NEUROPSYCHIATRY MODULE PRACTICAL MANUALstaff.ui.ac.id/.../material/translatedpanduanprmodulsy-jiwa.pdf · Different species may have different effects from a drug. ... Buku Farmakologi

NEUROPSYCHIATRY MODULE

PRACTICAL MANUAL

Copyright 2007 by the Faculty of Medicine, University of IndonesiaAll rights reserved. This book or any parts there of, may not be used or reproduced in any manner without written permission from the writer/publishers.Printed in Jakarta, Indonesia

ISBN

Translator: Siti NurhayatiEditor: Jeanne Adiwinata Pawitan

Faculty of MedicineUniversity of Indonesia

2007-2008

Author: Wawaimuli ArozalPerson in charge: dr. Instiaty, SpFKTutors:

1. Azalia Arif2. Sulistia Gan3. FD Suyatna4. Melva Louisa5. Dewi Selvina

Objective:At the end of the lab activity/practical students should be able to:

1. Explain the effects of morphine in various species (species difference).2. Explain the effects of morphine in humans, based on observations from

animals.3. Relate the effects of morphine in cats, rats and mice, to the effects of

morphine in humans.4. Explain the indications for morphine and its derivatives in therapy.

Laboratory animals, equipment, and substances:Lab animals : rabbit

cat rat mouse

Equipment : 1 ml tuberculin syringe 2 ml syringe ruler

Substances : 4% morphine sulphate solution 4% caffeine benzoate solution Naloxone

For the demonstration, administer:- morphine : cat 20 mg/kg BW

rat 40-60 mg/kg BW mouse 40 mg/kg BW

- naloxone : rabbit 0.01 mg/kg BW, intravenously

Pharmacology Practical

Method:

1. Effects of morphine in rabbitsRabbits are used as lab animals because the effects of morphine in rabbits are similar to those in humans.a. Observe and record:- depth and frequency of breathing- heart rate- reactions in muscle tone towards intensity of pain stimulation- muscle tone and reflex- attitude of lab animal- general behavior of lab animal (calm, agitated, etc)- pupil diameter

b. Inject subcutaneously 0.5 ml/kg BW 4% morphine sulphate solution into a rabbit, then

- Repeat all observations and make recordings every 5 minutes. If after 45 minutes the depressive effects are no longer observed, inject more morphine as much as half the initial dose.

- Note the reactions to certain stimuli, that previously would have elicited pain; after the administration of morphine such reactions would decrease heavily or dissipate all together. Reactions towards abrupt changes in stimuli intensity do not change.

- If the breathing frequency has decreased to 30 breaths per minute, inject subcutaneously 0.5 ml of 4% caffeine benzoate to each rabbit.

- Repeat all of the above observations every 5 minutes. If after 10 minutes no significant changes are observed, or if the respiratory depression is too great, inject the rabbits with naloxone or nalorphine.

2. Different effects towards different animal species (species difference)

Different species may have different effects from a drug. For instance: morphine causes excitation in cats and horses but have depressive effects in rabbits. One thing in humans that is similar to species difference is the event of idiosyncrasy (certain drug effects occurring in certain individuals that are different from the effects in the general population, due to genetic abnormality). For example: morphine causes depression in most people, but in certain people, especially women, causes excitation.

a. Inject 4% morphine solution subcutaneously and interscapularly to the different animal species below in the appropriate dosage.

b. Observe and take note:- cat : shows great excitation, dilated pupils, hypersalivation.- rat : shows changes in body tone. The body will remain in the

position arranged by the researcher (cataleptic).- mouse : shows moderate excitation, its tail rising and forms the

letter S (Straub effect).

3. Morphine derivates used as non-analgesicsOf all morphine derivates there are two drugs that are sometimes used, apomorphine and naloxone. Apomorphine is a strong emetic that works by stimulating the chemoreceptor trigger zone in the postrema area of the medulla oblongata. This stimulation is then passed on to the vomiting centre to produce vomiting. This drug is used to treat poisoning and Parkinson’s disease. Naloxone is a morphine derivate that is purely antagonistic in character. It is very useful to relieve respiratory depression caused by opioid substances.

Questions:1. What is the difference of idiosyncrasy and species difference in the

administration of morphine?2. What are the trias symptoms in the acute poisoning of morphine?3. Why is morphine only indicated in the relief of great pain such as renal

colic, cancer, and post surgery?4. What is the difference between pure antagonist and partial antagonist of

morphine?5. What is meant by endogenic morphine? Provide an example and explain

its functions.6. How many types of opioid receptors do you know? Explain the roles of

those opioid receptors!

You can look up the answers in:1. Buku Farmakologi dan Terapi. Edisi IV. Jakarta:1995. pp. 189 - 206

(chapter 14).2. Gutsein HB, Akil H. Opioid Analgesics. In: Goodman and Gilman’s, The

Pharmacological Basis of Therapeutics. 10th ed. New York; McGraw-Hill: 2001. pp.569-619 (Ch 23).

3. Schumaker MA, Basbaum AI, Way WL. Opioid Analgesics & Antagonists. In: Katzung BG. Basic & Clinical Pharmacology. 9th ed. New York; McGraw Hill: 2004. pp. 497 - 517 (Ch 31)

Author : Diana Aulia

Person in charge: dr. Diana Aulia, Sp PK(K)

Tutors:

dr. Diana Aulia, Sp PKProf. dr. Suzanna Immanuel, Sp PK(K)dr. Ina S. Timan, Sp PK(K)dr. Dewi Wulandari Sp PKdr. Eckydr. Anti

The laboratory tests to evaluate the condition of the nervous system and detect disturbances or abnormalities of the nervous system may be non specific and specific. Non specific clinical laboratory tests are, among others, tests to identify the effects of abnormalities in the process of the nervous system, such as hematological examinations to detect inflammation, infection and malignancy (infiltration in leukemia). Specific tests are, among others, protein or tranferrin electrophoresis examinations to help identify cerebrospinal fluid from nasal secretion or rhinorrheae or otorrheae. Glucose in the cerebrospinal fluid originates from active transport by endothelial cells and diffusion due to the difference in glucose level of the plasma and the cerebrospinal fluid. Achieving a balance between glucose level in the cerebrospinal fluid and the blood takes 30 minutes. Therefore, blood extraction (to examine glucose level in the plasma as comparison), should be done minimally 30 minutes before puncture is initiated. The increase of glucose in the cerebrospinal fluid does not have diagnostic value and may be found in hyperglycemia, or puncture trauma. The decrease of glucose level in the cerebrospinal fluid may be found in a few cases, such as hypoglycemia, meningitis, and primary tumor infiltration or metastasis. This decrease is caused by a disturbance in transport through the brain barrier and an increased in glycolysis by bacteria and leukocytes.

Objectives: 1. to know the various laboratory tests that can be used, among others, to

establish a diagnosis, monitor therapy, assess prognosis and epidemiology of the disease.

2. to know the many kinds of tests that will be used to treat a patient3. to know how to prepare a patient before the retrieving of laboratory

specimens, how to retrieve and transport it to the laboratory.

Clinical Pathology Practical

4. to be able to interpret laboratory test results5. to know the limitations of laboratory tests

Types of examinations:1. Cerebrospinal fluid examination2. Hematological examination3. Urinalysis 4. Enzyme and clinical chemistry examination

Cerebrospinal analysis:

No.. Pract

No. Result(Drawing)

Explanation

1. Lumbar puncture procedure

2. Specimen collection tubes for:1. Chemistry &

Serology2. Immunology/

additional tests3. Hematology4. Microbiology

CSF specimen collection tubes

3. Specimen collection:Transportation media for culture.

CSFspecimen collection transport media

4. CSF: normal subjectReport normal CSF appearance!

CSFMacroscopic

5. CSF: trauma capitisReport normal CSF appearance!

CSFMacroscopic

6. CSF: old trauma capitisReport abnormal CSF appearance!

CSFMacroscopic

7. CSF: infectionReport abnormal CSF appearance!

CSFMacroscopic

8. CSF: infectionReport abnormal CSF appearance!

CSFMacroscopic

9. CSF: pre-analysis CSFMacroscopic

10. Cell count:Counting chamber

CSFCell count

11 Differential count:Specimen processing

CSFDiff cell count

12 CSF: normal smearReport CSF’s smear! Slide no.:

CSFsmear


CSFsmear

14 CSF: meningitisSlide no.:

CSFsmear

15 CSF: smearErythrophagocytosis.Slide no.:

CSFsmear


CSFsmear

17 CSF: metastaticmalignant cells Slide no.:

CSFsmear

18 CSF: choroid plexus cells.Slide no.:

CSFsmear

19 CSF: parasitic infection Report CSF’s smear!Slide no.:

CSFsmear

20 CSF: contamination during the spinal tap

CSFsmear

21 CSF: smearReport CSF’s smear! Slide no.:

CSFsmear

22 CSF: smearReport CSF’s smear! Slide no.:

CSFsmear

23 CSF: smearReport abnormal CSF appearance!Slide no.:

CSFsmear

24 CSF: smearReport abnormal CSF appearance!Slide no.:

CSFsmear

25 CSF: Infiltrative leucemic cells.Report CSF’s smear! Slide no.:

CSFsmear

26 CSF: infiltrative leucemic cellsReport CSF’s smear! Slide no. :

CSFsmear

27 CSF: smearMyeloblast from acute myelocytic leukemia (prominent nucleoli)Slide no. :

CSFsmear

28 PANDY test result is: CSF

29 NONNE test result is: CSF

30 Mr. S., age 28, is admitted to the hospital ward with a temperature of 105oF, lethargy, and cervical rigidity. A lumbar spinal tap is performed, and tests result are:Slide no.:

Analysis of CSF

31 A clear CSF specimen from 23 year old patient experiencing mild motor difficulties and the tests results are :Slide no. :

Analysis of CSF

32 Examination of CSF specimen from 28 year old man suspected having meningitis reveals a slightly elevated white blood cells count consisting primarily of mononuclear cellsSlide no. :

Analysis of CSF

33 31 + the physician must make a preliminary diagnosis of viral meningitis. Name of the tests that would provide the most valuable information in the diagnosis of meningitis type!Slide no. :

Analysis of CSF

34 31 + the physician must make a preliminary diagnosis of tubercular meningitis. Name the tests that would provide the most valuable information in the diagnosis of meningitis type!Slide no. :

Analysis of CSF

35 31 + the physician must make a preliminary diagnosis of fungal meningitis. Name of the tests that would provide the most valuable information in the diagnosis of meningitis type!Slide no. :

Analysis of CSF

Author: Conny Riana Tjampakasari

Person in charge: Dra. Conny Riana Tjampakasari, MS

Tutors:

Conny Riana TjampakasariMardiastuti HWAnis KaruniawatiT. Mirawati SudiroRetno KadarsihYeva RosanaBudiman Bela

PATHOGENIC MICROORGANISM IN THE INFECTION OF THE CENTRAL NERVOUS SYSTEM

Objective1. To understand the various causes of infection of the central nervous

system2. To understand the microbiological examination procedures to identify the

organisms causing the infections

Introduction

A. Bacterial causes of central nervous system infections

1. Neisseria meningitdis

N. Meningitidis is widely referred to as meningococci. This bacterium causes meningitis, especially in children. The port d’entree of these bacteria is the nasopharynx. Meningococci are negative Gram diplococcic bacteria, that grow well in the brown agar or Thayer Martin medium incubated at 37°C in an environment of 5% CO2 (candle jar).

The specimen can be obtained from throat swabs, blood or cerebrospinal fluids that must be planted immediately in the medium. Pure culture of blood or cerebrospinal fluids give specific biochemical reactions: glucose (+), maltose (+),

Microbiology Practical

and sucrose (-), a positive oxidase test. These bacteria can be agglutinated by specific polyvalent serum.

2. streptococcus pneumoniaeThis bacterium looks like a lancet, joined together two by two, is positive Gram, with a capsule that can be observed by special staining like Gins-Burry. It is difficult to cultivate, destroyed in gal fluid, has a positive inulin reaction, and a positive optochine reaction. Just like other streptococcus sp., streptococcus pneumoniae also reacts negative for catalase. Identification is based on morphology and colony, and immunology (with quellung/swelling reaction).

3. Mycobacterium tuberculosisThis bacterium looks like a rod, positive gram, difficult to see when stained from specimen. With acid fast staining, the body of the bacteria will appear red. These bacteria grow very slowly in artificial culture.

Examination from direct specimen is done with Ziehl-Neelsen acid fast or Kinyoun-Gabett staining. Further identification is done through biochemical reactions such as neutral red, catalase reaction, peroxidase reaction, niacin test and nicotinamide test.

4. haemophilus influenzaeHaemophilus influenzae live in the mucosal membrane of the upper respiratory tract and may cause infection in children and adults. In severe cases it can also cause meningitis in children. This bacterium looks like a short coccoid rod, but after prolonged storage may become pleomorphic.

To grow, this bacterium depends on factor X and factor V as growth factors. Factor X can be obtained from blood, whereas factor V can be obtained from yeast extract and is also produced by certain bacteria like Staphylococcus aureus. The medium used for culture is usually brown agar medium, which is heated blood containing medium. In this medium Haemophilus influenzae grows by making small round, convex, and shiny colonies. If they grow around a colony of Staphylococcus aureus, this colony will grow larger (satellite phenomena). This bacterium has a capsule that can be observed with a serological reaction (capsule swelling test).

5. Listeria monocytogenesThis bacterium looks like small positive gram coccobacillus. Listeria move with a peritrich flagella. These bacteria grow well in blood agar and triptose agar. In blood agar culture, the colony is surrounded by a beta hemolysis zone, whereas in triptose agar, the colony is clear. This bacterium is aerobic/microaerophyllic. The optimum temperature for its growth is 37°C, but this bacterium can still grow at 2.5°C.

In humans, listerosis occurs in the form of abscess or widespread granuloma. Abnormalities can be found in the heart, adrenal gland, respiratory tract, digestive tract, central nervous system, and skin.

6. Clostridium tetaniThis bacterium is the cause of tetanus in humans. It is abundant in nature. It can be found in the earth, and in the feces of horses and other animals. There are many types, differentiated by the antigen of the flagella. All types produce the same toxin. The tetanus toxin is a thermolabil protein, with a molecule weight of 70.000, and can be digested by the proteolitic enzymes of the stomach. This bacterium is not invasive. It will stay put in a wound, when conditions are suitable, meaning anaerobic, due to necrotic tissue, calcium salts, or other pyogenic bacteria. In this condition the spores will become vegetative and the exotoxin will be formed and spread to the central nervous system through the perineural tissue, blood vessels, or lymph vessels.This bacterium is positive gram, forms a terminal spore (drum stick), is obligatively anaerobic, slightly proteolytic, but not saccarolytic.

7. Clostridium botulinumThis bacterium is abundant in nature, sometimes it can be found in animal feces. There are 6 types according to the toxins, they are A, B, C, D, E, F. In humans, type A, B and E can be found. The secreted exotoxins are thermolabil proteins with 70.000 molecular weight.

This bacterium usually does not cause infections in wounds, but causes food poisoning by the toxins ingested with food. The toxins work by blocking the formation or release of acethyl choline in the motor end plate, causing muscle paralysis.

Clostridium botulinum is obligatively anaerobic, has a subterminal spore, very proteolytic, but not saccarolytic. In egg yolk agar, this bacterium forms a specific colony, that is, a pearly layer covers this bacterial colony (due to the degradation of lipoid by lipase).

B. Fungi causing infections in the central nervous system

1. Cryptococcus neoformans

C.neoformans is considered a chamire with a capsule that can survive in dry conditions. This chamire reproduces through budding.Infections occur through inhalation of the spores. In the lungs it causes local damage and seldom produces symptoms or produces only mild ones. From the lungs, the fungus may spread to other organs such as skin, bones, and especially the brain.

C.neoformans in the tissue can be seen as a round cell with HE staining. To see the capsule clearly we can use, among others, Indian ink.Culture from clinical specimens can be obtained with Sabouraud dextrose agar medium, if necessary antibiotics should be added to prevent the growth of bacteria. The colony of this fungus has a soft consistency and appears yellow and slime-like.

2. Coccidioides immitis

This fungus is classified in the dimorphic group. In room temperature it forms a filament colony. Its hyphas easily fragmentize and form artospores. The artospores are lightweight and easily carried away by the wind and inhaled into the lungs.

Humans get infected through inhalation of the spores. Primary coccidiomycosis usually affects the lungs with symptoms similar to infection of the lungs by any other microorganism. Progressive coccidiomycosis can be fatal when left untreated. Only few of primary coccidiomycosis become progressive, spreading to the brain, skin, or other organs.

In a direct specimen made with 10% KOH solution, the fungus appears as a spherule with clear walls filled with endospores. When the spherule ruptures, the endospores will exit into tissue and grow into new spherules. When cultivated in Sabouraud agar medium in room temperature, the colony will grow as a filament.

B. Viruses causing infections in the central nervous system

Etiologically, viral infections in the nervous system are classified into three groups:

a. Primary neurotropic infection, when the virus attacks the meninges, the brain, and the spinal cord.

b. Post-infection encephalitis can occur due to complications after infections by viruses such as variola, varicella, influenza, morbilli, mumps, and rubella.

c. Post-vaccination encephalitis can occur due to vaccinations with varicella, rabies, morbilli, and yellow fever vaccines.

Rabies virus

Rabies is an acute central nervous system infection that is almost always fatal when not treated immediately. Transmission usually occurs through saliva in the bites of animals infected with rabies.Rabies is classified in the family of Rhabdoviridae, is an RNA virus, and looks like a bullet.

Laboratory diagnosis is made based on the finding of Negri bodies in the cytoplasm of the neural cell (ganglion) of the victim or in the brain tissue of the animal suffering from rabies. The negri body appears to have basophilic granules in an acidophilic matrix. If the Negri bodies are not found, specimens from the victim’s saliva or the infected animal’s salivary gland can be extracted to be injected into the cerebrum of lab animals such as rats or rabbits. These lab animals will become paralyzed and eventually die. From their brain tissue we can further look for the Negri bodies.

Observation

1. Neisseria meningitidis

Gram staining

Shape : Characteristic :

Growth in Thayer Martin medium Growth in CTA (Cysteine Trypticase Agar)

2. Streptococcus pneumoniae

Gram staining Gins-Burry staining


Growth in blood agar culture Optochine test

3. Mycobacterium tuberculosis

Ziehl-Neelsen staining Growth in Lowenstein –Jensen medium

4. Haemophilus influenza

Growth with factor X and factor V

5. Clostridium tetaniGram staining


6. Clostridium botulinumGram staining Growth in

Egg Yolk Agar

Shape : Characteristic:

7. Cryptococcus neoformansIndian Ink smear Growth in Sabouraud agar

8. Rabies virusNegri inclusion bodies (Negri Bodies) in the neural cell cytoplasm

References 1. Jawetz, Melnick, Adelberg’s. Medical Microbiology. 23rd ed. New York;

Mc. Graw Hill: 2004.2. Mahon CR, Manuselis G. Diagnostic Microbiology. London; WB

Saunders: 1995.3. Mims C, Dockrell HM, Goering RV, Roitt I, Wakelin D, Zuckerman M. Medical Microbiology. 23rd ed. London; Mosby: 2004. 4. Murray PR, Drew L, et al. Medical Microbiology. 5th ed. St. Louis; Mosby: 20055. Staf pengajar Departemen Mikrobiologi FKUI. Penuntun Praktikum Mikrobiologi Kedokteran. Jakarta; Medical Multimedia Indonesia: 2006.6. Wilson WR, Sande MA, et al (Eds). Current Diagnosis and Treatment of Infectious Disease. New York; Lange Medical Books: 2001.

Author: Noenoek Poerwaningsih

Person in charge: Noenoek Poerwaningsih

Tutors:

1. Noenoek Poerwaningsih 2. Agnes Kurniawan 3. Taniawati Supali4. Agus Aulung 5. Yenny Djuardi

The material for Parasitological practical consists of demonstrations, student independent work, and exercises.

A. Demonstrations 1. Toxoplasma gondii tachizoit stadium 2. Toxoplasma gondii cyst stadium 3. Plasmodium falciparum in brain capillary4. Plasmodium falciparum starry sky (thin blood smear)5. Plasmodium falciparum starry sky (thick blood smear)6. Trypanosoma sp promastigote stadium 7. Cysticercus sellulose8. Taenia sp egg stadium 9. Taenia sp proglotide 10. ELISA Toxoplasma gondii 11. Acanthamoeba castelanii culture12. Malaria ICT

Parasitology Practical

Demonstrations Illustrations

1. Toxoplasma gondii Specimen from peritoneal fluid Tachizoid stadium Giemsa staining

Observe: - Crescent shape- Located outside or inside the cell- Singular or grouped outside the cell

Magnification: 6 x 100

2. Toxoplasma gondii Brain specimen cyst stadium Giemsa staining

Observe: - Round, thick-walled cyst - Containing plenty of bradyzoit


3. Plasmodium falciparum brain specimen HE staining

Observe:- malaria pigment inside the brain capillary


4. Plasmodium falciparum thick blood smear young trophozoid stadium Giemsa staining

Observe:- parasite: uniform morphology, ring shape, open

ring, comma, exclamation point, flying bird wings


5 Plasmodium falciparum thick blood smear specimen young trophozoid stadium Giemsa staining

Observe:- parasite: ring-shape, open ring, comma,

exclamation point, flying bird wings



6. Trypanosoma sp. Blood specimen promastigot stadium Giemsa staining

Observe: - size: 15-30 µ (erythrocyte 7 µ)- nucleus: nucleus of entamoebae- vacuolated endoplasm- unclear ectoplasm


7. Taenia spp. Fecal specimen eggs

Observe:- shape: round- size: + 35 micron- wall: thick, radiated structure- contains: hexacant or oncospheric embryo

Magnification: 10 X 45

8. Taenia solium Proglotida gravid Borax-carmine staining

Observe:- shape: round- uterus branch: 15 – 30 branches- uterus foramen: non existing- genital foramen: located on the side of proglotide


9. Cysticercus sellulose HE staining Slice from subcutaneous bulb

Observe:- Sliced bulb- Suction pod- hooks


10. Toxoplasma ELISA

- Well 1: control –- Well 2: control +- Well 3: calibration

- Well 4: negative patient- Well 5: positive patient - Well 6: positive patient



11.Acanthamoeba castelanii culture

Observe the movement of amoebas in vegetative and cystic form in culture medium.

12. RAPID DIAGNOSTIC TEST IMMUNO CHROMATOGRAPHIC TEST (RDT ICT) FOR MALARIA

In recent times, many methods beside the conventional method (microscopic) have been developed to diagnose malaria, among others through immunological approach, one of them by detecting antigen from the metabolic end product of the Plasmodium parasite, in the form of a protein excreted extracellularly by the asexual stadium in the blood.

One of the methods being developed to detect the Plasmodium antigen is by Rapid Diagnostic test ICT (Immuno Chromatographic Test) Pf/Pv.

Demonstration RESULT1. Plasmodium falciparum

2. Plasmodium vivax

3. Negative

B. Student Independent Work

1. Examine a box of specimens of Toxoplasma gondii in the tachizoid stadium and Plasmodium falciparum in the trophozoid stadium (starry sky).

C. EXERCISE

1. What are the ways to diagnose toxoplasmosis?2. What does it mean if you find Toxoplasma gondii cyst in the brain biopsy?3. Can feces excreted the previous day still be used to examine for the existence of cysts?4. Besides thorough anamnesis and clinical symptoms, what methods do you need to use

to diagnose malaria falciparum?5. When is it indicated to examine inner organs to establish a diagnosis for malaria?6. In microscopical examination of inner organs, what do you have to find to establish a

diagnosis for malaria?

Author: Rino Pattiata

Person in charge: dr. Rino Pattiata,SpPA

Tutors:

1. dr. Rino Pattiata,SpPA 2. dr. Esti Soetrisno,SpPA(K)3. dr. Endang SRH,MS,SpPA(K)4. dr. Lisnawati,SpPA5. dr. Ening Krisnuhoni,SpPA

The practical of Pathological Anatomy is composed of independent practical and demonstrations. This practical includes macroscopic and microscopic specimens.

INDEPENDENT PRACTICAL

MACROSCOPIC

NS. 1 ANENCEPHALUS

Intra uterine fetal death shows prominent disorganogenesis i.e. the failure to develop the head and the two hands. In the autopsy, in the chest there is no chest cavity content (heart and lungs). Other than that, the intra abdominal system/organs are macroscopically small, and microscopically composed of immature cells and tissue, with uneven spotting and a minor inflammatory reaction. The inflammatory cells are dominated by lymphocytes.

Comprehensive exercise:a. In your estimation, in which week of embryogenesis did the

cellular injury occurred in this case? What are the characteristics of injury at that time? (Thus resulting in the failure of some vital organs to develop!)

b. What inflammatory/infectious process can elicit the reaction of inflammatory cells, primarily lymphocytes? What is the mechanism that produces an inflammatory reaction in the fetus during macroscopic examination?

Pathological Anatomy Practical

c. Should the mother be further managed? (to secure future pregnancies)

NS.2 MICRO (EN) CEPHALUS WITH MENINGOENCEPHALOCELE GLABELLAE

The fetus is stillborn with a prominent abnormality in head size and its contents, which were very small, with a soft elastic protrusion in the glabellae area.

Comprehensive exercise:a. Is there a definitive cause of microencephally? Explain the ones you know!b. Why does a meningoencephalocelle occur in the glabellae area?c. Name the types of cele that you know! (based on the composition and

localization)d. Is there a predilection of cele localization? Name them one by one!

NS.3. HYDROCEPHALLUS AND SPINA BIFIDA

The baby is born through cesarean section because of a large head proportion, with a homogenously enlarged ventricular system, and a protrusion at the lumbar area observed through USG (Ultra Sono-Graphy)

Comprehensive exercise:a. Why does the baby’s skin have folds? Explain the various types of

hydrocephalus!b. Explain about Spina Bifida! How does it relate to hydrocephalus?

NS.4. AGANGLIONIC PERIPHERAL NERVE OF THE DIGESTIVE SYSTEM: HIRSCHSPRUNG MEGACOLONIC DISEASE (MORBUS HIRSCHSPRUNG)

Autopsy was performed and the inner organs extracted in toto from the 5 month old baby. The baby was born at term, and according to the parents had difficulty to defecate since birth, thus causing the abdomen to extend progressively. At times a tumor with changing locations was observed. The baby died while the mother was away at the market.The specimen showed an enlarged segment of the colon with a relatively thin wall (proximal of the lesion) and a segment with a small lumen with thick walls (the pathologic area, does not contain ganglion and/or plexus).

Comprehensive exercise:a. What ganglions can be found in the various layers of intestinal wall?

b. Which ones form a plexus? What are the functions of each of the above ganglions?

c. Explain the functions of various peripheral nerve system ganglions!

NS.5. MENINGITIS PURULENTA

Meningitis is an inflammation of the meninges. Commonly it occurs in the piamater and arachnoid. Thus, to identify the etiology, a sample of cerebrospinal fluid will have to be obtained by lumbar puncture.

Observe that the meninx has turned a yellowish white color, and is thick in the sulcus area. Meningo-encephalitis is often found secondarily, originating through hematogenic spreading from pathology or lesion in the tissue-organ outside the central nervous system.

Comprehensive exercise:a. From which germinal layer do the piamater & arachnoid (leptomeninx)

originate from?b. When inflamed/ mildly infected it can recover, or sometimes will result in

fibrosis when local-systemic conditions are not favorable. What about superficial meningoencephalitis? Or deep infection that forms an abscess? Which will cause permanent damage? Based on what?

c. Explain the route of central nervous system infection?

NS.6 CEREBRAL SANGUINE APOPLEXIA (RUPTURE OF CEREBRAL BLOOD VESSEL)

In the brain macroscopic specimen there is a black area with sharp borders. This area is caused by blood clot after a massive intracerebral bleeding accompanied by liquifactive ischemic necrosis process (liquefactive encephalo malacia). It is sometimes difficult to differentiate from neoplasm with cystic degeneration accompanied by bleeding in radiological imaging without contrast/ sophisticated device.

Whether occurring spontaneously or caused by trauma, the naming of intracerebral bleeding is not different and based on location and clinical symptoms when afflicting the same blood vessel, with the cerebral parenchyma area and the duramater as reference.

Comprehensive exercise:a. Explain schematically the system of intracranial and intraspinal blood

supply clearly, each with their special characteristics.b. What are the consequences of aseptic and septic emboli to the central

nervous system?

c. Explain the cerebral infarction process and the progression of the repair effort!

NS. 7. CEREBRAL GLIOMA

In the central area of the cerebellum there is a black mass (prolonged bleeding) that has a relatively sharp border, but then there is also a vague grayish white mass with unclear borders unlike in NS.6, because it is a neuroglial tumor mass.

Neoplasm: uncontrollable growth, without function, growing parasitically from its host. Especially malignant neoplasm, have severe implications on the host’s stamina and may cause paraneoplastic syndrome. Manifesting symptoms depend on the location, progression of growth that pressures/ injures/ infiltrates directly the neuron or pathway, and the implications of SOL (Space Occupying Lesion).

Comprehensive exercise:a. Explain the components of neuroglia and their main functions/ roles!b. Are you familiar with the stages of degeneration of the astrocyte,

oligodendroglia, microglia, ependymal cell, and the neuron? Name each special characteristics! If neoplastic degeneration has occurred, and the cause eliminated, could the affected cell return to normal?

c. What are the neuronal implications of some degenerative diseases that you have studied?

MICROSCOPIC

ns. 1 MENINGOENCEPHALOCELLE

The microscopic specimen is made from tissue obtained from surgery on the fronto-nasal prominence of an 8 month old female baby; it has a soft elastic consistency. There are islands of cerebral tissue in between connective tissue, some are fibrillar; sometimes you can find immature neurons.

ns. 2. MORBUS HIRSCHSPRUNG

In each numbered specimen boxes there are transverse/circular slices or longitudinal slices of pathological lesions of the distal colon. The part with the small lumen, apparently has thickened layers of the wall, and has no Auerbach ganglion-plexus but between the muscular layers you can find thickened neural fibers. In the submucosal layer a Meissner ganglion-plexus also can not be found, and the neural fibers are also thickened. That is why this abnormality is also called AGANGLIONIC MEGACOLON OF HIRSCHSPRUNG, because the

proximal segment is dilated and enlarged due to the digested food from the upper digestive tract, that is difficult to pass through the restricted lumen without proper peristaltic movements, thus the primary clinical symptom is difficulty to defecate: once every few days and of very little amount.

ns. 3 PERIPHERAL NERVE DISORDER

As in No. 2, in each box of specimen there is only one specimen from a biopsy of a 12 year old boy’s peripheral nerve with clinical symptoms similar to ascending paralysis based on the immunological reaction defect, that caused myelin damage through inflammation, especially elicited by lymphocytes. The sample of N. Suralis obtained is very small, but you can find that there is an inflammatory reaction in the complex area of the nerve fiber-capillary where sometimes you can even find amorphous substances, supporting the finding of neuritis/neuropathy that can be found in Guillain Barre Syndrome (acute fibril polyneuritis).

Other specimens were obtained from the nodule in the scapular region. They show an indefinitive proliferation of the local tissue, without regular composition, non functional, but does not threaten the health/ quality of life of their host. In a proper slice, the prominent components are lobules of fatty proliferative tissue and bundles of spotted fine nerve fibers. PROLIFERATION/ HYPREPLASIA OF THE PERIPHERAL NERVE FIBRE in a HAMARTOMA lesion.

ns. 4. ACUTE SUPURATIVE MENINGOENCEPHALITIS AND FORMATION OF CEREBRAL ABSCESS

The specimen shows an inflammation-bleeding process and contains a lipophage-hemosiderophage reaction that usually originates from systemic blood circulation that enters the parenchyma of the central nervous system when there is a process that produces so much/ wide spread debris, that the local macrophage need help from outside. In the central nerve system, the microglia (mesoderm) acts as a macrophage and is able to move towards a target, and may turn itself into a Road cell/ gitter cell/ scavenger cell.

In the specimen there is a liquefactive necrotic area with packed groups of PMN (polymorphonuclear) neutrophil cells, indicating an inflammation/ acute supurative infection and/or the formation of a micro-macro abscess. In a new process, there have not been local reactions yet in an effort to isolate/organize-repair. An old focus of cerebral abscess is surrounded by edematous tissue. The leptomeninx area is still undergoing bleeding of the subarachnoid-cerebral cortex.

The neural cell (neuron) is a permanent cell (does not have the ability to proliferate); whereas the neuroglial cells (astrocytes, oligodendroglia, ependymal cells, and microglia) still have the potential to proliferate when induced.The astrocyte plays a role in the blood-brain barrier. When an abnormal chemical substance/poison/metabolite in the blood circulation enters the central nerve system, the astrocyte will anticipate, thus eliciting an adaptive/degenerative change, in the form of: gemitocyte, Alzheimer I/II cells, Rosenthal fibers.

In the repair process, the astrocyte will fill the destructed area, thus many glial fibrils can be found and at the end of the repair there will be a gliosis. When many of the neurons are destructed, repair may give an appearance of spongiosis: this is very prominent in Prion Disease (Transmissible Spongioform Encephalopathy), Creutzfeldt-Jacob Disease.

ns. 5. BLEEDING OF THE CEREBRAL CORTEX, PERIPHERAL MEDIAL/ TOP AND SULCUS AREA OF THE PARIETAL LOBE

In each box, the specimens complete each other about the position of bleeding. The peripheral position of the intracerebral bleeding ofcourse gives more hope of better treatability, in opposite to a deeper location of bleeding/ or a position closer to the centre of a vital organ, also to those that does not reach the ventricular system and the subarachnoid (an immediate diluting process with cerebrospinal fluid), bleeding is difficult to stop (disturbed clotting mechanism)).New recent bleeding does not yet create a local tissue reaction, but the ischemic neuronal impact is apparent, like tissue edema, and ischemic neuronal acidophilic degeneration.

Bleeding near the Pacchioni granulations and Intrasulci may cause complications of communicating hydrocephalus when resorbtion is not adequate. This bleeding will cause the result of lumbar puncture of the cerebrospinal fluid to appear reddish (positive).

ns.6. BLEEDING OF PRIMARY NEOPLASM OF THE CENTRAL NERVOUS SYSTEM: ASTROCYTOMA GEMISSTOCYTIC Gr. II

Bleeding is not yet massive; no bleeding cysts have been formed. Observe the large cells with large cytoplasm, and large eccentric hyper chromatic nucleus; mitosis/ atypical mitosis (tripolar/more) are not prominent.

Neoplasm is an uncontrolled, uncoordinated, and non functioning growth of body cells, that is parasitic towards its host. It can be benign or malignant. The benign ones differentiate well (is similar to its parent cell), usually grows expansively pressuring the surrounding tissue, has thin connective tissue capsule, when extracted operatively in toto is rarely recurrent, and does not metastasize.

Malignant neoplasm shows changes in morphology-biomolecular-genetics as well as behavior; the differentiation varies from good to poor; it grows infiltratively, metastasizes, and when extracted surgically often recurs when surgery is not performed in the early stage of the neoplasm. Bleeding and necrosis can be found in neoplasm with bad differentiation/anaplastic (unknown origin), high degree of malignancy or due to distortion/pressure and/or infiltration - metabolite of malignant cells (TNF: Tumor Necrosis Factor).

In the central nervous system, especially in the intracranial space in the form of SOL (Space Occupying Lesion), there is a characteristic for age, sex, localization, and malignancy.

ns. 7. MIXED GLIOMA WITH HIGH DEGREE OF MALIGNANCY

Under cautious observation there is a differentiation towards astrocytoma and dominant oligodendroglia. Throughout the whole tissue extracted surgically, there are cells not easily recognized as parenchymal cells of the central nervous system. The cells primarily have a high N/C ratio (Nuclear/Cytoplasm ratio), (highest normal range is 1:4). They have a hyper chromatic nucleus, with a pleomorphic cellular and nuclear shape.

They appear to form an alveolar/diffuse/pseudo-rosette configuration, some with clear cytoplasm (haloed), and some spiked.

The most common glioma is astrocytoma, and the most malignant is GBM (glioblastoma multiforme). Gliomas rarely metastasize outside the cerebrospinal axis.Cerebellar glioma that is most common in children is medulloblastoma. Gliomas are more often found in men, while meningiomas are more often found in women.

CPA= Cerebello-Pontine Angle Tumor = Neurilemmoma/Schwannoma N.VIII.

Capsular neurilemmoma (NF2 defect/ Merlin)Uncapsular neurofibroma (NF1 defect)Von Recklinhausen neurofibromatosis: neurofibrous lumps distributed throughout the body; potentially undergo malignant degeneration; heredofamilial factor exists.

DEMONSTRATION SPECIMENS

Demo 1. HYPERGANGLIONOSIS

The specimen originates from an appendix with abundant Auerbach plexus-ganglion in the muscular layer, irregularly positioned. Clinical symptoms: CHRONIC APPENDISITIS

Demo 2. GLIOSIS (GERIATRIC)

Limited number of specimens, tissue from cerebral cortex does not show viable neurons, with grayish purple spotting that appears to be an early focus of corpora amilasea. Mild gliosis, base of the parenchyma is vacuolated/ early stage of spongiosis. In GERIATRICS, dementia due to numeric atrophy of the neuron, the astrocytes are responsible to fill in the space of degenerative neurons accompanied by compensatory enlargement of the ventricular system in the effort to substitute the volume of atrophic parenchyma. The type of hydrocephalus that occurs is COMPENSATORY HYDROCEPHALUS (HYDROCEPHALUS EXVACUO).

Author: Tjhin Wiguna

Person in charge:dr.Gitayanti H, SpKJ(K)

Tutors:dr.Gitayanti H, SpKJ(K)

dr.Heriani, SpKJ(K)

The Practical of Psychiatry consists of 4 sessions, chosen from a selection of 5 psychopathology practical sessions 1-5.

Psychopathology Practical 1

Psychopathology practical 1 consists of assessment of patient’s general condition and his psychomotoric activity (2 hours).

Objective: The student is able to identify: Various general conditions of patients Various psychomotor activities in a patient

Method: demonstration through video (PANSS and ESRS video)

Process: 1. The session is opened by reviewing the various pathologies that may be found in the assessment of a patient’s general condition and psychomotor activity (10 minutes) 2. Watching a PANSS video segment that is related to the general condition of a patient (30 minutes)3. Watching an ESRS video segment that is related to the psychomotor activity of a patient (30 minutes)4. Discussion on the segment of psychomotor activity (30 minutes)

Evaluation: Hand out evaluation forms to the students and ask them to fill in the

forms completely (20 min)

Psychiatry Practical

Psychopathology practical 2

Psychopathology practical 2 consists of the identification of hallucinations (2 hours).

Objective: The student is able to identify: Various types of hallucinations

Method: demonstration through video (PANSS video)

Process: 1. The session is opened with a review of the various disturbances of perception (20 minutes)2. Watching PANSS video, the assessment of hallucination segment (P3, 45 minutes)3. Discussion of the assessment of hallucination segment, and further discussion related to the other various types of disturbances of perception that were not displayed in the video. (30 minutes)




Psychopathology practical 3 consists of identifying various moods and affects (2 hours).

Objective: The student is able to identify: Various moods and affects

Method: demonstration through video (video of psychiatric interview of depression and anxiety disorder)

Process: 1. The session is opened with a review of the various moods and affects (20 minutes)2. Watching a video segment of psychiatric interview of depression (60 minutes)3. Discussion on the findings from student observation on moods and affects (20 minutes)




Psychopathology practical 4 consists of the identification of various types of disturbances in the process of thinking (2 hours).

Objective: The student is able to identify: Various delusions

Method: demonstration through video (PANSS video, segment on delusions, P1-2, P5-7)

Process: 1. The session is opened with a review on the various types of disturbances in the process of thinking (20 minutes)2. Watching a PANSS video segment on assessment of delusions. (45 minutes)3. Discussion on the results of student observation (30 minutes)




Psychopathology practical 5 consists of the various types of assessment on patient’s insight (2hours).

Objective: The student is able to identify: Process of speech and insight of the patient

Method: demonstration through video (PANSS video, segment on insight and G12)

Process: 1. The session is opened by reviewing the various types of assessments of insight (20 minutes)2. Watching a segment of PANSS video on assessments of insight (45 minutes)3. Discussion on the results of student observation (30 minutes)



Author: Diatri Nari Lastri

Person in charge:dr. Freddy Sitorus,SpS(K)

Tutors:1. dr. Freddy Sitorus, SpS(K)2. dr. Adre Mayza, SpS(K)3. dr. Eva Dewati, SpS(K)4. dr. Al Rasyid, SpS(K)5. dr. Mursyid Bustami, SpS(K)6. dr. Manfaluthy Hakim, SpS(K)7. dr. Yetty Ramly, SpS8. dr. Diatri Nari Lastri, SpS9. dr. Darma Imran, SpS

Objective:1. Increase the skill to identify nervous system dysfunctions through the

showing of clinical neurological examination video2. To understand the clinical relevance of neuroanatomy and

neurophysiology to various nervous system disorders (signs and symptoms)

Method:1. Tutors hand out papers containing patient data and questions.2. A neurological examination video is shown to complete the previous data.3. Students are asked to answer (write answers) the questions presented by

tutors.4. Students are asked to write a clinical and a topical diagnosis.5. At the end of the event, the tutor summarizes the results of the practical.

Neurology Practical

Documents

NEUROPSYCHIATRY MODULE PRACTICAL MANUALstaff.ui.ac.id/.../material/translatedpanduanprmodulsy-jiwa.pdf · Different species may have different effects from a drug. ... Buku Farmakologi