weight of 80 kg and body height of 160 cm working

as a high school teacher went to ICU due to feeling weak. The man has been diagnosed as

suffering from DM since 5 years ago and conduct irregular control. Since ½ month ago,

there has been a wet wound on his leg. Medication has been given in Community Health

Center (puskesmas) but it has not been recovered yet.

SCENARIO 2

An 18-year-old swimming athlete weighed 50 kg, height 160 cm has been

diagnosed as suffering from DM since 1 year ago. The athlete has to plan a good diet to

support his carrier. Due to ASEAN championship, the athlete actively rehearses twice a

day, morning and afternoon. Each exercise takes 2 hours. Plan a well-arranged diet for the

athlete correctly.

Page 38: Buku Modul Endokrin 2010

LEG TREATMENT

Things to know:

- Diabetic leg problems

- All tool types of leg treatment.

- Ways of cleaning legs

- Ways of cutting toenails

- Choosing footwear

- Things endangering legs that should be avoided

- Legs exercise

- Ways of choosing shoes / requirements of good shoes for DM sufferers

Example of Leg Exercise

Initial Position:

Sit down straight up on a bench and do not

lean

1st exercise (10 times)

1. Move the toes from both legs like

pawing

2. Straighten them back

2nd exercise (10 times)

1. Lift the toe tips, heels remain on

floor

2. Put down the toe tips, then lift the

heels and then put down back again.

Page 39: Buku Modul Endokrin 2010

3rd exercise (10 times)

1. Lift toe tips of your both feet.

2. Spin your ankle sideways.

3. Put them down on the floor and

move to the central side.

4th exercise (10 times)

1. Lift your both heels.

2. Spin your heels sideways.

3. Put them down again on the floor

and move to the central side.

5th exercise (each leg 10 times)

1. Lift one of the knees

2. Straighten your legs.

3. Move your toes forwards.

4. Put your leg down again, left and

right legs take turns.

6th exercise (each leg 10 times)

1. Straighten one of your legs on the

floor.

2. Lift the leg.

3. Move the toe tips towards your face.

Put down back the hell on the floor

7th exercise (10 times)

Like the prior exercise (exercise 6) but this

time, with both legs at the same time.

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8th exercise (10 times)

1. Lift your both legs, straighten and

hold on the position.

2. Move your ankles forwards and

backwards.

9th exercise (each leg 10 times)

1. Straighten one of your legs and lift

it.

2. Spin the ankle.

3. Write on the air number 0 – 10 using

your leg.

10th exercise (once)

1. A piece of newspaper folded in the

form of a ball using feet. Then make

it as before folded using both feet

and afterwards, tear it up.

2. Collect the torn pieces with both feet

and put on other piece of newspaper.

Finally, wrap all in the form of a ball

with your both feet.

WORK PAGE

I. Students conduct practice of leg exercise for DM sufferers.

II. Students conduct counseling for DM diet through the following scenarios:

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CHECK LIST

EDUCATION ON DM DIET

ACTIVITIES SCORE

0 1 2

1 Explain the diet objectives in DM management.      

2 Count calorie needs of DM client diet:      

A. Count the ideal body weight      

B. Determine client’s normal/under/over weight      

C. Count the calorie basal total relating to sex.

D. Count the basal calorie correction (regarding the age,

activity, and body weight)

3 Implement the result of calorie counting (no. 2d)      

A. Into the table of diabetic standard diet (in food

exchange)

     

B. To arrange menu example relating to food exchange

table (exchange list) relating to the result of 3a.

     

4 Explain about the needs of pair/family support towards

the success of DM diet.

TOTAL SCORE      

Page 42: Buku Modul Endokrin 2010

EXAMINATION OF BLOOD GLUCOSE

Various blood glucose examination tools (in line with those available in exercise place) :

- Accutrend (common, mini, GC)

- Adbantage

- Glucometer – 4

- Glucometer – Gx

- One touch – basic

- One touch II

- Surestep

Tools/ materials:

- Autoclix/vaccinostyle

- Alcohol 70%

- Cotton

- Blood glucose examination tools and strip test ( test carik)

How to take the blood:

1. Clean patient’s ring finger using cotton that has been give alcohol 70%, dry it.

2. Prick the ring finger tip using vaccinostyle vertically, fast and not deep.

3. after blood comes out from the finger, sweep it with dry sterililzed cotton.

4. Push the fingertip outward.

5. Turn the hand up side down. Allow the blood drop alittle.

6. Drop the blood on the strip test.

7. Conduct the examination procedure in line with the instruction of each testing tools.

How to use glucometer

1. If the strip test picture appears, put the strip test in

2. Touch the blood drop until filling the central test area.

3. Read the blood glucose that appears.

1. A piece of newspaper folded in the form of a ball using feet. Then make it as before

folded using both feet and afterwards, tear it up.

2. Collect the torn pieces with both feet and put on other piece of newspaper. Finally,

wrap all in the form of a ball with your both feet.

Page 43: Buku Modul Endokrin 2010

INSULIN AND WAYS TO USE IT

Things students should know:

- Introduction to any types of insulin

- Introduction to insulin injection tools: various injection tools with various scale

(injection tool BD, Terumo 1 cc and ½ CC)

Novo – pen II (novo Nordisk)

Novo – pen III (Novo Nordisk)

medijector

BD – pen (Becton Dickinson)

Preparation:

- Injection location

- Preparing insulin in accordance with the dosage, ways of mixing insulin.

- Sterilize location and tools.

- Cleaning the tools.

- Storing insulin and the tools.

- Self-performed injection

- Complication of insulin injection

Injection techniques for people with diabetes

Tools required:

- Insulin

- Injection tools with the needle

- Disinfectants

- Cotton

- Hand-washing container

Patients’ preparation:

- Fasting begins at night, at least 8 hours, last meal at 20.00 – 22.00 pm

- If thirsty in the morning, patients are allowed to drink fresh water or tea with no

sugar, do not take any medicine in the morning.

- After finishing taking fasting blood, medicine-taking or insulin injection may take

place two hours post pandrial.

- Patients eat some diets usually taken.

- After exactly 2 hours, blood is taken for examination.

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(Gloves are used when injecting others. Gloves are useful as self-protection against other

people’s body liquid, so that sterilization is not required. As a result, it can be used

repeatedly).

Injection procedures:

1.Prepare injection

equipments and avoid

touching the needle.

2. If using insulin

suspension, move the

bottle up side down so that

the suspension will mix

perfectly and also sterilize

the rubber cap with

disinfectant.

3. Take some air into

the injection tube with

the same volume as the

insulin amount to be

injected.

Slowly stick the needle into

the vial insulin with vertical

position parallel with eyes.

Insulin goes into injection

equipment, knock slowly

on the injection equipment

so that the appearing air

bubbles are gone.

Store back the

exceeding insulin into

vial insulin so that the

sucked air is also

away.

Page 45: Buku Modul Endokrin 2010

Ways of injecting: needle’s

position may be at 45

degrees or vertical.

Inject it slowly, then

push with finger on the

area where injection

took place after the

needle was drawn away.

To avoid injury on the

skin tissues due to the

repeated injection in one

area, it is advised that

each injection moves on

different areas.

WORK PAGE

I. Students conduct blood glucose examination.

II. Students conduct insulin injection.

CHECK LIST

EDUCATION ON HOW TO INJECT INSULIN PEN

ACTIVITIES SCORE

0 1 2

1 Explain how to put insulin tube on pen.      

2 Explain how to put on pen needle.      

3 Explain how to arrange dosage/unit required by the

equipment.

     

4 Explain how to conduct disinfectanization on the

injection area.

     

5 Explain how to conduct injection.      

6 Explain the locations that injection may take place.      

7 Explain how to recognize the symptoms of complication

due to injection (signs of infections and hypoglycemia)

     

TOTAL SCORE      

Page 46: Buku Modul Endokrin 2010

ANAMNESIS OF THE BLOCK

GENERAL OBJECTIVES:

Students are able to conduct anamnesis on cases of endocrine diseases.

SPECIFIC OBJECTIVES:

1. Students are able to conduct anamnesis of main complaints and explore well and

properly on cases of endocrine diseases.

2. Students are able to conduct anamnesis about recent diseases history and explore

well and properly on cases of endocrine diseases.

3. Students are able to conduct anamnesis about past diseases history and explore well

and properly on cases of endocrine diseases.

4. Students are able to conduct anamnesis about family and socio culture history and

explore well and properly on cases of endocrine diseases.

5. Students are able to summarize well and properly the problems faced by patients

6. Students are able to determine properly the possibility of comparing diagnosis on

the problems faced by patients.

ASSIGNMENT:

Each big group is divided into small groups of 2-3 people. One person plays the role of a

doctor, one plays as a patient and the other one is the observer. This assignment is done

exchangeably. Conduct the anamnesis for cases like the following:

SCENARIO 1

A 52-year-old woman who live in Merbabu mountain area feels upset due to the emergence

of a bump on the front area of her neck since last few months. Each time she wants to do

her activity, she also feels harder heart beats. She also feels that her hands are trembling

and she has swollen legs.

SCENARIO 2

A 32-year-old woman, who was just married, conducts a complete laboratory examination

for general check-up. She really wants to have a baby because she feels that she is now

turning quite old. Her body weight is 65 kg and with body weight of 155 cm. Lately she has

been complaining of feeling sleepy easily and often urinate. There are members of her

family who have suffered from the same complaint.

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SCENARIO 3

A married couple that has been married for 6 months sees a doctor because the wife is not

pregnant yet. The wife feels upset due to her irregular menstruation since she was young,

even, he has not had the menstruation in three months long.

SCENARIO 4

A 48-year-old woman, experiencing premenaupause is interested to conduct hormone

replacement therapy (HRT) to prevent osteoporosis. She feels hot on her face and sick with

intermittent sharp pain on her back. She has been a smoker since 20 years ago and has a

family history of breast cancer and heart disease.

CHECK LIST FOR ANAMNESIS

NO ASPECTS TO BE SCOREDSCORE

0 1 2 3I Maintaining courtesy

1. Say salaam at the beginning of interview, ask to sit

down

2. Ask the identity

3. Ask about the main complaints

Nice, sympathetic and friendly appearance

II Able to collect needed information:

4. Use understandable language to the respondents.

a. Interview is not impressed as investigating or

interrogating

b. Exploring the main complaints

Ask about RPS

a. Ask about patient’s other complaints

b. Explore patient’s other complaints

c. Ask about RPD

d. Ask about personal history

e. Ask RPK

f. Conduct cross-checking to ensure patient’s answers

III g. Be neutral with patients

h. Able to take note clearly

IV Possess interviewing appearance properly

i. Work consistency and discipline

j. Polite and sympathetic

V Able to summarize patient’s problems well and properly

a. Able to draw conclusion about recent condition.

Page 48: Buku Modul Endokrin 2010

b. Able to determine the opportunity of comparing

diagnosis on diseases suffered.

Note:

0 : not done

1 : done but less properly

2 : done properly

3 : done properly and perfectly

Page 49: Buku Modul Endokrin 2010

Patient education of Diabetes Mellitus

Role Play:Conduct a role-play in running skill of patient educating about Diabetes Mellitus (DM) completely with your friend. Make a couple of 2 persons by turns to play role as: Doctor who will conduct patient educating Patient DM sufferer The student who is acting as a patient is also act as the observer to evaluate the doctor by using List of

Anamnesis Observation hereunder.Good Luck!

The Patient’s Guidance: You act as a patient who has been diagnosed as DM Evaluate your friend who is acting as the doctor in conducting patient educating about DM based on the

observation list.

The Doctor’s Guidance: Educate about DM comprehensively to the patient; if necessary, you may use leaflet and poster about DM. Do not forget to pay attention the verbal and non-verbal communiation

Observation List of Patient Educating about Diabetes Mellitus

No Assessed Aspect Parameter Score0 1 2 3

1. To create communication by greeting the patient and introducing himself, and also make a comfortable environment for the patient.

“Assalamu’alaikum, Mr. Ali, I’m Budi, school of medicine student/ young doctor.. I’m a part of medical team who will treat you.”

Recite it naturally and do not make a formal impression

2. To check the patient identity Name Age Address Work Marital status

3. To ask the patient understanding about DM

Use open-ended questions“What do you know about your disease, sir?”

4.

4. To explain the general description about DM

Use daily communication, not medical one

5. To explain about DM sympthom Childhood disease

6. To ask about the history of family disease (RPK)

Disease in his family Death, the cause and age of die time of his family

member Draw it into FAMILY GENOGRAM

7. To ask about history of social personal ADULT:* Education* Work environment* Home/family/mariage environment* Habit/lifestyle (diet, physical activity, smoking, alcohol, drug,

etc) CHILDREN:

* History of mother pregnancy (ANC, medication, etc)* History of mother delivery* History of prenatal* History of nutrition (ASI, etc)* History of immunization* History of growth development

8. Anamnesis system (review system) Skin Head Eye Ear Nose & sinus Throat (mouth& faring) Neck Breast Lungs Heart Digestion Ureter Genital: male / female Vein perifer Muscle & bone Psychological Nerve Blood Endocrine

9. To embrace the gained history of the patient

To embrace the finding of history of yang retell it to the patient To give a chance the patient to check the reality

10. Non-verbal communication aspects Eye contact maintaining

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Friendly expression, smile Open ended gesture, to face the patient with 45 degree Clear voice articulation & prompt intonation Clean & neat appearance

11. Aspects of emphaty and skill of active hearing

Content reflection Feel reflection

Explanation:0 = Not conducted 1 = Conducted but improperly 2 = Conducted properly 3 = Conducted properly and perfect

Observation List of Genogram Family MakingAnd Family Life ciclus Identification

No Assessed Aspects Parameter CheckNo(0)

Yes (1)

1. Made of minimum 3 generations

2. The symbol made for male and female family member and marital status

3. The first birth of each generation is located at the most left and followed by the next birth at the right side.

4. The family name is on the top

5. Name and age are under each symbol

6. The patient is identified with an arrow

7. Writing down the date of diagram making

8. Taking a note about health problems of each family member (into symbols with explanation)

9. Taking a note about important dates in family history: Death, birth (age), marriage, divorce

10. Identifying the family member who live in the same house to identify family type of the patient:nuclear family; extended family, etc

11. Taking a note about name and main role /function of the family member:B = Breadwinner D = Decision maker C = CaregiverPN=Pencari nafkah PK=Pembuat keputusan POS= Pengasuh OS

12. Explanations of all the used symbols

13 Cyclus identification of family life:

TOTAL

EXAMINE OF THE THYROID GLAND

Page 51: Buku Modul Endokrin 2010

GENERAL OBJECTIVES:

Students are able to examine the thyroid gland .

SPECIFIC OBJECTIVES:

1. Students are able to examine of the normal thyroid gland.

2. Students are able to examine of the abnormal thyroid gland.

3. Students are able to interpret the result of the examine thyroid gland.

EXAMINE PROCEDURE:

1 . Inspect.

a.Ask the patient to bend the head back a bit.

b. Inspect the region below the cricoid cartilage for the thyroid gland.

c.Then ask the patient to take a sip from a glass of water, again extend the neck and

swallow.

d. Watch the movement of the thyroid gland, nothing its countour and symmetry.

An enlarged thyroid gland, and also many normal ones, may be visible even

before swallowing. An enlarged thyroid gland is called a goiter

2 Palpate.

Palpation is probably best done from behind the patient. Because you cannot see what

you are doing, you may initially find this position awkward. Orient yourself first to the

patient’s cricoid cartilage- the basic landmark for the examination. Feelings any visible

thyroid tissue form in front of the patient first may also give you guidance

a. from behind, place the fingers of both hands on the patient’s neck so that the

index fingers are just below the cricoid.

b. The patient’s neck should be extended, but not far enough to tighten the

muscles

c. As the patient’s swallows the thyroid isthmus should rise under your fingers.

Page 52: Buku Modul Endokrin 2010

d. By rotating your fingers slightly downward and laterally, feel as much of the

lateral lobes as possible, including their lower borders.

e. During both maneuvers the patient should sip water as necessary to swallow

as you repeat your palpation.

Note the size, shape, and concistency of the gland and identify any nodules

or tenderness.

The anterior surface of a lateral lobe is approximately the same size as distal

phalax of the thumb, its consistency is somewhat rubbery

3. Auscultate

If the thyroid gland is enlarged, listen over the lateral lobes with a stethoscope to

detect a bruit ( a sound similar to a cardiac murmur but of noncardiac origin).

A localized systolic or continous bruit may be beard in hyperthyroidism.

CHECK LIST FOR THYROID EXAMINATION

NO ASPECTS TO BE SCOREDSCORE

0 1 2 3I Maintaining courtesy

a. Say salaam at the beginning of interview, ask the

objective of examination

II A. Inspect

1. Ajust patient’’s neck for extention

2. Inspect lower os cricoid to examine the glandula

thyroidea and report the result of the examination

B. Palpate

1. Examiner stands behind the patient’s

2.Put his two fingers below os cricoid, patients is asked to

swallow

Page 53: Buku Modul Endokrin 2010

3. Examiner checks thyroid and reports the result of

palpate examination.

e. When enlargment happens, auscultation is done.

Examiner can put stethoscope on lobus lateralis glandula

thyroidea and report the bruit.

A. Examiner cincludes the result of the examination in

general.

Note:

0 : not done

1 : done but less properly

2 : done properly

3 : done properly and perfectly

Page 54: Buku Modul Endokrin 2010

GUIDELINES FOR PRACTICUM

BLOCK OF ENDOCRINE

Contributor:

dr. Agus Suharto, SpPA

ENDOCRINAL SYSTEM

Page 55: Buku Modul Endokrin 2010

I. ENDOCRINAL SYSTEM GENERAL DESCRIPTION

A. Component system

Endocrinal system in the body consists of some endocrinal organs, those are:

- adenohipofisis

- thyroid gland

- adrenal gland

- endocrine tissue in exocrine gland, such as insula pancreatic

- and some endocrine cells with “DNES” function in the alimentary canal mucosa

B. Endocrine origin

Endocrine gland is a gland that doesn’t have exit canal (ductus excretorius), it develops

as epithel surface invaginasi, such as oral ectoderm or colon endoderm, which finally

released, separated from the main epithel.

C. MICROSCOPIC STRUCTURE

Endocrine gland is specifically formed by lots of sekretorik cells which are arranged as

chorda, gathered or convex follicle which directly connects with blood capillary or

sinusoid.

D. SECRETION

Endocrine cells release their secretion, as hormone specially, into the blood circulation.

Other substances are not released into blood circulation but they are released into a

canal (ductus) (those substances are enzyme and albumin serum), but they are also

considered as hormone secretion. Hormone is a molecule which influences on the

special arrangement on target cells, a tissue or organ which is located far away from the

gland’s location. Hormone, even in a small portion, can give dramatic and specific

effects and it can also directly or indirectly influence all tissues. There are so many

hormones that can keep the environment in balance. Hormone plays important roles in

controlling the carbohydrate, protein, and lipid metabolism; mineral and water balance

in body liquid; growth; sexual function and body shape differences in terms of sex and

behavior, character or temper and emotion. There are two kinds of hormones, those are:

1. Peptide Hormone

Protein, glycoprotein, or short chain peptide hormones tie a special receptor in the

target cell surface. This kind of hormone sometimes stimulates the second

intracellular messenger production, such as Krebs cyclic (AMP cyclic) in the target

cell.

2. Steroid Hormone

Page 56: Buku Modul Endokrin 2010

Hormone that dissolves in lipid can easily go through target plasma cells and then

directly influences the cells’ function. This hormone binds in the special joint

protein in cytoplasm and nucleus.

E. NEUROENDOCRINE SYSTEM

There is a complex connection of function in the cells, tissue and body organ is

monitored and coordinated by two interconnected system i.e. nervous and endocrine

system. With the increasing of attention on these two systems, it is considered as single

system that is neuroendocrine system. One of its glands is called “master gland”

because of its capability in controlling endocrine gland and nervous system. The

secretoric activities of these two parts of this hipofisis are neurohipofisis and

adenohipofisis, both are controlled by other part of the brain which is located near to

each other, that is hypothalamus.

The hypothalamus activities are controlled by:

1. Nerves connection with other parts of nervous system, and

2. Negative feedback from hormone that is produced by hipofisis target cells.

Diseases occur are related with hipofisis, especially as the result of hipofisis

hormone’s hyper-secretion or hypo-secretion; this hyper or hypo secretion is caused

by hipofisis, target organs or hypothalamus damage.

II. GENERAL ORGANIZATION AND HIPOFISIS EMBRYONIC ORIGIN

There are two parts of hipofisis those are:

Adenohipofisis, and

Neurohipofisis,

These two parts are difference on their origins, structure and function.

A. ADENOHIPOFISIS

1. Origin

It is rom evaginasi go up to ectoderm which layers the primitive mouth cavity. This

part makes contact and then intact with neurohipofisis that grows down.

2. General structure

Adenohipofisis consists of glandular capillary gully which is separated from one

another by a big amount of sinusoidal capillary from plexus capillary secundaricus.

Adenohipofisis does not directly get nerve from hypothalamic nerves.

3. Subdivision

Adenohipofisis is divided in to:

Pars distalis (pars anterior), which is the biggest part.

Pars tuberalis, which is an expansion toward superior area from pars distalis,

forming the “hand” part which is an infundibulum partial cover (neurohipofisis)

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Pars intermedia, a ribbon like part of hypofisis slender tissue which borders with

neurohipofisis

B. NEUROHIPOFISIS

1. Origin

Neurohipofisis is appeared as downward growth of ectoderm neural hypothalamus

and because of it; it becomes a part of the brain.

2. General structure

Neurohipofisis consists of a big amount of axon. The axon comes from nervous cell

body especially in supraopticus nucleus and paraventricularis hypothalamus

nucleus.

3. Subdivision

Neurohipofisis is divided into infundibulum which consists of “infundibular stem”

(“neural stalk”) and eminentia mediana. This “infundibular stem” brings axon from

hypothalamus to pars nervosa, it also contains capillary from plexus capillaries

primaries. Eminentia mediana from tuber cinerium forms hypothalamus floor. Pars

nervosa (infundibularis processus) is an expansion of neurohipofisis lobus; this pars

nervosa contains axon terminal and some big blood capillaries.

III. ADENOHIPOFISIS

Every secretor cell in adenohipofisis synthesizes and stores on of the following

hormones:

follicle-stimulating hormone (FSH)

thyrotropin (thyroid stimulating hormone : TSH)

luteinizing hormone (LH)

adrenocorticotropic hormoe (ACTH)

growth hormone (GH), and

prolactin

The secretion of those hormones, which control the activities of other glands, are

regulated or controlled by special “releasing” or “inhibiting” hormones which are

produced by hypothalamus and carried to adenohipofisis by blood in the hipofisis

portal system.

A. PARS DISTALIS

Consists of two cell groups, those are:

1. Chromophobus

This cell does not bind color, so it is in a pale color, looks transparent or white

in the tissue microscopic preparatory. There are three kinds of this

chromophobus cell, all of the three kinds are 50% epithel in the pars anterior;

the cells are:

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a. Non-secretoric cell which has not been differentiated, it might be a stem cell.

b. Cromofilic cell that some of it has been degranulated, which contains small

amount of granule, and

c. Foliker cell is a cromofob type cell which dominates in making stroma web

that supports other cell (cromofil). It’s a star-shaped cell (stelat) and can

have fagositic function.

2. Chromophylus

This hormone producer cromofil binds color tightly because there is a bug

amount of granule, where hormone is stacked or stores, in its cytoplasm. There

is a specific cell for every hormone. The cromofil cell has bigger size than

cromofob cell and it is divided into two classes, those are:

a. Acidophil

This cell is a simple protein producer, it is strongly painted with eosin and

orange G, but it isn’t painted with PAS. This cell stays in one group in the

edge of the organ; it has smaller size than basophile cell while its

sitoplasmic granule is bigger and in a bigger quantity. Acidophil cell

consists of two kinds of hormone producer cell; those are samototroys which

produces samototropin (growth hormone) and mammotrop cell which

produces prolactine. To remember hormones that are produced by acidophil

cell, the GPA (Growth hormone, Prolactine, and acidophil) abbreviation is

used.

b. Basophile

Basophile is painted with hematoksilin and other base colors and has PAS

positive character. The location of this cell is in the middle of the organ; it is

bigger than acidophil cell. This basophile cell consists of 3 kind of cell

which produces 4 kinds of hormones, those are:

Each cell from the two gonadotrops cells produces different

gonadotropin. One of the cells produces follicle stimulating hormone

(FSH); while the other cell produces luteinizing hormone (LH; it is also

known as interstitial cell-stimulating hormone = ICSH in men)

Kortikotrovik produces adrenocortitropin (ACTH).

Tipotropi produces thyroid-stimulating hormone (TSH)

B. PARS TUBERALIS

Pars tuberalis’ shape is like a ship’s chimney and is an upward expansion of pars

distalis which surrounds “infundibular stem”. The histological description is similar

to the pars distalis, but it mainly contains gonadotrops cells. Pars tuberalis is full of

blood capillary from plexus capillaries primaries of hipofiseal portal system.

C. PARS INTERMEDIA

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A pars intermedia looks like ribbon or adenohipofisis belt between pars distalis and

pars nervosa. It does not develop in human body. It contains Rathke’s cysts. This

Rathke’s cysts are small rooms with irregular shapes and contain colloid which is

covered with cuboids epithel. These cysts are the remains of Rathke’s pouch. Pars

intermedia also contains groups and basophile cell gullies or melantrops which

produce melanocyte-stimulating hormone (BMSH)

D. VASCULAR AND HIPOFISIS PORTAL SYSTEM

1. Plexus capillaries primaries

This plexus is located in the upper part of “infundibular stalk” = truncus

infundibularis and in the lower part of emenentia medianal widen into pars

tuberalis. These plexus capillaries get the blood from hypophysealis anterior and

posterior superior (from circulus Willisi) arteries and flow into portalis

hypophysealis vena.

2. Portalis hypophysealis vena

Small vena or venula is mainly located in the center and lower part of truncus

infundibularis and in the pars tuberalis. This portalis vena accepts blood from

plexus capillaries and is directly carried to plexus capillaries secundarius in the

pars distalis. Blood vessels carry blood directly from a certain plexus capillaries

to other plexus capillaries without returning to main circulation that is portal

vessel.

3. Secondary Plexus Capillaries

Plexus which is rich with full of holes capillaries is located in the whole part of

pars distalis; it goes also trough pars tuberalis and pars intermedia. In this

plexus, it is also found the connections between these capillaries and the

capillary which is located in pars nervosa. Capillaries which are located in gland

cell lines in the pars distalis, belong to this plexus, get blood directly from

portalis vena and arterial blood from hypophysealis anterior-superior. The blood

flows from inferior hypophysealis inferior into the internal jugulars vena.

E. RELEASING AND INHIBITING HYPOTHALAMUS HORMONES

This peptide hormone with light molecule is synthesized in the neuron

(neurosecretoric cell body) with nucleus in hypothalamus and released from its

terminal axon into primer capillaries plexus. That hormone flows through

hypophysealis portalis venula into secondary venous plexus. Then, it goes trough

the adenohipofisis to stimulate or hamper the release of hormone by acidophil and

basophile cells (endocrinocytus acidophilicus dan endocrinocytus basophilicus).

1. Releasing Hormone

Hormones that are included in this hormone are:

a. “Corticotrophin-releasing hormone” (CRH)

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It is a peptide hormone which consists of 41 amifio acids and is synthesized

in the paraventricularis nucleus and also spur the Corticotrophic/

Corticotrops cells to produce ACTH.

b. “Gonadotropin –releasing hormone” (GnRHI)

It consists of 10 kinds of amino acid, synthesized in the preopticus and

arcuatus nucleus; it spurs the gonadotropic/gonadotrops cell to stimulate the

release of FSH and LH hormones.

c. “Thyrotrophin-releasing hormone” (TRH)

It is a peptide hormone which consists of 3 amino acids, stimulates the

thyrotrophic/ thyrotrops to release TH (tirotrophin).

2. Inhibiting hormones

a. Somatostasin (GHIH = “Growth hormone-inhibiting hormone”)

It is a peptide hormone which consists of 14 amino acids; synthesized in the

suprachiasmaticus nucleus which inhibits somatotropic/somatotrops cells

which produce somatotropin (GH = “Growth Hormone”). This somatostatin

also inhibits the secretion of glucagons, insulin and other hormones related

to the digestive system (“gastrointestinal tract”)

b. Dopamine (“Prolactin-inhibiting hormone = PIH)

It is a neurotransmitter which is synthesized in the arcuatus nucleus which

inhibits the mamotropic/mamotrops to release prolactin.

F. SUMMARY OF ADENOHIPOFISIS HORMONES PRODUCTION

1. Neuron in nucleus in hypothalamus synthesizes inhibiting and releasing

hormones and packs them in neurosectorial vesicle.

2. Neuron carries this neurosecretoric vesicle downward into the

tuberoinfundibularus tractus axon and hypothalamohypophysealis tractus into

the axon terminal which surrounds primaries plexus capillaries.

3. Nervous or hormonal reciprocal stimulation from adenohipofisis target organ

causes this nerves stimulate the action-potential which releases correct

inhibiting and releasing hormones from axon terminal.

4. And then, inhibiting and releasing hormones go into the primaries capillaries

plexus and flows through portae vena to the secondary capillaries plexus.

5. In this secondary capillaries plexus, hormones ooze out from capillary lumen

through “windows” or holes (fenestratum) and stimulate or inhibit the releasing

of adenohypofisis hormones which is stored in it from acidophil and basophile

cells.

6. Adenohipofiseal hormone goes in through secondary capillaries plexus; and

then, leaves adenohipifisis through anterior-inferior hypophysealis vena into the

big circulation.

G. THE HISTOPHYSIOLOGIES OF ADENOHIPOFISIS HORMONES

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1. Somatotropin = GH = “growth hormone” (STH)

Somatrotopin is a protein with a small molecule, consists of 190 amino acids

and never has “target organ”, but it influences the cells in entire body, raises the

protein synthesis ratio. Another metabolic influence is raising the fat acid from

adipose tissue and lowering the ratio of glucose use. The most prominent

influence is the growth ratio of young animals. The absent of this hormone can

cause “pituitary dwarfism”. The excessive amount of this hormone can cause

“pituitary gigantism”. The overproduction of this hormone is caused by a tumor

in pars distalis in adulthood which causes acromegali, a typical condition which

is marked by disproportional/imbalance bone thickening.

2. Prolactine

It is a protein with molecule weighting 25.000 D and consists of 205 amino

acids. Its prime role is to stimulate the development of mammary and lactase

glands. During the pregnancy, the concentration of this hormone growths

rapidly, starting from the fifth week until aterm pregnancy.

3. Thyrotrophin (thyroid stimulating Hormone = TSH)

It is a glycoprotein hormone with molecule weighting approximately 2.8000 D.

This hormone holds tiroglobulin proteolysis and releases thyroid hormone to

blood. This hormone can also cause gland cells become hypertrophy and cause

the ratio of thyroid hormone increasing.

4. Gonadotropin: FSH and LH

The two hormones are produced by pars hipofisis hormone which is called

gonadotropis. FSH is a glycoprotein with molecule weighting about 30.000 D.

In women, this hormone undergoes the secretion circulation which goes up and

down every month. The increasing of this hormone stimulates the development

of some follicles in the ovarium as a preparation to one or two ovulation in the

middle of the cycle. For men, FSH plays an important role in the initiation of

spermatogenesis during the puberty period. The role of this hormone in

adolescence human in not clear but it seems it plays the roles in sertoli cell

(endocrinocytus interstitials) in the seminiferus tubules, stimulates the synthesis

of androgen hormone which binds protein. LH is a gicoprotein with molecule

weighting 26.000 D. In women, the function in the ovarium is to increase

estrogen hormone secretion by developing its follicles, and in the middle of the

cycle, it increases the LH hormone peak level. After ovulation, this hormone

causes differences in luten cells which creates luteum corpus. In men LH

hormone stimulates interstitial in testis, discharges testosterone which is

important in keeping the process of spermatogenesis.

5. Adrenokorticotropin = adrenokortikotrop hormone

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This hormone is included in polypeptide with 39 amino-acid chains, with

molecule weighting about 4.500 D. This hormone stimulates cortex of adrenal

gland to produce/discharge cortisol kortisol hormone.

IV. NEUROHIPOFISIS

Neurohipofisis has three structural components, those are;

A. NEUROSECRETORIC AXON CELL

Neurohypofisis contains lots of nervous fiber (axon) without myelin cover

(neurofibra non-myelinata). This axon comes from nervous cell body (corpus

neurocyti) which is mainly located in supraopticus nucleus and hypothalamic

paraventricularis nucleus. This axon spreads from both nucleuses to the hipofisis

nervosa, together forming hypophysealis hypothalamo tractus. This axon contains

granule neurosecretoric and show granule with neurosecret in big size, which is

called Herring bodies (corpusculum neurosecretorium accunulatum).

Neurosecretoric materials which are located in the granule are produced and packed

in those nucleuses.

1. Neurohipofisial Hormone

Neuron hypothalamus which is terminated in the neurohipofisis releases

oxytosin and anti-diuretic hormones, around blood capillaries in that hipofisis

part.

a. Oxytocin is a peptide with 9 amino acid chains, especially synthesizes by

hypothalamic paraventricularis nucleus. This hormone stimulates the breast

milk from mammae granule and stimulates the contraction of uterus’ smooth

muscle when copulation and child birth.

b. Antidiuretic hormone (ADH = arginine vasopressin)

It is a peptide which consists of 9 amino acids and is synthesized mainly by

cells in supraopticus nucleus. This hormone stimulates the reabsorbing of

water by ductus collectivus renalis.

2. Neurofisin as protein-binding which binds the two neurohipofisis hormones

3. ATP = Adenosin triphospate

B. PLEXUS CAPILLARIES FENESTRATUM

It surrounds the axon terminal. The blood capillaries accept the secretic products

and carried them to the big sirculation.

C. PITUICYTUS

Pituicytus is a glia cell with branches, and its taju surrounds and supports axon

without covering myelin.

D. SUMMARY OF NEUROHIPOFIS HORMONE PRODUCTION

1. Each Neuron in supraopticus nucleus synthesizes ADH and oxytocin hormones

2. Its neuron packs those two hormones with neurofisin and ATP in the

neurosecretoric vesicle.

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3. The vesicles are transported by neuron with its axon faces downward from

tractus hypothalamohypophysealis into axon terminal among the blood

capillaries in nervosa pars.

4. In the right stimulation, neurosecretic cells arouse the action potential along its

axons, causing exocytose with vesicle in terminal axon.

GLANDULE ADRENALIS

1. GENERAL DESCRIPTION OF HORMONAL SECRETORIC CELLS =

endocrinocytus: structure-function relation.

The knowledge about endocrinocytus structure can give a prediction or presumption

about ultra endocrinocytus which produces steroid hormones that contain more

reticulum endoplasmicum nongranulosum than reticulum endoplasmicum granulosum;

whereas endocrinocytus which produces peptide hormone contains a big amount of

reticulum endoplasmicum granulosum.

2. GLANDULE ADRENALIS = GLANDULE SUPRARENALIS

It forms a hat on top of renal (kidney). These glands are divided into two main

categories according to their origin, structure and function, those are:

A. ADRENAL CORTEX

1. Embryonic origin

Adrenal cortex comes from mesoderm coelom intermedia

2. Structure of mature glands

Gland cell in adrenal cortex has a special structure as a steroid hormone producer.

Adrenal cortex is divided into three layers, those are:

a. Glomerulosa Zone

Glomerulosa Zone is the outer layer of adrenal gland and it is located right

under the capsule and occupies 15% of adrenal volume. Its cells cluster looking

like archer’s bow (glomerulus) surrounded by blood capillaries. Endocrinocytus

in this zone produces mineralocorticoid.

b. Fasciculate zone

This middle layer of adrenal cortex occupies approximately 65% of adrenal

gland. Its cells are arranged like straight lines forming fascicules which are

perpendicular with organ surface. Endocrine-ocytus in this organ produces

gukokortikoid and some adrenal androgen hormones.

c. Reticularis Zone

This zone is the inner layer and occupies about 7% of adrenal volume. Its cells

are arranged like ‘cordial’ or irregular rope which braids anastomosis

(reticulum). Its cells are similar to the fasciculate, but smaller and more asidofil.

The cells contain lesser lipid than those cells in fasciculate zone and have more

lipofuscin granule. Reticularis and fasciculate zones forms single functional

zone with retucolaris zone forming most of the glucocoticoid and adrenal

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androgen, while fasciculate zone plays role as a reserve zone which is activated

by long term stimulation.

3. Normal Function

Adrenal cortex produces three kinds of steroid hormones; those are:

a. Mineralocorticoid

It is mainly consisted of aldosteron which is produced by glomeru-losa zone as

its response to stimulus, especially for angiotensin II stimulus, and also by

ACTH. Aldosteron organizes the balance of water and electrolyte by stimulating

the absorbing of Na by renis distalis tubulus, it also has influence on gastrica

mucose and saliva gland.

b. Glucocorticoid

It is mainly consisted on cortisol and corticosteron. Both hormones are

produced by reticularis zone with the stimulus from ACTH and fasciculate zone

with the long term stimulus. Glucocorticoid organizes carbohydrate metabolism,

especially by stimulating carbohydrate synthesis in hepar (liver). Glucocorticoid

has opposite role in other tissue; that is as catabolism (degradation) of

carbohydrate to get the carbohydrate base material for hepar. Glucocorticoid

also suppresses the responds of body immune by decreasing the amount of

lymphocyte and eosinofil circulation.

c. Adrenal Androgen

Adrenal androgen is mainly consisted of dehidro-epi-androsteron, which is

discharged as a responds to ACTH by recticularis and undergoes the long term

stimulation, it is also produced by fasciculate zone. The influence of this

hormone is its masculinis-asi and anabolic characters which are similar to the

testosterone, but it is less patent.

4. Abnormal Function

a. Hyper secretion

Cushing’s syndrome is an example of the existence of cortisol hypersecretion and

more often androgen. the sympthoms cover trunchus obesity (body), moon face,

high blood glucose degree, diabetes mellitus, hirsutism, amenorrhea, acne and

unstable emotion.

B. Hypersecretion Aldosteron,

For instance sindroma conn, causing retention of water and Na, and hypertension.

hyposecretion: Hypofunctional chronic of adrenal cortex, such as Addison’s desease

causing blood glucose degree, Na, Cl, and carbohydrate low and K degree in serum

high. this casues body weaknesses, nausea, losing body weight, and increasing

ACTH degree (causing hyperpigmentation). In this case, there is no compensation

for androgen from testis, decreasing synthesis androgen adrenal on women can

cause the loss of pubes and armpit’s hair.

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5. Cortex Foetalis or Provisional Cortex

The thickest adrenal layer before birth is located in between medulla and thin

permanent immature cortex. it causes ‘sulfated androgen’ which is activated by

placenta and come into material circulation. after birth, foetalis cortex experiences

regression, and permanent cortex develops into three layers such as described

above.

B. MEDULLA ADRENAL

1. Origin: It originates from crista neuralis.

2. Structure: composed of two primary cells, they are:

A. Cromaphin Cell

It is also called phoechromocytus. It is a cell type that predominates medulla. This

cell is a modification of neuron postganglionic symphatic that loses axon and its

dendrite. It has big neculceus. Granula secretoric is solid electron. This granula

contains catecholamine (epinefrin or nore-pinefrin). Complexus golgiensis grows

well. There are only some reticulum endoplasmicum granulosum, and very many

oval mitochondrion are found. The secretoric granula has strong affinity towards

cromium color substance. Cromafin cell synthesizes and releases the catecholamine

content facilitated by neuron preganglionic sympatic.

B. Ganglion Cell

Some existing parasimphatic ganglion cells perform morphology of ganglion cell

type of specific autonomy.

3. Normal Function

The normal function of medulla adrenal covers the production of 2 types of

catecholamine, that is, epinephrine and norepinephrine, on the response to stimulation

ganglion simpatico (such as stress). The two catecholamine hormones increase blood

glucose degree by stimulating glicogenolisis in hepar; this hormone increase the blood

circulation to the heart.

a. Epinephrine

It causes harder heartbeats and blood vessel dilatation, which is required by organs to

prepare or avoid sties, such as heart muscles and skeletal muscles. Perform dilatation of

bronchioles and perform contraction of blood vessel in organs (such as on skin,

digestive system, kidneys) that is not important to react against stress.

b. Norepinephrine

It causes blood vessel contraction on unimportant organs. It increases periphery

resistance so that it increases blood pressure and blood circulation to the heart, brain

and skeletal muscles.

4. Abnormal Function

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Tumor hypersecretion of chromafin cell (pheocromocytoma) causes the increase of

stress respons (mainly hypertension) although without the existence of stress. Tumor cell

ganglion (neuroblastoma and ganglion neuroma) often occur, mainly on children but they

manifest clinically various.

C. ADRENAL VASCULARISATION

1. Artery

Three main arteries supply blood to every adrenal gland. they are:

- A. suprarenalis superior, originating from a. phrenicus inferior.

- A. suprarenalis medialis from aorta,

- A. suprarenalis inferior from arterial rhenalis.

The three arteria penetrate capsula separately, and the branches of anastomose create

plexus arteria subcapsularis. From this plexus, three groups of arteries emerge:

a. arteria in capsule

b. arteria in cortex, that has many branches forming cortical capillary that runs in

between secretoric cells and flow into medularis capillary; and

c. arteria in medulla

This arteria runs through cortex without the branches until it reaches medulla, and

this artheria forms medullaris capillary.

2. Medullaris Capillary

Which accepts double blood, that is, from both artheria in cortex and medulla,

meeting to form several medullaris vena.

3. Medularis Vena.

These medularis vena meet each other to form one big suprarenalis vena.

4. Suprarenalis Vena

Located in the middle of the medulla, and this vena flows into renalis vena or

directly comes into vena cava inferior.

INSULA PANCREATICA

This insulae pancreaticae is a building like endocrine cell nest (endocrinocytus) that spreads

all over pancreas. Each insula contains four types of cell producing peptide hormones.

A. ALFA CELL = ENDOCRINOCYTUS ALPHA.

This cell produces glucagons hormone, playing a role of increasing low blood glucose

degree, and this hormone works on the reverse of insulin hormone.

B. BETA CELL = ENDOCRINOCYTUS BETA

This cell is found abundant inside insulae pancreatincae and produces insulin. The

insulin works at the condition of high blood glucose degree and can decrease the high

degree of blood glucose to be normal again. Insulin increases the blood glucose intake

by most cells; increasing glycogen synthesis by hepatocytus and grigliserid synthesis by

adipocytus. Malfunction of beta cells may cause diabetes mellitus, a condition as a

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manifestation due to excessive glucose blood degree (hyperglycemia), that is released

through urine so that glicosuria takes place. Hyperplasia and neoplasia of bheta cell can

cause hiperinsulism syndrome, with the specific symptom of hinoglikemia.

C. DELTA CELL = D CELLS = ENDOCRINOCYTUS DELTA

Somatostatin that suppresses insulin release, glucagons and growth hormones, is

produced by this delta cells. Besides, this cell also produces gastrin that triggers gland

secretion in digestive system mucosa. Syndrome zollinger-ellison (gastrinoma) is

caused by the excessiveness of acid. Gastric produced by parietal cell on gaster

mucosa/gastric, is singed by ulcus pepticum. Somastostatinoma is a tumor that is hardly

found and has various effects.

D. F CELL = PP CELL

This type of cell secretes polypeptide pancreatica that slow pars exocrine pancreas to

produce enzyme and bicarbonate. This hormone causes vesica fellea relaxation and

reduces bile secretion.

GLANDULA THYROIDEA

Is located on neck, anterior larynx. This thyroid gland is composed of two lobus connected

by isthmus. This gland is composed of follicles in great amounts and in the form of spheres

and wrapped by thin capsules penetrating into parenchyma, creating septas.

B. THYROID FOLLICLES

each follicle is composed of epithelium simplex cuboideum/one-layered cuboids

epithel rotating/limiting a lumen containing colloid. These follicles have various

sizes, enlarging if there is stimulation.

C. THYROID FOLLICLES CELL

1. Structure

The thyroid follicles cell that originates from endoderm has its ultra structure that

performs specific cell that produces peptide hormone. The cell size is ranging from

flat on inactive glands until columnar if there is stimulation.

2. Normal Function

Thyroid follicles cell is different from other endocrine gland cells that store half-

made hormone (intermediate) (thyroglobulin) extracellularly inside colloid, but it is

not stored inside the granula cytoplasm. Stimulation by TSH that is generally

followed by the increase of energy need. Synthesis and secretion increase.

a. Synthesis and thyroglobulin storage

Required steps to perform this process are:

Synthesis of tirosin-rich protein = tiroglobulin, on reticulum

endoplasmicum granulosum.

Protein glicosilation in reticulum endoplasmicum and complexus

golgiensis.

Wrapping in vesicles on complexus golgiensis, and

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Fusion of vesicles on apex membrane cell, resulting in exsositosis

tyroglobulin into colloid on lumen follicles.

b. Absorption and iodide oxidation

Molecular pump in plasma membrane of follicle cells move iodide in the

circulation into cytoplasm. This iodide is oxidized by peroksidase and then

moved to cell apex. Iodide absorption is also triggered by TSH.

c. Iodination of tiroglobuline and the formation of tiroid hormone

Enzymes that are found on the tips of microvilli plasma membrane penetrate

into colloid catalyzing iodination of tirosin residue in tiroglobulin. The

reaction is in between bending microvillus surface. One iodide molecule is

added with tirosin, creating monoiodotyrosine (MIT). The second iodide

molecule is then added into some tyrosine residue, forming diiodotyrosine

(DIT). The pair of two tyrosine that has been iodized forms tyronine

molecules. The combination of two DIT molecules forms tetra-iodo-

thyronine (thyroxin; T4), while the combination of one MIT and one DIT

forms triiodothyronine (T3). Although T4 is the producer of 90% thyroid

hormone, this hormone is not strong in general.

d. Secretion of thyroid hormone

Stimulation by TSH causes follicular cells to perform pinositosis on colloid

part, creating vesicles that contains tiroglobulin that has been iodized. These

vesicles run fusion with lisosoma containing enzyme that smashes

tiroglobulin. T3 and T4 are released, spreading outside from secondary

lisosoma. this vesicles penetrate cytoplasm and membrane plasma to reach

blood circulation.

e. Target and the effect of thyroid hormone

T3 and T4 affect whole body cells. it increases basal metabolism ratio (i.e.,

ratio on the time the cell uses glucose), increases cell growth, increases

heartbeat, increases energy-user cells. this hormone also affects on TRH-

producing cells on hypothalamus and thyrotrops on adenohipophisis to

reduce TSH secretion (negative feedback).

3. abnormal function

a. hypothyroidism

Excessive production of thyroid hormone is also known as thyrotoxicosis,

causing some symptoms such as nervousness, palpitation, fast polls, muscles

weaknesses, fatigue. Weight loss with good appetite, drench in sweat, do not

stand sun heat and unstable emotion. Hyperactive follicles thyroid due to

additional length of epithelia follicles and the increase of tiroglobulin sediment

causes swelling of the thyroid gland and it is called goiter.

b. hypothyroidism

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Hypothyroidism is called cretinism on children and myxedema = mixoedema on

adults. Hypothyroidism causes less glucose use. The symptoms appearing

among others are: ‘lethargy’, unable to stand cold weather, slow inttellctual and

motoric skills, storage of glicosamino-glican on dermis (skin) with the

consequence that the skin becomes bump and sometimes body weigh increases.

Because iodide is needed for normal thyroid function, lack of iodide on food

diets reduces the production of functional thyroxin and often cause cretinism

and myxedema. Because thyroxin that is not iodized is caused by iodide

deficiency does not give negative feedback on TSH production, follicle and

goiter enlargement often comes along with this type of hypothyroidism.

D. PARAFOLICULAR CELL = CELL C

This cell is found on thyroid glands, spreading among between follicular cells or

clustering among follicular cells. On human being, the cytoplasm of parafolicular cell is

colored pale with standard and specific color substance that look transparent and white.

The structure of the ultra cell plays a role to increase Ca (calcium) degree in blood.

Calcitonin causes Ca absorption by cell and increase Ca deposition on bones, so that it

causes the decrease of Ca degree in blood.

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GLANDULA PARATHYROID

There are 4 parathyroid glands, located in posterior surface of tiroid glands; coming from

endoderm (3rd and 4th pharynx bags). in adults, this gland is composed of two types of

primary cells; chief cell = cellula principalis and oxyphil cell = cellula oxyphylus.

A. CHIEF CELL = CELLULA PRINCIPALIS

is a parenkim cell in large amount.

1. Structure:

This cell has small size (proximately 4-8 micron in diameter), polygonal and ultra

structure illustrates cell type that produces peptide hormone. This cytoplasm cell that is

coloured pale is full of small granula secretoric.

2. Normal function

This principal cell secretes paratiroid hormone (PTH = parathyroid hormone) in

response to stimulation of low Ca blood degree with 3 targeted areas, they are:

a. In bones, PTH increases bones reabsorption.

b. In kidneys, it inceases phosphate excretion and Ca reabsorption as well as causes

precursor activities of vitamin D.

c. In intestine, PTH (may be due to the vitamin D activity causes the increase of Ca

absorption from foods by intestinal mucosa.

3. Abnormal function

a. Hyperparatiroidism

Excessive secretion of PTH increases serum Ca (hyperphosphatemia) and

decreases serum phosphate degree (hypophosphatemia). The effect includes Ca

urine, abnormal Ca sedimentation in artheria and kidneys, and loses Ca from

bones excessively that will cause osteomalacia and osteitis fibrosa cytica.

b. Hypoparatiroidism.

Insufficiency of PTH secretion distracts neuromuscular function. due to low Ca

blood degree, it tends to reveal spontaneous action potency and the flash of

action potency is out of control. on the edge nerve, it can cause spontic muscle

contraction called tetanus. neutron spontaneous flash on brain may influence

behaviors.

B. OXIPHYL CELL

This cell has bigger size compared with principal cells, but the amount is less than that of

principal cells. This cell contains much mitochondrion so that it is so acidophil. The

function of this cell is not yet recognized clearly.

EPIPHYSIS CEREBRI

Is small organs with the size of 3-5 mm X 5- 8 mm, in the form of conus/conical (called

epiphysis cerebri as well), clinging on the branch on diencephalons roof near ventriculus

tertius cerebri (the posterior aspect). Epiphysis cerebri contains globular building that is

basophile and calcifies in groups called brain sand or corpora arena-cea, that increases in

amount and sizes and calcification increases as age goes on.

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epiphysis cerebri contains two primary cell types:

A. PINEALOCYTUS.

1. Structure:

This cell has nucleus in big size and has irregular shape and also has nucleolus that

can be seen clearly/bumping and the cytoplasm is pale basophile. With silver dyeing

method according to Del Rio Hortega, this cell performs ; long cytoplasmic crowns

and terminate as bubbles on septa near blood vessels. this inervation epiphysis

cerebri (both symphatic and through the branch from commissural posterior) plays

unknown roles.

2. Normal Function

Pinealocytus secretes melatonin. The cycles of melatonin degree change in blood

plasma follow the environment shining changes, but this relationship is not yet

known. Melatonin may help determine circadian rhythm and has antigonadotropic

influence that flees when sexual maturity appears in puberty. The other pinealocytus

product is ‘arginine basotocin’ and the opportunity of increasing substance that use

antigonadoptropic influence through hypothalamo-hypophysealis fuse.

3. Abnormal Function.

Glandula damage. This pinealis happens to mostly young men and may cause

praecox puberty and decreases sexual maturity. Due to the organ location, pineal

tumor may disturb the flow of cerebrospinal fluid through aqueducts sylvii, so that it

causes hydrocephalus and the following symptoms.

B. ASTROGLIAL CELL

This cell is also called interstitial cells. This cell is like glia and has lengthening nucleus

heterocromatic and simpthoplasmic crowns containing philamentum intermedium. This cell

is commonly found around blood vessels and amongst the groups of pinealocytus.

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PRACTICUM OF ANATOMY PATHOLOGY OF ENDOCRINE BLOCK

1. STRUMA COLOIDES MACRO ET MICRO FOLLICULARIS

Is the enlargement of thyroid gland mostly observed. This struma occurs due the

short of iodine intake, the increasing need of thyroxin (for instance on growth time,

lactation, stress), the existence of goitrogenic materials that hamper the production of

thyroxin hormone (such as cabbage, cassava, radish), as well as the existence of familial

defect on synthesis or thyroxin hormone transportation.

Clinic:

A 35-year-old woman suffers from an egg-sized bump on neck front area that

moves when swallowing saliva. This has been happening in the last 3 years.

Macroscopic:

Capsulated egg-sized tissue, elastic consistency. Brownish white spongius profile.

Microscopic:

Weak Enlargement

- Small and big follicles are seen, all containing red colloid mass.

- Most of these colloids flee from follicle wall and located in the middle.

Strong Enlargement

- Big follicles wall consists of flat one-layered epythel.

- Epythel wall of small follicles is still in the form of one-layered cuboids.

2. STRUMA LIMPHOMATOSA HASHIMOTO (LIMPHOSITIC THYROIDITIS)

This occurs mostly in menopause women, although it can also occur in any age.

Occurrence on women is 10-20 times more than on men. Struma Hashimoto is tyroiditis

autoimmune, with the existence of autoantibody circulation towards thyroglobulin and

follicular cell antigen especially thyrotropin (TSH) receptor. Clinic is indicated with the

enlargement of thyroid gland, that in the initial phase may be still in the form of eutiroid. in

advanced phase, hypotiroid may occur, and in some cases, it is followed by tirotoxicosis

symptoms. Sometimes, clinic is difficultly differentiated with carcinoma.

Clinic:

A 40-year-old man with a lanseh-sized bump in neck front area. it moves when

swallowing saliva.

Microscopic:

Weak and strong enlargement

o Thyroid gland Asini is mostly penetrated by lymphoid tissue by forming

lymphoid follicles.

o Asini becomes small with very narrowing lumens.

o Inside the lumens, colloid is sometimes seen.

o Asinus lumen is limited by polyhedral-forming cells.

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1. Grave’s disease

Clinic:

A 35 –year – old woman has a duck egg-sized symmetric bump on neck front area and

it moves when swallowing saliva. In the last 3 years, the bump enlarges. Besides, the

sufferer feels his eyes become bump, often feels hard heartbeats, drenching in sweat

and increasing blood pressure that was once only 120/70 and now becomes 170/100.

Thyroidektomy is conducted and the result was sent to pathology anatomy laboratory.

Macroscopic:

Brown and elastic tissue with the diameter of 6 cm, reddish brown profile with the

gland that is seemingly composed of translucent mass.

Microscopic:

Thyroid tissue with small-sized gland follicles with irregular edge and hyperplasia,

some papillary grow into the lumen. Papillary epythel cell has the core in basal cell

area. Lumen contains sufficient colloid mass.

2. Parathyroid Adenoma

Clinic:

a 40-year-old woman with a pigeon egg-sized bump on neck front area. it moves when

swallowing saliva and it has been 2 years and enlarging. besides, the sufferer conducts

blood examination and it is found in the blood that the calcium degree increases.

extirpation is conducted and the result is sent to pathology anatomy laboratory.

Macroscopic:

parathyroid tissue with arranged tubular/granular tumor. small-sized follicle gland. cells

with small core with cytoplasm are sufficient and very vacuolar.

3. Phaeochromocytoma

Clinic:

A 34-year-old man with a bump on his belly on his left upper waist. It is felt to enlarge

since the last 6 months. He then met a surgery and operation is suggested.

Durante operation: left kidney is identified, macroscopic is good. Capsulated tumor

intoto is identified outside the kidney. Glandula suprarenalis is not identified.

Macroscopic: tissue with the diameter of 15 cm is capsulated, blackish brown with

elastic consistency. Some are fluctuated, on kidney fission, yellow profile with brown

part, some are blackish, fragile, some has cavity containing red blackish liquid.

Microscopic:

Ephytelial tumor tissue is composed solidly, some have band around with blooding area

and necrosis is large. atipi and polymorph tumor cells are medium to big, cytoplasm is

eosinofil or granular. The core is sometimes vesicular chromatin. Core is irregularly

rough. Some of core descendents are obvious. Few big cells with more than one core

are found. There are several mitosis.

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4. Pituitary adenoma

Clinic:

A 25-year-old girl complains of her enlarging breast in the last few months. White

liquid comes out from the nipples and she has not had menstruation in 3 months. She is

reffered by the doctor to RS PKU Muhammadiyah and CT scan is conducted. CT scan

suggests the existence of mass in sella tursica with diameter of ± 2 cm. extirpation is

performed by a surgery and the result is sent to pathology anatomy section.

Macroscopic:

Tissues with diameter of 2 cm, white brownish and elastic, with while brownish profile.

Microscopic:

Tumor tissues are composed of uniform cells of polygonal shape in groups that is

limited by supportive tissues or reticulin. Tumor cells have monomorf cores. Some

cytoplasm is reddish or bluefish. Mitosis can be found.

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