FMS 1 Final Exam – 2013

1. Draw the components of cell and their functions (10 items)

- nucleus  merupakan pusat seluruh aktivitas sel, mengandung materi genetic yg
menyimpan informasi genetic yg mempengaruhi sifat dan fungsinya dan dapat
diturunkan kepada keturunannya
- lysosome  mengandung digestive enzyme, dimana organel ini berfungsi untuk
fagositosis (mencerna benda asing), autofag (mencerna organel yg sudah tdk
berfungsi/sdh tua), dan autolysis (mencerna diri sendiri saat sudah tdk dibutuhkan)
- ribosome  tempat sintsis protein, dibagi jadi 2 : free ribosome (menghasilkan protein
yg akan dipakai internal sel) dan ribosome pada RE (mensintesis protein yg akan
disekresikan keluar sel)
- RER  terdapat ribosome, berperan dalam sintesis protein
- SER  berperan dalam sintesis lipid dan steorid
- apparatus golgi  tempat mempackage dan memodif protein sebelum direlease
- mitochondria  merupakan power house of cell, berperan dalam respirasi intracellular
dan menghasilkan energi
- cytoskeleton (microtubule)  berperan dalam transport intracellular, memaintain cell
shape, dan berperan dalam cell division dimana akan membantu pergerakan sentromer
menuju kutub2 yg berlawanan dan membentuk sentriol pole??
- sentriol  berperan dalam cell division dimana akan menarik kromosom menuju kutub2
berlawanan dalam proses segregasi
- peroxisome  berperan dalam metabolisme FA dan metabolit2, memiliki enzyme
peroxisome yg berfungsi untuk menetralkan racun (ubah H2O2 jadi H2O)

2. What is the mechanism of cell death & their differences? (8)

Necrosis
Morphology feature Loss of membrane integrity
Dimulai dgn swelling
cytoplasm & mitochondria
Ends with lysis
Complete lysis, no vesicle
formation
Biochemical feature No regulation
Post-lytic DNA
fragmentation
Physiological feature Affect group of cells
Ada inflammatory response
Disebabkan karena non-
physiological disturbance
Apoptosis
Ada blebbing, no loss of
membrane integrity
Sitoplasma menyusut,
nucleus condensed
Ends with fragmentation,
formation of smaller body
Terbentuk apoptotic bodies
Ada regulation, use
enzymatic step
Pre-lytic DNA
fragmentation
Ada release caspase cascade
Ada release various factor
dari mitokondria ke
sitoplasma
Affect individual cells
No inflammatory response
Akibat physiological
disturbance
3. Explain the differences between DNA and RNA? (5)

DNA RNA
Kadar Tidak dipengaruhi oleh Dipengaruhi oleh
kecepatan sintesis protein kecepatan sintesis protein
Letak Nucleus, mitokondria, Nucleus, sitoplasma,
kloroplas ribosom
Ukuran Sangat panjang Pendek
Bentuk Double helix Tunggal
Basa Pu : A,G ; pi : C,T Pu : A,G ; pi : C,U
Gula Deoxyribosa Ribose
Fungsi Mengendalikan factor Sintesis protein
keturunan & sintesis protein

4. Explain the 2 types of DNA damages and the repair mechanisms involving cell?
- single strand DNA damage  damage terjadi hanya pada salah satu dari 2 strand DNA.
Dapat direpair dengan cara :
* MMR (mismatch repair)  dilakukan pada damage dimana terjadi kesalahan pasang
(mismatch) dari sequence nukleotida yg ada. Repair dilakukan agar tidak terjadi mutasi
permanen.
* BER (base excision repair)  dilakukan untuk damage akibat alkilasi, deaminasi, atau
oxidasi, dimana terjadi perubahan sequence nukleotida skala kecil yg tidak menyebabkan
distorsi (non-helix distortion).
* NER (nucleotide excision repair)  dilakukan pada damage akibat radiasi sinar UV,
carcinogen, dimana terjadi perubahan sequence nukleotida skala besar yg telah
menyebabkan distorsi (helix distortion). Repair dilakukan dgn mengganti suatu region.

- Double strand DNA damage  damage terjadi pada kedua strand DNA yang ada. Dapat
direpair dgn cara :
* homologous end joining  breakage akan direjoined menggunakan DNA ligation,
merupakan pathway cepat
* non-homologous end joining  menggunakan DNA pairing sbg template untuk hasil
lebih akurat namun lebih complex dan lama

5. Explain the herediter Mendellian inheritance with cystic fibrosis as example!

Autosomal resesif
• phenotype expressed only in homozygote rr • traits are masked by normal gene
• both males and females may be affected
• many AR diseases are the result of an enzymatic defect (inborn errors of metabolism)
caused by mistakes/mutations in the DNA of a single gene
• mutation in Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene
• chloride channel • controls the regulation of transport pathways
Over 300 CFTR variations have been identified
most common: deletion of amino acid Phenylalanine at position 508 (ΔF508)
Mutations can cause: • reduction of synthesis
• prevention of the protein from reaching the plasma membrane
• incorrect function at the membrane
6. Explain the chromosome in general and chromosome abnormalities which is related to
down syndrome!
 Kromosom merupakan struktur dalam sel yg mengandung banyak gen dari seseorang.
Kromosom berbentuk kumparan, bersifat kompak, dan terdiri dari DNA + protein
(histone) yg dipackage sedemikian rupa hingga muat di nucleus.

Double helix  nukleosom oleh 8 histone  solenoid  loops  kromosom

Kelainan Down syndrome dapat disebabkan karena 3 hal :

- non disjunction (pada meiosis)  dimana terjadi kegagalan segregasi/pembelahan yg
tidak sempurna shg muncul trisomy/kelebihan satu kromosom pada kromosom 21
- robertsonian translocation  terjadi pada 2 kromosom akrosentrik (kromosom 21 dan
kromosom lain), dimana terjadi breakage pada daerah dekat sentromer, kemudian lengan
panjang kromosom yg satu akan bergabung dengan lengan panjang kromosom lainnya,
dan lengan2 pendek kromosom2 tersebut akan hilang. Pada saat segregasi, maka dapat
menimbulkan trisomy 21 (lih ppt week 3)
- mosaicism (non disjunction pada mitosis)  memiliki populasi sel yg sama tapi jumlah
kromosom nya berbeda2, sehingga menghasilkan individu yg seperti mosaic. Terjadi
akibat non disjunction pada mitosis pada masa post zygotic development

7. Mention and explain classification of protein based on their location in living cell!
- transmembrane protein (protein membrane)  lokasi pada lipid bilayer membrane,
tertanam atau nempel/sebagian tertanam
- internal protein  di dalam sel, berfungsi utk keperluan internal sel (biasa larut dalam
sel & bebas/tidak terikat pada struktur tertentu)
- xternal/secretion protein  disekresikan keluar sel dan berfungsi utk keperluan
xtracellular, mengalami modifikasi dan ditranspor keluar sel
- virus protein  pada virus

8. Explain the process of protein secretion

Sekresi merupakan proses pengeluaran protein dari sel. Protein yg akan dipakai sel
tersebut tidak akan disekresikan/dikeluarkan. Protein yg akan disekresi punya signal
sequence sbg tanda utk memandu protein agar sampai ke tempat tujuan. Pada proses
translasi, signal sequence dibentuk dan translasi tdk akan selesai sblm protein menempel
dgn RE, lalu sintesis protein akan dilanjutkan, protein di package di vesikel, keluar dari
RE dan masuk ke apparatus golgi, dimodifikasi, membentuk vesikel pada trans golgi,
keluar dari golgi, ke plasma membrane, exocytosis (melalui secretion vesicle)

## vesicle ada 2 : transport vesicle (berperan pada constitutive secretion/sekeresi yg terjadi

scr terus menerus,gada regulasi) dan secretory vesicle (berperan dalam regulated
secretion/sekresi yg terjadi saat ada perintah/sinyal, baru akan terjadi exocytosis)

9. Describe by your own word about induced pluripotent stem cell/iPSC in general and its
challenge and treatment
Pluripotent stem cells that are generated from differentiated (non-pluripotent) cells.
Or a Pluripotent cells derived from dedifferentiating and reprogramming cells
whose developmental fate have been determined.
Challenge
1. Finding approaches for delivering reprogramming factors into nucleus a
drawbacks viral integration?
Retrovirus will use host cell to replicate, viral transgene.
2. Difficult to yield high number iPSC a different cell different efficiency.
3. Minimizing DNA alteration on reprogramming.
4. Developing more safely programming for clinical application

Treatment for
1. Amyotropic Lateral Sclerosis (ALS)/Lou Gehrig’s disease
2. HIV AIDS patients
Because HIV/AIDS can mutate and become immune to treatments at an accelerated
pace, most treatments involve a chemical cocktail
– 47 (give or take) different medications
– Not a simple method
– This treatment carries with it many complications
• Patients play the side effect game
The chemical compounds are a burden on the body
– Extremely large structures
– Designed now so the body to not be able to break it
down
• Intended to extend the length of treatment
3. Mesenchymal stem cells for Autism and Autism Spectrum Disorders (ADS
Treatment of chronic spinal cord injured patients with autologous bone marrow-derived
hematopoietic stem cell transplantation
• Cairo University conducted human trial of hematopoietic progenitor stem cells in SCI
Patients
• Results: Improved functions
• Not FDA approved
• MRI showed no tumors
• Awaiting 1 year follow up

10. Explain about the immunology of hematopoietic stem cell transplantation and its way out
to rejection

3 criteria Graft versus Host Disease:

1.Immunocompetent graft is administered.

2.Recipient is immunology disparate – histoincompatible.

3.Recipient is immunocompromised therefore cannot destroy the transplantated cells.

Way out to rejection due transplantation

1.Match the donor and recipient

2.Immunosuppressive agents

3.Nuclear transfer

4.Adult stem cells

Why do stem cell transplants fail?

•Immune issues impact stem cell therapies

•Major Histocompatibility Complex is a person’s combination of cell surface proteins that

lymphocytes use to tell “self” from “non-self”

•Allogeneic transplants fail because there isn’t a match, and lymphocytes destroy the non-self
cells

11. Explain the differences between lactose intolerance and hyperglycaemia based on
biochemical process

For the people that are lactose intolerance, they lack of enzyme to digest lactose. Therefore,
the lactose passes to small intestine until colon. In the colon, some bacteria are able to
digest lactose and break it to glucose and galactose for their own (bacteria purpose).
During breaking down the lactose, the bacteria will produce hydrogen gas and make the
lactose intolerance people pass out gas (gassy) through lungs (by breathing) or flatulence
(kentut). The unused lactose will cause the people to have a watery stools or diarrhea.
Lactose is diglucose that formed by glucose and galactose. Lactose is not in the form that can
be stored in the body. Therefore, it may not accumulate in the body. It finds its way out
of the body system via stools or gas.
Hyperglycemia is the condition when glucose concentration is high in the blood. When that
happens, it iniates some pathway to reduce it or the attempt to store it by the action of
insulin (that convert glucose to glycogen for storage). When glucose concentration
increases, glucose will be converted to sorbitol (by aldose reductase via pulyol pathway)
and then oxidized to fructose (by sorbitol dehydrogenase. When the enzyme is so
saturated by too much glucose, the glucose will be accumulated in sorbitol forms in
several organs such as kidneys, nerve tissues or the lens of the eyes. The sorbitol is
accumulated because no membrane transport system to quit sorbitol from these tissues.

KETERANGAN DARI POWER POINT:

Symptoms occur because the unabsorbed lactose passes through the small intestine and into
the colon. In the colon, one type of normal bacterium contains lactase and is able to split the
lactose and use the resulting glucose and galactose for its own purposes. Unfortunately, when
they use the glucose and galactose, these bacteria also release hydrogen gas. Some of the gas
is absorbed from the colon and into the body and is then expelled by the lungs in the breath.
Most of the hydrogen, however, is used up in the colon by other bacteria. A small proportion
of the hydrogen gas is expelled and is responsible for the increased flatulence (passing gas).
Some people have an additional type of bacterium in their colons that changes the hydrogen
gas into methane gas, and these people will excrete only methane or both hydrogen and
methane gas in their breath and flatus.
Not all of the lactose that reaches the colon is split and used by colonic bacteria. The unsplit
lactose in the colon draws water into the colon (by osmosis). This leads to loose, diarrheal
stools.
The severity of the symptoms of lactose intolerance varies greatly from person to person. One
reason for this variability is that people have different amounts of lactose in their diet; the
more lactose in the diet, the more likely and severe the symptoms. Another reason for the
variability is that people have differing severities of lactase deficiency, that is, they may have
mild, moderate, or severe reduction in the amounts of lactase in their intestines. Thus, small
amounts of lactose will cause major symptoms in severely lactase deficient people but only
mild or no symptoms in mildly lactase deficient people. Finally, people may have different
responses to the same amount of lactose reaching the colon. Whereas some may have mild or
no symptoms, others may have moderate symptoms. The reason for this is not clear but may
relate to differences in their intestinal bacteria.

Sorbitol is formed in many tissues when blood glucose levels are increased. This occurs
through the "polyol pathway", a reaction sequence found in most tissues. Glucose is first
reduced to sorbitol in the aldolse reductase reaction. It is then oxidized to fructose by sorbitol
dehydrogenase.
The high blood glucose concentrations found in diabetic patients activate the aldolase
reductase enzyme, leading to sorbitol formation in several organs, notably the kidneys, nerves
and the lens of the eye. Sorbitol accumulates in these tissues because they lack a membrane
transport system for this sugar. They can reduce glucose, but cannot utilize or be quit the
resulting sorbitol. Cataract formation in the lens is believed to follow sorbitol accumulation.
Renal damage and neuropathy seen in diabetic patients is thought to be at least partially
triggered by sorbitol accumulation in these tissues.
12. Explain the membrane transport of substances through cell membrane
Transport membrane ada 2 :
- pasif  perpindahan zat dari [tinggil] ke [rendah] secara difusi, no need Energy,
membawa zat water soluble (molekul polar yg kecil, ion). Dibagi jadi 3 :
* simple/passive diffusion  ga butuh carrier protein/protein transpor, pada molekul
nonpolar-hidrofob, contoh O2, CO2, steroid
* facilitated dif  butuh carrier protein, pada molekul polar yg kecil, ion, cth : asam
amino, glukosa
* osmosis  air bergerak dari [air tinggi] ke [air rendah], cth : krenasi, lysis
- aktiv  perpindahan zat dgn melawan gradien [], dimana dari [rendah] ke [tinggi]
sehingga need Energy, cth : Na+ K+ pump (Na out K in) #Na byk di luar, K di dalam#

13. Explain the second messenger system that are present in cellular activity
13. Second messenger is one part of the mechanism called signal transduction. Signal transduction is
a process which involves first messenger (such as hormones) that gives instructions for cells
(particularly the nucleus) through specific signals to a certain receptor on the surface of cell
membrane, and when it reaches the receptor, corresponding signals appears inside the cell in order
to send the message from the first messenger to the nucleus. The concept of how second messenger
works can be seen through phosphorylation cascade to activate a protein channel.

In order to give signal, a G-protein receptor appears on the surface of the cell membrane to take the
code from the first messenger. As the first messenger attached to the receptor, the G-protein
attached, which consists of alpha, beta, and gamma protein with GDP, separates into alpha protein +
GDP and beta-gamma protein. As they are separating, GDP is replaced by GTP. Due to GTP
attachment now to alpha protein, the protein now moves forward to transmembrane enzyme
phosphorilase C. When alpha protein and phosphorilase C have joined together, GTP gave energy in
order to activate the enzyme by losing Pi. Now, the alpha protein is attached to GDP and will return
back to join beta-gamma protein. As phosphorilase C is now activated, it releases phospholipid to
produce two second messengers, such as IP3 and diacylglycerol. Then, IP3 goes and attached to a
receptor in the endoplasmic reticulum to release calcium ions. The released calcium ions and
diacylglycerol go and attach to another enzyme on the plasma membrane, protein kinase. By this,
protein kinase is activated and it moves to a protein channel (typically cation protein) on the plasma
membrane. When it reached cation protein, the protein channel is opened by the enzyme and with
the help of ATP. Therefore, the protein channel will be opened.

14. Explain with the help of diagram about cell cycle and explain 3 roles of critical cancer
genes
(Gambar diagram seperti roda cell cycle)
The cell cycle shown on the diagram visualized how cells reproduce. The cycle goes from G1
 S  G2  mitosis / meiosis
Stage G1: At this stage, the cell that is going to reproduce is just growing into a bigger cell.
Before moving on to the next stage, here lies a checkpoint in which to see that the grown cell
is normal, such as no cell inhibition, no DNA damage, enough space for replication, etc.
Stage S: At this stage, the cell’s DNAs inside the nucleus are duplicated and form into
chromosomes.
Stage G2: At this stage, the cell’s DNAs are shaped in chromosomes and getting ready for
cell division. In this stage, here lies another checkpoint. This checkpoint looks for any DNA
damage or any wrong base pairings before moving on to cell division.
Mitosis/Meiosis
Mitosis: This is where cell division happens for autosomal cells (diploid cells reproducing
diploid cells). It started from the release of chromosomes from the nucleus (interphase) and
the formation of spindle fiber inside the cell (prophase). As the spindle is forming, the
chromosomes must line up at the center of the cell and attach to the spindle at their
centromeres (metaphase). After metaphase happened, here lies another checkpoint in order to
see whether all spindle fiber is attached to the centromeres. When all centromeres are
attached, the spindle fiber will start to pull the chromosomes to different polar, making the
chromosomes separated into chromatids (anaphase). After the separation of the sister
chromatids, the nucleus started to form again while the cells are now separating as well
(telophase). The cell should separate perfectly in order for reach success in cell cycle
(cytokinesis).
Meiosis: This is where cell division happens for gametes (diploid cells reproducing haploid
cells). The basic of meiosis is similar with mitosis. The differences in meiosis is that it has 2
cycle of mitotic stage and involves exchanging genetic materials.
The basic of cell cycle was discussed above. By understanding cell cycle, therefore it is easier
to understand how cancer cells develop. There are 3 critical genes in controlling cancer cells,
DNA repair genes, proto-oncogenes/oncogenes, tumor suppressor genes.
DNA repair genes: This genes repair when DNA is broken.
 Single strand damage:
 o Mismatch repair – for repairing mismatched base pairing
o Base excision repair – for repairing damage due to point base mutation
o Nucleotide excision repair – for repairing base that connects to the consecutive
base on the same strand
 Double strand damage:
o Homologous recombinant end joining – for repairing broken part of DNA
o Non-homologous recombinant end joining – for repairing the loss base pair in
DNA sequence

Proto-oncogenes: This gene does not generate cancer cells, but when it’s mutated into
oncogenes, it generates cancer cells.
Tumor suppressor genes: This gene, particularly p53, suppressed the development of cancer.
When it is mutated, then there is nothing to suppress any cancer development. Therefore,
cancer cells might develop without inhibition.

15. Explain about epigenetics and their roles in cancer

Epigenetic merupakan prubahan heritable (bisa diwariskan) pada pattern gene expression
dimediasi oleh perubahan taq2/marker dari DNA tsb (DNA sndiri gak brubah). Dibagi
jadi 2 : DNA methylation and histone modification (methylation, acetylation,
ubiquination, phosphorylation).

Prinsip 22nya sama : kalo kbanyakan methyl (DNA methylation)/hypermethylation akan

menyebabkan DNA rigid dan susah diakses oleh transcription factor shg transkripsi
gakbisa jalan & less protein production. Hypomethylation : kebalikannya, kbanyakan
transkripsi jd too much protein production. Berlaku sama dgn histone modification

Peran dgn cancer : cth hypermethylation pd p53, hypomethilation pada cancer gene??

JAWABAN FMS 2
1. Patent Foramen Ovale

Pada hari ke-28, antara atrium communis dan ventrikel terdapat penonjolan
yang disebut endocardial cushion. Dari atap atrium communis terdapat
 penonjolan yang tumbuh kembang kea rah endocardial cushion, dinamakan
septum primum. Sebelum septum primum mencapai endocardial cushion,
mengalami absorbsi, membentuk foramen primum. Pada waktu yang sama,
sebelum septum primum selesai diabsorpsi, terbentuk penonjolan ke-2 dari atap
atrium communis yang juga tumbuh kembang ke arah endocardial cushion,
dinamakan septum sekundum. Sebelum mencapai endocardial cushion, septum
sekundum juga mengalami absorpsi. Terbentuk foramen diantara septum
primum dan septum sekundum dinamakan foramen ovale.

Pada kasus Patent Foramen Ovale, foramen ovale tidak menutup dan berubah
menjadi fossa ovalis, hal ini mengakibatkan darah yang kaya CO 2 dari atrium
kanan yang seharusnya masuk ke ventikel kanan, melewati foramen ovale ke
atrium kiri dan bercampur dengan darah yang kaya O2 di atrium kiri.

2. Situs Inversus

Pada minggu ke-6, midgut mengalami elongasi dan membentuk ansa intestine
primarus. Selain itu, pada waktu yang sama, terjadi pembentukan dan
pengembangan hati yang begitu cepat. Hal ini mengakibatkan cavum
abdominalis tidak dapat menampung seluruh ansa intestine sehingga sebagian
ditonjolkan keluar lewat umbilicus, disebut hernia umbilicalis physiologica.
Kemudian terjadi rotasi intra umbilical 90 oCCWR. Pada bulan ke-3, cavum
abdominalis sudah mulai membesar dan dapat kembali menampung seluruh
ansa intestine, maka terjadi rotasi reduksi 180 oCCWR sehingga ansa intestine
kembali masuk ke rongga abdomen dan mengalami elongasi di dalam cavum
abdomen.

Pada situs inversus totalis, terjadi malposition intestinalis dimana hal ini
disebabkan karena kesalahan saat proses rotasi.

3. Hydrocephalus

Pada minggu ke-3, neural plate mengalami lateral folding menjadi neural fold.
Neural fold, pada daerah cervical region (somite 4) mengalami fusi, membentuk
neural tube. Neural tube mengalami pemanjangan ke arah cranial dan caudal
dimana bagian ujungnya tetap terbuka. Ujung cranial yang terbuka dinamakan
neuroporus anterior dan ujung caudal yang terbuka dinamakan neuroporus
posterior. Neuroporus anterior akan menutup pada hari ke 25 (18-20 somite
stage) dan akan tumbuh menjadi otak. Neuroporus posterior akan menutup pada
hari ke 27 (25 somite stage) dan akan tumbuh menjadi spinal cord. Pada minggu
ke-4, neural tube akan membentuk 3 pembesaran : prosencephalon,
mesencephalon, dan rhombencephalon. Pada minggu ke 5, akan terdapat 5
pembesaran : telencephalon, diencephalon, mesencephalon, metencephalon,
myelencephalon. Terbentuk rongga di dalam pembesaran tersebut. Rongga di
dalam telencephalon dinamakan ventriculi lateralis, rongga di dalam
diencephalon dinamakan ventrikulus tertius, dan rongga di dalam
 rhombencephalon dinamakan ventikulus quartus. Di dalam rongga tersebut
membentuk system ventricular yang fungsinya untuk mengalirkan CSF.

Pada hydrocephalus, terjadi defect pada sistem ventricular. Defectnya dapat

disebabkan karena produksi CSF dalam jumlah berlebih obstruksi pada system
ventricular, atau karena absorpsi CSF yang terganggu.

4. Pendarahan di mid shaft humerus

Nerve : N musculocutaneous, N medianus
Pembuluh darah : A. brachialis, A. profunda brachii

5. Muscle pada sciatic nerve

Di paha : M. biceps femoris, M. semitendinosus, M. semimenranosus
Di betis : M. gastrocnemius, M. soleus, M tibialis posterior

6. Arteri besar di abdomen

Trunkus celiacus
Arteri mesenterica superior
Arteri mesenterica inferior

7. Alat genital
Pria : testis, prostat, epididimidis, vas deferens, vesicular seminalis
Wanita : ovarium, tuba fallopi, uterus, cerviks, vagina

8. Saraf
CNS → brain and spinal cord
PNS → cranial nerve → N. olfactori, N. opticus, N. oculomotori, N. trochlearis, N.
trigeminus, N. abducen, N. fasialis, N. vestibulocochlear,
N.
glosopharingeus, N. vagus, N acesorius, N. hypoglosus
spinal nerve → motoric, sensoric, autonomy

9. Mikroskopik dan Morphology dari Intramembranous Ossification:

Tampak trabekel – trabekel tulang.

Hasil: tulang – tulang pipih (cranium, sternum, pelvis)

Mikroskopik dan Morphology dari Endokondral Ossification:

Tampak zona – zona :
-Zona rehat: sel – sel acak
-Zona proliferasi: sel – sel gepeng berhimpitan
-Zona hipertropi: Sel – sel besar
 -Zona calcification: Kurang jelas (Sel pecah – pecah/mati, sel sudah tidak ada
inti)
-Zona osifikasi: merah – merah, mulai menjadi tulang
Hasil: Membentuk tulang – tulang pendek dan panjang

10. Otot Polos: bekerja secara involunter berfungsi dalam gerakan Peristaltik,
berbentuk spindle dengan nucleus satu di tengah, dan tidak mempunyai
striations

Otot Rangka: bekerja secara sadar/volunteer berfungsi dalam Pergerakan

sehari-hari serta keseimbangan, berbentuk silindris panjang dengan banyak
nucleus di tepi, dan mempunyai striations

11. Neuron Motoris: Letaknya di kornu Anterior Medulla Spinalis (sayap besar) dan
berfungsi untuk menghantar impuls dari Medulla Spinalis ke otot (efektor)
*ciri kornu anterior:
-Ada celah
-Sel multipolar (banyak dendrit),
-Terdapat beberapa sudut (tidak cuma bulat)

Neuron Sensoris: Letak di kornu Posterior Medulla Spinalis dan berfungsi

untuk menghantar impuls dari reseptor ke Medulla Spinalis
*ciri kornu posterior?
-tidak ada celah
-biasanya unipolar

12. Innervasi Otot Polos:

 It is activated unconsciously (Autonomic Nervous System)
 Innervates smooth muscles, cardiac muscle and glands
 Slow acting
 Respond to internal stimuli (GVA)
 Fibers nya: Preganglionic & postganglionic
 Innervasi Otot Rangka:

 Striated muscle
 Voluntary by Somatic nervous system with Ionotropic membrane
receptor/ Nicotinic acetylcholine receptor
 The terminal axon formed neuromuscular junction in which contain
neurotransmitter acetylcholine. & release into synaptic clefts
 Muscle fiber contraction is “all or none” muscle fibers within a given
motor unit will either fire & contract maximally or not at all
 Masuk ke Sistem Saraf Pusat which means Neuron Motoris dari Medulla
Spinalis berakhir di skeletal muscle nya

14. Three main components and function of bone development.

(intinya ada osteocytes, osteoblast dan osteoclast yg berperan dalam bone development saat
bone remodeling, bone growth in length or widening/thickening). Penjelasan di bawah lebih
merinci.
Osteoprogenitor / osteogenic cells make up the formation of 3 types cell of osseous tissue :
A. Osteoblasts: - bone forming cells - found on surface of bone

- no ability to mitotically divide - collagen secretors

 The initial stage in bone production is the secretion of collagen molecules (called
collagen monomers) and ground substance (mainly proteoglycans) by osteoblasts.

 The collagen monomers àpolymerize rapidly àto form collagen fibers;

the resultant tissue à becomes osteoid,

B. Osteocytes:

derived from osteoblasts trapped in the matrix they formed (osteoid) à Osteocytes
mature bone cells - do not secrete matrix material
cellular duties include exchange of nutrients and waste with blood. (concentrate Cal &
Phosphate in mitochondria)
C. Osteoclasts

- develop in bone marrow by fusion of 3-50 stem cells

- reside in pits that they ate into the bone - bone resorbing cells - bone
surface
- growth, maintenance and bone repair
Once a bone is formed, osteoblasts and osteoclasts still play a very important role in the bone
remodeling that takes place THROUGHOUT LIFE
• Bone remodeling is the result of the combined actions of osteoblasts and osteoclasts

 Osteoblasts SYNTHESIZE bone matrix, creating more osseous tissue =

BONE DEPOSITION

 Osteoclasts DISSOLVE bone matrix, removing osseous tissue = BONE

RESORPTION

The widening and thickening of bone (bone growth) is called APPOSITIONAL GROWTH
• A thin layer of osteoblasts (the bone forming cells) resides on the inner
surface of the periosteum

• As the osteoblasts lay down more and more osseous tissue, making the
bone thicker and wider,

• osteoclasts come behind from inside the marrow cavity and dissolve some
of that bone allowing the marrow cavity to grow as well

 This prevents bones from becoming overly dense and heavy due to
growth

21
BMU Remodeling Sequence
Osteoclasts and osteoblasts assemble into Basic Multicellular Units (BMUs)

Osteocytes

Activation

Quiescence
Resorption

Formation & Reversal

Mineralization

15. Describe the fetal circulation and difference between fetal and after born neonatal
circulation.
FMS III
PA
1. Difference between acute and chronic inflammation
2. Correlation between acute and chronic inflammation in systemic and clinical
changes
3. What happened when the formation of granuloma

Histologi
4. Difference between lymph nodes and spleen

Immunology
5. Explain the function of each component immune system (innate). Innate cellular
=> neutrophil, makrofag,basophil, eusinofil, dendritic, NL. Innate humoral =>
complement
6. Describe the cellular and humoral component of adaptive immune system with
each of its function. Adaptive cellular => limfosit T dan B. Adaptive humoral =>
antibody

Farmakologi

7. a. describe the mechanism why the man got rash & mechanism of
diphenhydramine => block histamin response, antagonist competitive
b. explain the mechanism of dexamethasone => anti inflammation (mengurangi
rash)
c. Why the man got sore throat & dry mouth? => efek samping rangsangan
antihistamin receptor cholinergic (parasimpatik)

8. a. describe the route of drug administration

b. best drug administration for the patient

Fisiologi
9. Explain the negative feedback mechanism and its role in maintain the body
homeostasis

10. Explain the mechanism of baroreceptor to maintain blood pressure that affects
Cardiac output, Heart rate , Stroke volume
 11. Describe the mechanism of heat transfer between the body and the environment
and also describe the influence factor in each mechanism of heat transfer!
12. Acid-base balance case
13. Mechanism of ADH release before-after exercise
14. Describe the mechanism of normal tissue perfusion
15. Explain the factors that maintain acid-base balance

Jawaban :

1.

Differences Between Acute and Chronic Inflammation

Features Acute Inflammation Chronic Inflammation
Onset Rapid onset Insidious/delayed onset

Duration of Course Short (Days) Long (Weeks to Months)

Specific as it involves Acquired

Specificity Non-specific
Immunity

 Pain (Dolor)
 Heat (Calor)
 Redness (Rubor)
Cardinal Signs  Swelling (Tumor) Absent in any of cardinal signs
 Loss of Function (Functio
Leasa)

 Physical and Chemical damages

 Presistent infection
 Pathogen invasion
 Presence of foreign bodies
Causative Agents  Tissue necrosis
Autoimmunity
 Immune response

Lymphocytes o T cells o B cells

Neutrophils
Fundamental Cells
Macrophages
Macrophages Fibroblasts

Fluid Exudation and

Present Absent
Edema
Fibrosis Absent Present
Angiogenesis Absent Present
  Low grade fever
 High grade fever
 Loss of weight
Systemic Manifestation  Other 5 cardinal signs
 Loss of appetite

 Neutrophil Leukocytosis  Often absent

Peripheral Blood (bacterial infection)  Increase in the level of
Changes  Lymphocytosis (viral infection) Antibodies

Vasoactive amines o Serotonin  Interferon Gamma

 TNF alpha
 Growth Factor
Primary Mediators o Histamine Eicosanoids
 ROS
 Hydrolyzing enzymes
o Prostaglandins o Thromboxane

2. Acute and chronic inflammation in systemic and clinical changes

(diambil dari Lange Medical Immunology)

Acute inflammation is associated with an infiltration of neutrophils. The local release of

inflammatory mediators produces swelling, redness, heat and pain at the injured site.

As early as 30 minutes after acute injuries, neutrophils accumulate to significant level within 8-12
hours and continue to increase until the production of chemotaxis subsides. The hallmark of the
acute inflammation is the pus production that is enzymes released from dying neutrophils and
liquefy nearby host cells to form semi fluid residue. The extracellular degranulation is observed
when neutrophils encounter target that larger than themselves.

Systemic (blood circulation. In severe acute infections, or other period of high demand, the rate at
which neutrophils are produced and released from storage in the bone marrow increases
dramatically, so the blood neutrophils concentration rises several fold. If marrow output is great,
immature neutrophils that have unsegmented, rod shaped nuclei (called bands) may be released in
the bloodstream.

Chronic inflammation.

The presence of macrophages in significant numbers (7-10 days pass) and the influx of lymphocytes
are the host response known as chronic inflammation. Macrophages aggregate around target are
known as granuloma formation and usually contain lymphocytes, fibroblasts etc.

Acute inflammation Chronic Inflammation

Clinical Changes Pus on the injuries Granuloma formation, observed
site epithelioid cells (macrophages form
continuous sheet of cells resemble
epithel) and multinucleated giant cells
(macrophage that fuse together)
Systemic Blood neutrophils Macrophages circulating in blood with
 concentration rises less abundant than neutrophils but with
many sub populations of macrophages.
Inflammatory cells that Neutrophils: Macrophages: tissue-resident
involved circulating in the
bloodstream
Time to response 30 min to 12 hours 7-10 days
3. Formation of granuloma.
Granulomas form when the immune system attempts to wall off substances that it perceives as
foreign but is unable to eliminate. This is initiated with the recruitment of cells from the blood
including macrophages and neutrophils. The macrophages and neutrophils try to contain the
infection. They are then arranged into a spherical structure surrounding a centrally necrotic area.
Then, the lymphocytes (CD4+ and CD8+ T cells, B cells) migrates as well and surround the necrotic
area forming small lymphocytes cuff. Often, the epitheloid macrophages then fuse to form
multinucleated giant cells, Langhans’ giant cells which participate in bacterial killing and prevent
excessive pathology. Hence, granuloma is formed.

4. Difference between lymph nodes and spleen

Lymph Nodes Spleen

Shape & Size Small bean-shaped Largest lymphatic organ
structures, usually less
than 2.5 cm (1 inch) in
length.
Histology Composed of lymphoid • Red pulp contains all the
tissue. components of circulating
Blood
Cortex > Germinal centers • White pulp (little
produce lymphocytes islands, mostly B cells
Medulla > Medullary cords
Location They are widely Located between the
distributed throughout the stomach & diaphragm
body along the lymphatic
pathways

Three superficial regions

where
lymph nodes tend to
cluster
1. Inguinal nodes in the
groin
2. Axillary nodes in the
armpit
3. Cervical nodes in the
neck
Afferent vessels or sinuses Present Absent
Function Important lymphocytes of • Blood formation
the • Blood filtration
immune response are • Blood storage
 matured here.
Lymphatic flow Lymph enters nodes
through afferent
Lymphatics > flows
through sinuses > exits
through efferent lymphatic
From trabecular artery >
central arteries > penicillar
arteries > Pulp arteries
(Sheathed arteries (Hülsen
arteries) & capillaries) >
Open and Closed
circulation > sinus venosus
> trabecular vein

5. a) Innate Immune System

b) Innate : thrombocyte, erythrocyte, eosinophils, basophils, neutrophils, monocyte, DC, NK cell

c) function of its component :

Komponen Cellular

Trombosit (untuk pembekuan darah saat luka), eritrosit ( sel darah merah dalam tubuh), eosinophil
(untuk infeksi parasite, ADCC, non phagocityc), Basophil ( nonphagocytic, allergies), NK cell (killing
stressed cells, killing infected cell, phagositosis), DC (utk APC), Monocyte ( untuk inflamasi kronik,
phagocytosis, APC), Neutrophil (utk fagositosis, inflamasi akut)

Komponen Humoral :

Memiliki fungsi complement seperti untuk fagositosis, menghancurkan microbe by leukosit, osmotic
lysis of microbe.

6. a) Adaptive Immune system

b) characteristic of this immune system :

Memory, clonal expansion, specialization, non reactivity to cell, specificity, wide diversity

c) humoral componentnya : antibody

d) fungsi humoralnya : untuk neutralisasi racun microbe, fagositosis microbe, ADCC,

complement activation yaitu : untuk inflamasi, melisiskan microbe, fagositosis

e) tipe antibodynya : Active artificial aqcuired

7a. Describe the mechanism why the man got rash & mechanism of diphenhydramine ? saat alergen
masuk -> berikatan dengan reseptor di cell mast -> cell mast lysis -> mengeluarkan histamin ->
histamin punya reseptor di beberapa tempat (skin, repsi, pembuluh darah) -> di kulit (gatal) di
pembuluh darah (vasodilatasi) di repsi (bronkokonsitriksi). Orang yang tidak punya hypersentivitas ->
tidak akan terjadi.

Pemberian diphenhydramine -> memblok reseptor dari histamin sifatnya antagonis – kompetitif.
Bisa menggeser jika diberikan dengan cepat dan kuat. Ketika terjadi alergi yang kuat dia akan
menduduki reseptor yang longgar (mencegah inflamasi berkepanjangan).
b. explain mechanism of dexamethasone

anti inflamasi (rubor, kalor, dolor)

c. why the man got sore throat & dry mouth?

Reseptor histamin sama dengan reseptor kolinergik (sifatnya parasimpatik). Jika dihambat akan
menghasilkan mulut kering keluar liur -> rangsangan kolinergik. Mulut kering ->tenggorokan kering

8a. Describe the route of drug administration

ADME

a. Obat awal harus di absorbsi

b. Lalu distribusi ke bagian apa saja melalui darah (sirkulasi sistemik)
c. Dibawa ke hati untuk biotransformasi (metabolisme), mengubah susunan kimianya.
d. Menjadi tidak aktif akan dibuang (ekskresi)

b. Melalui intravena.

10. ↑BP-> Baroreceptor -> Pusat kardiovaskular -> ↓ Akt. Saraf simpatis jantung -> ↓aktifitas simpatis
-> ↑Aktifitas parasimpatis -> ↓kec. Jantung -> ↓stroke volume -> vasodilatasi arteriol dan vena -> ↓
cardiac output -> ↓resistensi perifer total -> BP turun ke normal

(Termasuk sebaliknya, ada di Sherwood)

11. Describe the mechanism of heat transfer between the body and the environment and also
describe the influence factor in each mechanism of heat transfer.

Conduction – The transfer of heat between two objects of different temperature that are direct
contact with each other. Influence factor: Temperature difference between two surface in contact
(The greater is the temperature difference, the faster is the rate of heat transfer), Surface area in
contact (the greater is the surface area in contact, the faster is the rate of heat transfer).

Convection – The transfer of heat from one place to another by motion of heated substance.

Influence factor: Wind (the stronger the wind, the faster is the rate of heat transfer), Temperature
difference between two area (the greater is the temperature difference between the two area, the
faster is the rate of heat transfer)

Radiation – The transfer of heat between two objects through electromagnetic waves.
Influence factor: Surface area (the greater the surface area, the faster is the rate of heat transfer)

Evaporation – Changing a liquid into a vapor. Heat is loss through insensible water loss and
sweating. Influence factor: Body surface area (the greater the surface area, the faster is the rate of
heat transfer), Amount of sweat (the greater is the amount of sweat evaporated, the faster is the
rate of heat lost to the surrounding).

12. Acid Base Balance

Jika metabolik asidosis:

- di sebabkan oleh diare, dll

- Banyaknya HCO3- yangg keluar dan meningkatnya H+ di tubuh
- Respiratory yangg mengkompensasi dengan hipoventilasi
- Lebih sedikit CO2 yg masuk ke dalam tubuh sehingga mengurangi keasaman tubuh

Jika metabolic alkalosis:

- disebabkan oleh muntah-muntah atau konsumsi obat-obatan yang bersifat basa

- Karena perut sifatnya asam, jika muntah, banyak H+ dan Cl- yg keluar
- Level HCO3- akan meningkat
- Respiratory yang mengkompensasi dengan hiperventilasi
- Banyak CO2 yang masuk ke dalam tubuh untuk meningkatkan keasaman tubuh

Jika respiratoric asidosis:

- disebabkan oleh retensi CO2 di dalam tubuh

- Dikompensasi oleh ginjal dengan mengeluarkan H+ di dalam urin
- Ammonia juga disekresikan untuk membuat keadaan menjadi lebih basa

Jika respiratoric alkalosis:

- disebabkan oleh kehilangan banyak CO2

- Dikompensasi oleh ginjal dengan mengeluarkan HCO3- didalam urin
- Ginjal akan reabsorpsi H+ balik ke darah dengan pertukaran dengan K+ di darah

13. Mechanism of ADH release before-after exercise

After exercise:

- Water is lost through sweat in order to do remove excessive heat from the body
- Exercise increase production of heat due to the increase of metabolism to produce ATP for
muscle work
- More water loss, blood will be more concentrated, Na+ in blood will increase
- Na+ increase, stimulation of ADH secretion from pituitary gland
- ADH causes increase of water permeability by inserting aquaporin
- ADH causes reabsorption of water in distal convoluted tubule and collecting duct
- Concentrated urine is produced

14. Describe the mechanism of tissue perfusion

 - Diffusion: movement of particle from high concentration to lower concentration and down
the concentration gradient
- Contohnya glukosa, O2 dan ion-ion yg penting untuk tubuh akan di perfusikan melalui difusi
ke dalam tissue
- CO2, urea dan lain-lain akan dikeluarkan oleh tissue
- Osmosis: movement of water particle from higher water potential to lower water potential
through semi permeable membrane.
- Ada dua tekanan yang berperan penting dalam pergerakkan air seperti osmotic dan
hydrostatic pressure
- hydostatic pressure: sifatnya mendorong. Jika tekanan di dalam kapiler lebih tinggi dari
tissue, air akan terdorong untuk masuk tissue
- osmotic pressure: sifatnya menarik dan tergantung dengan banyaknya protein atau ion di
suatu tempat.
- Jika konsentrasi di dalam kapiler lebih tinggi dari pada tissue, akan ada pergerakkan difusi
seperti Na, Cl, albumin, dll.
- Air akan ditarik oleh protein atau ion tersebut. Pergerakannya mengikuti mereka.

15. 3 komponen homeostasis :

a. Receptor – monitors the environments and responds to changes (stimuli)
b. Control center – determines the set point at which the variable is maintained
c. Effector – structures that provide the means to respond to the stimulus and restore the
variables to the optimal physiological range.

FMS IV
1. Swab tenggorokan. Fever
A. Anaerobic cocci
B. Normal Flora Oral

2. Ambil sample darimana. Jawaban : Feces

3. X molecule can binds to receptors on certain B cells but does not stimulate them to
produce X molecule antibodies unless it is first conjugated to a larger, immunogenic
molecule such as albumin. These findings indicate molecule X is a(n):
A. hapten
B. antigen
C. adjuvant
D. tolerogen
E. Immunogen

4. Hydrocephalus. Jawaban : Cytomegalovirus

5. …
6. …
7. …
8. …
9. …
10. …

11. Patient: diarrhea, vomit. Gram negative. Virulence factor?

A. M protein
B. Polypeptide
C. Calcified protein
D. Peptide
E. Lipopolysaccharide

12. New vaccine. The one that induce greatest immune response?
A. 100.000 Da particulate protein. Human male. Intravenous
B. 100.000 Da soluble protein. Human female. Subcutaneous
C. 100.000 Da soluble protein. Chimpanzee. Subcutaneous
D. 100.000 Da soluble protein bacteria. Intravenous
E. 100.000 Da particulate protein. Bacteria. Subcutaneous

13. Rural area. Sterilization plastic/ rubber surgery tools

A. Boiling
B. Autoclaving
C. Uv radiation
D. Ultrasonic wave
E. Gaseous ethylene oxide

14. Mild fever, pain, swelling, redness in left knee. Accidents 5 days ago.
Yellow purulent discharge at wound. Grapelike clusters. Virulence factors?
A. Exotoxin
B. Flagella
C. Glycocalyx
D. Techoic Acid
E. Lipopolysaccharide
 15. Young boy. Brain abscess. Previously diagnose: chronic otitis media. Pus, culture:
gram positive cocci cluster transmission?
A. Sexual
B. Airborne
C. Fecal oral
D. Contagious
E. Hematogenous

16. Immunocompromised person with high fever, confused. Liver and kidney function
were normal. Blood pressure 60/40 and pulse 136x. Doctor diagnose sepsis caused by
fungi. Culture show true hyphae. What is the most appropriate drugs?
A. Nypsin
B. Intrakonazole
C. Griseofulvin
D. Ketokonazole
E. Ampotericin B

17. Baby 8 months old, fever, cough, diarrhea, swab faring appears to have gram positive
spherical. Keluarin toxin yg bikin toxic shock syndrome. What possible finding in the
swab?
A. Streptococcus spp
B. Staphylococcus spp
C. Clostridium spp

18. Mother, 43 years old. High in IgE. TH2 more than TH1 and Tc. What mechanism?
A. Non reactive to cell
B. Specific
C. Specialization
D. Diversity
E. Memory

19. 3 Years old female. Fever. Lethargy. Irritability. Apnea. Projectile vomiting. Nuchal
rigidity. Diminished deep tendon reflexes. Bacterial meningitis by gram negative
cocci. Bacterial structure that can prevent infection of pediatric population?
A. Haemophilus influenza
B. Polyribose

20. A 6 years old girl presented a dry cough, fever, runny nose and sneezing. After about
two weeks, this condition progresses to a spells of paroxysmal coughing. This episode
worsen and characteristic of whoop begins. For confirming the diagnosis, a
nasopharyngeal expirate will be culture on Bordet-Gengou medium and the result of
gram staining is gram negative coccobacilli. The immunization was questionable.
Which of the following cells is the most appropriate for the respiratory tract?
A. Giandiasis
B. Leukocytes
C. Lymphocytes
D. Ciliated cells
E. Muscular cells
21. Cewe vagina kena penyakit. DNA virus, sexually active. What virus? Jawaban : Herpes
22. Penyakit Ascaris. Specimen?

23. Sore throat. Bacteria gram positive. Cocci in cluster.

24…
25…
26…
27…
28…
29…
30…

31. During S.pyogenes infection, individual generated high levels of IgM and IgG antibodies
against S. Pyogenes antigen yang strukturnya sama dengan subtance yang ada di jantung dan
menyebabkan cardiac damage. Mekanisme apa yang terjadi?
C. Mimicry Molecule

32. seorang anak lumpuh sebelah kakinya thin, weak, and wasted. Imunisasinya gak lengkap.
What vaccine can be used to prevent this condition?
A. BCG
B. DPT
C. MMR
D. OPV
E. HIB

33. HIV. Struktur yang mudah bermutasi :

A. Protease
B. Dismutase
C. CD 4 receptor
D. Viral structure
E. Reverse transcriptase

34. Laki2 ada pus di urine terdeteksi gram negative diplococci, Lupa neh

35…

36. 13 Years old. Fever. Watery diarrhea. Active bowel sound. Non-tender. Viral. Daycare,
teman2nya kena. Transmission? Droplet.

37. Anak kecil. Low fever. Skin rashes. Self-limiting. Transmission?

38. Danny. 10 years old children has lesion on his thumb but he doesn’t notice it. Adaptive
immune system hasn’t worked so he rely on his innate immune system what signal induce
innate immune system?
A. Complex peptides from infectious agent with MHC class II
B. Complex peptides from infectious agents with HLA
C. Enzyme wall lipid bilayer of infectious disease
D. PAMP
E. Cytokine from infectious agents

39. Bacteria gram positive. Streptococcus. Virulence factor, “spreading factor”

A. Deoxyribonuclease C
B. Streptokinase
C. Hyaluronidase
D. Protein M

40. Runny nose. Rash. Fever. Punya anak umur 9 bulan. Immunisasi apa untuk mencegah
penyakit ibunya?
A. BCG
B. OPV
C. HiB
D. MMR
E. Hepatitis B.

41. Seorang pasien dgn keluhan demam, mual, muntah, sakit kepala, ada petechie. Apa yg
menyebabkan dia bisa gini? a. droplet inhalasi dari orang dgn gejala sama ; b. digigit
artropoda ; c. kontaminasi makanan ; d. kontak langsung dgn pasien gejala sama

42. Mutasi pada gen AIRE dapat berdampak pada immunotolerance apa? a. T regulatory ;
folicular exclusion ; c. receptor editing ; d. anergi T cell ; e. apoptosis T cell

43. Seorang pasien dgn gejala flu-like syndrome, limfadenopathy, hepatosplenomegaly. Ia ke

dokter dan dokter mendiagnosis bahwa penyakitnya disebabkan oleh sesuatu yang
berhubungan dengan Burkhit Lymphoma. Apa causative / etiology nya? a. EBV ; b. CMV ;
c. HPV ; d. retrovirus ; e. lupa apa satu lagi pilihannya

44. nyamuk pembawa penyakit dengan ciri ada bintik2 putih di kaki dan badan, serta
gambaran lyre putih pada mesonotum nya adalah nyamuk? a. Aedes aegypti ; b. Aedes
albopictus ; c. Mansonia family ; d. Anopheles barbirostus ; e. Culex quequinfasciatus

45. Seorang pasien dengan gejala left ear pain dan ada pus. Pus kemudian dikirim ke lab
untuk pemeriksaan dan ditemukan gram + cocci in chains. Pasien punya history alergi dengan
B-lactam. Antimicrobial apa yg harus dikasih pada pasien? a. azole ; b. macrolide ; c.
aminoglycoside ; d. cephalosporin ; e. lupa apa kl gak salah metronidazole atau apa

46. 69 years old man undergo to bypass coronary surgery. 10th day postoperative, he got
pneumoniae. multy drug resistant streptococcus pneumoniae. what action do you need to
prevent this disease?
a. immunization
b. Hand hygiene
c. aseptic
d. antibiotic prophylactic
47. Mother and father with the blood type O. How do we know if the offspring has blood type
O? No agglutination when the blood mix with the serum that have anti A antibodies and
anti B antibodies.
48. Severe arthralgia.
A. Japanese encephalitis
B. Chikumungyah
C. Yellow fever
49. Mechanism of Beta Lactams?
Inhibit cell wall synthesis.
50…
51. 31 years old man, pain while swallowing for 2 days, coughing, sneezing, kasi obat apa?
A. Antimicrobial
B. Antifungal
C. Antiviral
D. Drug according to symptom

52. 31 years old female has herpes and prescribed a drug earlier. What drug to give?
Acyclovir
53…
54…
55…
56. HLA match dalam sebuah persidangan:

Person HLA-1
Mother 3,1
Son 1,5
Daughter 3,9
Defendant 6,8
Jawaban: daughter bukan anak nya si defendant soalnya HLA no-match
57. Seorang ibu yang dirawat di ICU, tiba-tiba mendapat pneumonia di hari ke-3 nya. Saat
dilihat, ada yeast-like & pseudohyphae di kultur Saboroud Agar. Siapa penyebab nya?
Jawaban: Candida spp.

58. Seorang bayi dikasi vaksin DPT dan seminggu setelah setalah vaksinasi tersebut, serum
nya diambil untuk dilihat sifatnya. Bagaimana seharusnya perbandingan antara serum
sesudah vaksinasi toxoid ketiga dan pertama? Jawaban: antibodi terhadap toksoid jadi
lebih banyak dan reaksi lebih cepat

59. Seorang farmasis datang ke dokter karena sakit flu. Dokter minta dia minum antibiotic
untuk mencegah secondary infection caused by bacteria. Tapi karena dia seorang
farmasis, dia tau bahwa flu yang disebabkan oleh virus sifatnya self-limit dan
pencegahan terhadap secondary infection dari bakteri itu salah soalnya ga efektif dan
bisa cause Resistance of Bacteria. Bagaimana sikap kita? Jawaban: Kita harus setuju
sama dia.

60. Seorang bayi berumur 1 tahun datang ke dokter dengan X-linked defect calls Burton
Tyroid Kinase (BTK). System apa yang akan terganggu di bayi ini? Jawaban: ketidak-
mampuan T cell untuk membedakan self dan non-self antigen
61. Sakit. Obat Fluoroquinolone. Spontaneous mutation.
62. HIV
A. HLA I
B. HLA II
63. …
64. Penyakit. Secondary infection: IgG
65. Male. 23 years old. Antibody terhadap Hepatitis B sudah tinggi. Pekerjaan dari?
A. plasma Cells
B. Memory B cells
66: ambil csf diagnosis penyakit gejala criptococosis apa yang didapat : large transpant
capsule
67: AFP tinggi menandakan apa?
68: ada kasus infeksi setelah operasi. Propalaxis  treatment berguna untuk kasus: sebelum
heart surgical
69:candidiosis vagina, obat topikal: kotakonazol
70: nudule pada lymphatic drainage -> penyakit ini didiagnosis dengan?

71. Male 23 years old. His mother 44. Father 50. The son genotype: a3/16, b27/b35, c1/c7.
Mother a6/a6, b27/b45, c1/c1. Father a6/a6, b27/b35, c2/c7. Greatest effect on
transplantation:
A. Graft size
B. Age donor
C. Sex donor
D. Genetic mismatch
E. Heterotropic or otherotropic graft

72. 67 tahun, batuk2, chest pain, shortness breath, radiologi ada lower left lobe, Gram
positive diplococcus with PMN
A. 23 valen polisakarida
B. Hyperimmune
C. Antitoxoid serum
D. Oral Pennicilin V
E. Oral Rimfapin
73. 14 tahun.batuk. high fever sejak 5 hari yg lalu. Sebelum sakit dia main on the soil. BP
130/90. HR 100. Temp 38.3. RR 24. Diff count: 1/8/7/56/25/3. X rays thorax ada mild bilated
seral:
A. 7 hari
B. 14 hari
C. 30 hari
D. 45 hari
E. 60 hari
74. Putih, abu2, fishy odor, pH 5.5 Ada gram variable rods. Infeksi ini disebabkan oleh
karena:
A. lactobacillus turun
B. Resisten Clostridium
C. Turunnya provetella
D. E. coli naik
E. Mix Candida albicans
75. 25 tahun facial rash. Pain dan bengkak di joint. Abnormal kidney. Disease?
A. Contact sensitive
B. Immune complex
C. Drugs induced anemia
D. Hipersensitif
E. Delayed hypersensitivity.
76. 7 years old boy. Serpeginous urticaria on face. Have pet dog at home. Liver biopsy shows
presence of larvae and eosinophilia. Diagnosis ?
A. creeping eruption
B. fungi infection
C. Loeffler syndrome
D. dog bite
E. lupa 
77. 8 months baby. Parents both HIV negative. C3 deficient. Mekanisme apa yang
terganggu?
A. activating T cell
B. activating B cell
C. cytotoxic activity of T cell
78. 12 years old child. Presence of N. Americanus dan A. Lumbricoides. Pake obat apa?
A. Ivermectin
B. mebendazole
C. Carbamaxymine
D. lupa jga 
79. 25 years old boy. Undergoes blood transfusion. Gol darahnya O. Pas lagi transfusi ada
hypotension and abdominal pain. Blood not match. Hypersensitivity type?
A. Type I
B. Type II
C. Type III
D. Type IV
E. Type V
80. 28 years old woman. Vaginal dischargenya white milky purulent. Ada erythema at vagina
and labia. Periksa lab nya apa?
A. Gram staining
B. Vaginal discharge culture
C. India Ink
D. lupa
E. ini jga lupa
81...
82..
83. Pasien post-operasi terkena infeksi. Hasil swab darah dan pus pada jahitan menunjukan
bakteri gram(+) streptococcus. How to prevent the infection?
a. UV
b. autoclaving
c. gamma radiation
d. …
84...
85...
86. Bentuk telur ada 2 benjol di kedua kutub dan ukuran. Ciri2 T. trichuris
A. A. duodenale
B.
C. Trichuris trichura
D.
87.Ditemui ada flagella anterior 4 dan flagella posterior.
Trichomonas vaginalis
88. Di check dari mana
A. Urine
B. Stools
C. Urethral discharge
D.
89. Cewe ditemukan protozoan flagel.
Infeksi? Trichomoniasis
90.Ttg Toxoplasma gondii. Pasien punya banyak binatang peliharaan di rumah.
Cek konfirmasi dari?
A. Oocyt in stools
B. Trophozoites in tools
C. IgM and IgG
D. Trophozoites in blood
E. Trophozoites in CSF
91. A 30 years old woman came to the linic with complaints of swelling eyelid as big as quail
egg. This swelling has been suffered for 1 year since returning from Africa. On physical
examination was found calabar swelling. The transmission of the disease is through the bite
of the insect of:
a. culicoide
b. glossina
c. simulium
d. chrysops
e. phlebotomus
92. Many people in the mountainous village in Africa suffer from onchochercoma. The
transmission of this disease is through the bite of the fly of:
a. glossina
b. simulium
c. chrysops
d. Triatoma rubrofasciatus
e. phlebotomus
93. A 5 years old girl brought to the hospital caused of itched and rashed on the feet, looked
pale, no appetite and abdominal discomfort. The girl likes barefoot when plays on the ground.
From the feces found adult worm 1 cm shaped C, sharp tail, and has 2 pairs of teeth. What is
the probable cause?
a. Ascaris lumbricoides
b. Ancylostoma duodenale
c. Toxocara sp.
d. Strongyloides stercoralis
e. Trichostrongylus sp.
94. A 50 years old male patient was known with extreme swelling of his scrotum and legs
like elephant feet (elephantiasis). The transmission of this disease is through bite of mosquito
of:
a. Aedes aegypti
b. Aedes albopictus
c. Mansonia uniformis
d. Anopheles barbirostris
e. Culex quiquefasciatus
95. in the rural area with vast savannah in Africa, many residents died after having seizures
and decrease of awareness. They also previously had the symptoms of high fever,
enlargement of the posterior cervical lymph nodes (winterbottom’s sign) followed by
enlargement of the liver and spleen. Savannah is known to be a good breeding place for the
flies of Glossina morsitans. The MOST likely species of parasites that can be the cause of
this disease is:
a. Leishmania tropica
b. Trypanosoma cruzi
c. Leishmania donovani
d. Leishmania brasiliensis
e. Trypanosoma rhodisiense
96
97
98
99
100
FMS 2
Embriologi common arteri (aku jabarin dari awal)
1. Pada hari ke 18: mesoderm spalchincus yang berada disekeliling prochordal plate
akan membentuk sel  blood island

Pada hari ke 19, blood island akan bergabung membentuk 2 buah tabung/sepasang tabung
yang disebut Endocardial heart tube. Endocardial heart tube mengalami cephalo caudal
folding dan lateral folding  PRIMARY HEART TUBE pada hari ke 21.
FORMATION OF THE HEART TUBE
a. Sinus venosus akan berdifferensiasi menjadi:
- Vena umbilikalischorion
- Vena vitellina  system porta (pembuluh darah balik)
- Vena cardinalis communis  vena cava superior dan inferior
b. Primordial artrium
c. Ventricle
d. Bulbul cordis

Kemudian ada bentuk 5 pelebaran (dari cranial ke caudal secara berurutan)

1. Truncus arteriosus
2. Bulbus cordis
3. Ventricle
4. Atrium
5. Sinus venosus

Bulbus cordis dan ventricle akan bergabung mementuk BULBOVENTRICULARIS. Dan

kemudian bulboventricularis mengalami elongasi.
FORMATION OF THE HEART LOOP
Elongasi dari bulboventricularis terjadi pada hari ke 23-28.
Pada saat elongasi, bagian cranial dan caudal dari bulboventricularis mengalami fikasasi
sehingga elongasinya tidak bergerak memanjang melainkan bergerak ke ventral-caudal
dan agak ke kanan.
Antara bulbus cordis dan ventricle terdapat suatu alur yang dinamakan sulcus
bulboventricularis dan didalamnya akan tampak bahwa sulcus bulboventricularis membetuk
suatu tonjolan disebut plica bulboventricularis.  disini atrium terletak diisebelah dorsal
dari truncus arteriosus dan terbentuk jantung sederhana dengan 3 rongga:
 a. Atrium communis
b. Ventricle dextra
c. Ventricle sinistra

Pada hari ke 28
Diantara atrium communis dan ventricle terdapat suatu tonjolan yang disebut endocardial
cushion.
Akibat dari pergerakan truncus arteriosus kearah dorsal, maka bagian cranial dari atrium
communis akan membentuk suatu lekukan yang menghasilkan suatu tonjolan yang disebut
septum primum yang tumbuh kembangnya kearah endocardial cushion.
Tetapi pada saat septum primum memanjang menuju ke endocardial cuhion terdapat
pembentukan satu lubang yang disebut foramen primum, sehingga septum primum tidak
dapat mencapai endocardial cushion karena menyalami absorbsi (septum primum dari arah
cranial tidak dapat mencapai endocardial cushion, tetapi bagian caudal dapat mencapainya)
sehingga diantara septum primum bagian caudal terdapat lubang kedua yang dinamakan
foramen secundum.
Pada saat sebelum seluruh bagian septum primum habis diserap, pada sisi kanannya
terbentuk tonjolan baru  septum secundum, yang tumbuh kembangnya sama seperti
septum primum: mengarah ke endocardial cushion dan mengalami absorpsi bagian
caudalnya  terbentuk septum primum dan secundum yang diantaranya terdapat lubang
berbentuk ovale  foramen ovale (menghubungkan left and right atrium). Jantung ada 4
ruang… 