WEEK 1

Question 1

Parkinsonism

Answer 1

Rest tremor, rigidity, bradykinesia, postural instability

Question 2

Etiology parkinsons

Answer 2

α-Synuclein
immunoreactive deposits in neurons
(LBs) and dystrophic neurites
throughout the CNS

Question 3

Pathophysiology parkinsons

Answer 3

lesions in nigrostiatal, excessive inhibitory output of GPi and SNpr, decreased dopamine neurotransmission

Question 4

supporting factors parkinsons

Answer 4

levadopa, olfactory loss, limb rest tremor

Question 5

treatment parkinsons

Answer 5

Activating Dopamine receptors in Substantia Nigra :
- dopamine precursor (levadopa),
- dopamine agonist (amphetamine, apomorphine),
- dopamine receptor agonist (bromocriptine)
Limit dopamine changes :
- MAO-B inhibitor (Selegeline),
- COMT inhibitor (Entacapone and Tolcapone),
- Dopa-decarboxylase inhibitor (carbidopa)
Antagonize Acetylcholine receptors (Benzatropine),
- extra = amantidine buat less use more produce, Anticholinergic (benztropine) antagonis si asetilkolin

Question 6

Levadopa bad symptoms

Answer 6

Cardiac Stimulation Due to Beta Adrenergic Effect on Heart (tachycardia, cardiac arrhythmias, hypertension)
= treat with propanolol (b-blocker)
GI nausea, vomiting
on/off efek = kayak bisa normal bisa tb2 full parkinsonism

Question 7

Cognitive

Answer 7

memory and attention

Question 8

Memory

Answer 8

prefrontal cortex = sequence of events
frontal lobe = short term 
amygdala = emotional memories
medial temporal lobe = explicit to long term
Hippocampus = explicit to long term 
cerebellum = movement memories

Question 9

Amnesia

Answer 9

anterograde - hipocampus damage, no new explicit memories

retrograde - episodic memory of the past

Question 10

Chondrocyte

Answer 10

Regulate the synthesis & produce enzymes for degradation of Extra Cellular Matrix (ECM)
kartilago –> balance synthesis & degradation ECM

Question 11

Cartilage consists of

Answer 11

Chondrocyte = Regulate the synthesis & produce enzymes for degradation of Extra Cellular Matrix (ECM)
Extracellular matrix :
collagen = resist tension (II, IX, XI)
Aggrecan/acan & proteoglycan = resist compression
Water

Question 12

osteoarthritis risk factors

Answer 12

trauma
aging
obesity
inflammation
loss of joint stability

Question 13

Etiology osteoarthritis

Answer 13

joint trauma/overuse –> damage-associated molecular patterns (DAMPs) –> Synovial macrophages, Fibroblast-like
synoviocytes (FLS) chondrocytes –> inflaammatory mediators

Question 14

pathophysiology osteoarthritis

Answer 14

cartilage destruction –> chondrocyte react –> degradasi enzym –> kartilago pecah fragmentasi

OR

kartilago weakening –> metaloproteinase (mengandung metal) –> Collagen Catalysation (kek lebih cepet dibikinnya), Proteoglycan Degradation –> banyak inflamatory IL-1, TNF-alpha, Cytokine, Nitric
Oxide

Question 15

Interleukin oesteoarthritis

Answer 15

Interleukin-1 (IL-1) is the prototypic pro-inflammatory cytokine.

Kalo yg 6 bukan krna itu both pro and anti inflamatory

Question 16

Progress OA (diabet, trauma)

Answer 16

Diabet –> loading dari tubuh ke joints lebih berat, build up lemak sehingga kartilago ga balanced
Trauma/overuse –> build up damage-associated molecular patterns (DAMPs) –> sel2 kek makrofag & inflamasi mediators

Question 17

Synovitis

Answer 17

Synovial inflamation, when the synovium of a joint becomes inflamed

Question 18

osteoarthritis treatment

Answer 18

NSAIDs, acetaminophen, surgery

Question 19

osteoporosis

Answer 19

low bone mass + micro-architectural deterioration, sehingga lebih fragile dan gampang patah

Question 20

Bone remodelling

Answer 20

osteoclasts –> resorption tulang –> osteoblast nempel–> produksi osteoid (matriks tulang) –> mineralized bone

Question 21

etiology osteoporosis

Answer 21

glucocorticoids, secondary (nutrition, endocrine, systemic, tumor), primary (postmenopausal, aging)

Question 22

UMN lesions

Answer 22

weakness
reflex increase
tonus increase
pathological reflexes

Question 23

LMN lesions

Answer 23

weakness
atrophy
fasciculations
reflexes decrease
tonus decrease
no pathological reflexes

Question 24

Peripheral Nervous disorders

Answer 24

motor neuron/spinal cord
radix
plexus
nervus perifer
neuromuscular junction
otot

Question 25

Myasthenia Gravis

Answer 25

autoimun pd neuromuscular junction Antibodi menyerang reseptor Acetylcholine (Ach) di motor end plate --> reseptor asetilkolinnya nurun --> si membran postsinaptik turun --> mencegah pengikatan asetilkolin dan perangsangan kontraksi otot -->kelemahan pada otot

Question 26

MG Antibodies

Answer 26

``` Antibodi asetilkolinesterase (AChR) (seropositif) --> pergantian si ach cepet dan ganggu postsinaptik Antibodi Muscle Spesific Tyrosine Kinase (MuSK)(seronegatif) --> langsung memblokir pengikatannya ```

Question 27

Clinical symptoms MG

Answer 27

* Kesulitan berbicara (dysarthria) * Kesulitan menelan (dysphagia) * Kelopak mata jatuh (ptosis) * Penglihatan berbayang (diplopia) * Nasal-sounding speech * Kelemahan otot leher

Question 28

Tests for MG

Answer 28

Waternberg (suruh liat keatas), Cogan Sign (suruh liat kebawah lama baru naik normal nanti agak twitch), ice test

Question 29

Treatment MG

Answer 29

Endrophonium Chloride, – Beta blockers, calcium channel blockers, quinine, quinidine, procainamide, some antibiotics, neuromuscular blocking agents

Question 30

Markers of Aging?

Answer 30

1. Oxidative stress and mitochondria 2. DNA &chromosomes : telomere, DNA repair, Epigenetic modifications 3. RNA and transcriptome 4. Metabolism 5. Cell senescence 6. Inflammation and intercellular communication

Question 31

Etiologi aging

Answer 31

1. akumulasi waste, mutasi genetik, wear and tear 2. free radicals --> oxidative stress/mutant mitochondria --> apoptosis 3. advanced glycation endproducts 4. circadian rhythm --> oxidation 5. telomere shortening

Question 32

Presbycusis/presbyacusis

Answer 32

damage to cochlea, cochlea neurons --> hearing becomes bad, loss of sensitivity for high frequency sounds

Question 33

Brain Aging

Answer 33

Atrophy, Cerebrovascular changes, Neuronal, axonal, and neurotransmitter changes, Increased numbers of amyloid plaques (AP) extracellular and neurofibrillary tangles (NFT) intracellular in the brain

Question 34

Physiological CNS Aging

Answer 34

White matter = reduksi volume/atrofi krna tractus berkurang, banyak lesi kecil, myelin degenerasi Cerebrovascular = intinya kek vasa2 biasa menebal, pecah, ga cepat regenerasi neuroglial = banyak fagosit

Question 35

Cellular hipocampus aging

Answer 35

oxidative stress, protein misfolding, senescence, inflamasi -lesions to the anterior impair spatial learning, -lesions to the posterior impair fear-conditioning and anxiety related behaviors. extra : ada HPA disfungsi yg bikin more stress dan inflamasi, VEGF menurun sehingga neurogenesis nurun, klotho gene bantu supress stress dan apoptosis

Question 36

Bone remodelling

Answer 36

▪ Activation ▪ Resorption (osteoclast & mononuclear cells) ▪ Reversal (pro-osteoblast) ▪ Formation (osteoblast) ▪ Termination/resting phase (lining cells, mineralization)

Question 37

Calcium/Magnesium/Phosphate

Answer 37

Mineral - ion - protein - complex calcium - 50 - 40 - 10 phosphate - 55 - 10 - 35 magnesium - 55 - 30 - 15

Question 38

calcium disorder

Answer 38

hypo = pth turun, calcium di darah ga banyak or hypercalcemia = pth kebanyakan, di darah kebanyakan Total calcium in normal adults ranges between - lower limit : 8.5 – 8.8 - upper limit: 10.1-10.5 Ionized (free) calcium : 4.6–5.3

Question 39

phosphate disorder

Answer 39

hypo = high pth, phosphate excretion naik atau dari extracel masuk ke intracel hyper = low pth, excrete turun Serum phosphate: normal 2.5 and 4.5 mg/dL children : 4.0–7.0 mg/dL Urinary phosphate excretion: 0.4 – 1.3 g/24 h

Question 40

magnesium disorder

Answer 40

``` hypo = fluid drop, diabetM, gabisa absorpsi hyper = renal failure, intake naik, tb2 dibutuhin mislanya shock burns adults = 1.7–2.4 mg/dL ```

Question 41

hormone bone metabolism

Answer 41

pth, vitamin D

Question 42

diagnosis bone metabolism

Answer 42

bone imaging techniques, bone biopsy, biochemical markers of bone turnover.

Question 43

bone turnover marker

Answer 43

``` resorption = calcium, TRAP formation = P1NP & P1CP (kolagen), osteocalc & Bone Alkaline Phosphatase (dibikin osteoblast) ```

Question 44

bone disorder

Answer 44

osteoporosis : decreased organic bone matrix & deterioration of bone tissue normal - osteopenia - osteoporosis - severe osteomalacia (failure to mineralize) & rickets (di anak2 yg XO) failure to mineralize osteoid in the mature skeleton

Question 45

osteomalacia why?

Answer 45

1. vitamin D deficiency states, 2. phosphate depletion, 3. systemic acidosis, 4. inhibitors of mineralization