buku modul endokrin 2010
TRANSCRIPT
Modul Practicum Guidelines Laboratory Skills Guidelines
BLOCKS OF ENDOCRINE
FACULTY OF MEDICINEMUHAMMADIYAH UNIVERSITY OF YOGYAKARTA
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
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
.
TOPIC TREE
BLOCK OF ENDOCRINE
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
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)
C.Learning of Competence
Level of expected ability
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
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%
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
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.
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
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)
SUPPLEMENTS OF
BLOCK OF ENDOCRINE
GUIDANCE OF TUTORIAL
BLOCK OF ENDOCRINE
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.
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
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
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)
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!
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!
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
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.
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.
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
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.
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 →
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
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
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
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
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
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
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
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
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
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.
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.
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.
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:
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
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.
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.
(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.
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
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.
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.
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
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
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
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.
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
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
GUIDELINES FOR PRACTICUM
BLOCK OF ENDOCRINE
Contributor:
dr. Agus Suharto, SpPA
ENDOCRINAL SYSTEM
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
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)
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:
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
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)
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
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
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.
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
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.
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
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
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
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
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.
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.
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.
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.
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.
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.