Exam paper answer and discussion

GOOD LUCK EVERYONE!!!

No 2015/2016?

2008
SAQ
1. MSK pathophysiology - Rheumatoid Arthritis lab markers
a. Increased CRP
i. Macrophages, fibroblasts, endothelial cells release IL-6 -> trigger hepatic acute
reaction -> release C-reactive protein in response -> elevated CRP
b. Increased ESR
i. Macrophages, fibroblasts, endothelial cells release IL-6 -> trigger hepatic acute
reaction -> fibrinogen released
ii. Fibrinogen is a factor in clotting cascade -> blood clots faster due to elevated
fibrinogen level -> increased ESR
c. Increased ALP in LFT
i. Inflammation in RA damages bone -> ALP is released during bone remodelling
process.
2. MSK pathophysiology - Metastasis sites to bone
a. Thyroid cancer
b. Breast cancer
c. Lung cancer
d. Kidney cancer
e. Prostate cancer
i. Any 4 of them
3. Neuro pathophys - Cerebral infarct morphology
a. I dunno wat they mean by established cerebral infarct?
b. TIMELINE
i. In the setting of global ischemia, the brain is swollen, with wide gyri and
narrowed sulci. The cut surface shows poor demarcation between gray and
white matter.
ii. Histopathologic changes on irreversible ischemic injury
iii. Early changes - 12 to 24 hours after
1. Acute neuronal cell change - red neurons
2. Microvacuolization
3. Cytoplasmic eosinophilia follows
4. Later nuclear pyknosis and karyorrhexis.
5. Similar changes occur somewhat later in astrocytes and oligodendroglia.
6. After this, tissue damage begins with infiltration by neutrophils
iv. Subacute changes - 24 hours to 2 weeks
1. Necrosis of tissue
2. Influx of macrophages
3. Vascular proliferation
4. Reactive gliosis and repair,
 v. After 2 weeks
1. Removal of all necrotic tissue
2. Loss of organized CNS structure
3. Gliosis
4. distribution of neuronal loss and gliosis is uneven with preservation of
some layers and devastation of others
a. pseudolaminar necrosis

vi. The macroscopic appearance of a nonhemorrhagic infarct

1. First 6 hours the tissue is unchanged in appearance
2. 48 hours, the tissue becomes pale, soft, and swollen.
3. Days 2 to 10
a. Brain turns gelatinous and friable
b. Boundary between normal and abnormal tissue becomes more
distinct as edema resolves in the adjacent viable tissue.
4. Day 10 to week 3
a. Tissue liquefies, eventually leaving a fluid-filled cavity lined by
dark gray tissue
vii. Microscopically
1. 12 hours
a. Ischemic neuronal change - red neurons
b. Cytotoxic and vasogenic edema predominate
c. Endothelial and glial cells swell, and myelinated fibers begin to
disintegrate.
2. 48 hours
a. Neutrophilic emigration
3. 2 to 3 weeks
a. Followed by mononuclear phagocytic cells during the
b. Macrophages containing myelin or red cell breakdown products
may persist in the lesion for months to years
4. As the process of phagocytosis and liquefaction proceeds, astrocytes at
the edges of the lesion progressively enlarge, divide, and develop a
prominent network of cytoplasmic extensions.
5. After several months
a. Astrocytic nuclear and cytoplasmic enlargement regresses
b. In the wall of the cavity, astrocyte processes form a dense
feltwork of glial fibers admixed with new capillaries and a few
perivascular connective tissue fibers.
c. In the cerebral cortex, the cavity is delimited from the meninges
and subarachnoid space by a gliotic layer of tissue, derived from
the molecular layer of the cortex.
d. The pia and arachnoid are not affected and do not contribute to
the healing process.
4. Mental health pathophysiology - psychosis and schizophrenia
a. Delusion
i. Delusion - Fixed beliefs that are not based on fact
ii. Hallucination - False sensory perception without real external stimulus
iii. Illusion - Misinterpretation/misperception of real external stimulus
b. Delusion criteria
 i. certainty
ii. Is maintained even if argued with facts
iii. impossibility/falsity of content
c. (My pure assumption)
i. General appearance and behavior
ii. Thought content
iii. Mood and affect
iv. Thought content
v. Speech
vi. Hallucination (disorders perception)
vii. Cognitive function
viii. Psychomotor activity/general observation
1. MSE assesses
a. Appearance
b. Behaviour
c. Speech
d. Content of speech
e. Mood and affect
f. Thought
g. Perception
h. Cognition
i. Insight
5. Neuro pathophysiology and pharmacology - Dopamine antagonist + PD and Schizophrenia
a. Parkinson disease is caused by destruction of substantia nigra -> decreased [dopamine]
in basal ganglia -> decreased dopamine effect -> disinhibit indirect pathway + does not
stim direct pathway -> hard to initiate movement
b. Dopamine antagonist will block dopamine receptors in basal ganglia -> further decrease
dopamine effect in basal ganglia -> worsens PD symptoms
6. Pharmacology - prescribing to elderly
Vd
a. Half life = , Vd = volume of distribution, CL = clearance
CL
b. In lipophilic drug, Vd is fat/adipose tissue
c. Vd is increased in obese patients, and assuming Clearance between elderly are equal,
half life of the drug is increased in the elderly obese patients
d. So plasma conc. of the drug will fall further in lean elderly subjects
7. Pharmacology - osmolarity
a. Plasma osmolarity approx 260~280 mOsm, so 700 mOsm solution is hyperosmolar
b. NaCl in water dissociates into 2 molecule i.e. 1 mol of NaCl = 1 mol Na + 1 mol of Cl in
water
i. 340 mOsm/kg
c. Water will flow out from RBC to solution to balance electrolyte equilibrium -> RBC will
shrink
8. Neurophysiology - somatotrophic organisation
a. Dunno how2 answer tbh
b. Distribution of areas of motor and somatosensory cortex that relates to the activities of
skeletal muscle
c. Stroke/amputation - damage
d. Perseverance - cortical plasticity
 i. Ability to change neuronal properties on cortex to refine movements and to
recover from injury
ii. Ocular dominance columns
1. Covering one eye during infancy will cause other eye to be dominant on
the rest of the life
iii. Auditory cortex plasticity
1. Auditory cortex is organised tonotopically - represent frequency in orderly
manner
2. Higher frequency normally inhibit lower frequency
3. On damage/hearing loss - this inhibition is lifted -> excitability is
increased in restricted frequency band (normally inhibited band)
4. These frequencies may dominate when competing for cortical space ->
reorganisation of the tonotopically organised cortex
iv. Long Term Potentiation
1. Glutamate released to synaptic cleft -> binds to postsynaptic receptor
AMPA -> if continuously stimulated (high frequency stimulation) will push
Mg2+ blocking NMDA receptor (glutamate also binded to it) and cause
calcium to flow into the postsynaptic neuron.
2. When calcium is in high concentration will lead to activation of protein
kinases (it regulates synaptic strength) and cause more AMPA
expressed on the postsynaptic surface
3. High calcium in post synaptic neuron also has feedback effect on
presynaptic neuron -> enhances neurotransmitter release
4. Used to strengthen memory - working memory -> long term memory
v. Long Term Depression
1. Opposite of LTP, caused by prolonged depression of synaptic
transmission (low frequency stimulation)
2. Used to clear old memory traces + control of LTP
vi. Somatosensory cortex plasticity
1. Removal of a digit on hand caused reorganisation of somatosensory
cortex
2. Areas that represent the digits adjacent to the amputated digit later
occupies the areas that represent the removed digit
3. Phantom limb pain
9. Neurophysiology - proprioception
a. Muscle spindles
i. Detect static length changes (stretch receptor) + small movement and vibration
b. Golgi tendon organ
i. Detect force on tendon
c. Joint receptor
i. Detect edge of range of movement of joints
d. Cutaneous mechanoreceptors
i. Bidirectional detection (doesn’t contribute to proprioception a lot normally, but
when there is disease like HSAN where muscle spindles doesn’t function)
10. MSK physiology - Knee movement
a. Slight medial and lateral rotation
b. Unlocks femur and tibia during locomotion
c. Locking of the knee is a result of medial rotation of the femur during the last stage of
extension
 d. Unlocking therefore requires lateral rotation
11. Renal physiology - Defence mechanism
a. Urine
i. Low pH
ii. Mechanical flushing of urineo
iii. Chemicals in urine inhibits bacterial adherence - bladder mucopolysaccharides,
oligosaccharides, uromucoid
b. Mucosal immunity
i. Mucosal IgA
ii. Mucosal lining makes it difficult for bacteria to penetrate and adhere
iii. Normal bacterial flora
12. Renal physiology - RAAS and ACEI
a. Angiotensinogen from liver --(renin from kidney)---> Angiotensin I
b. Angiotensin I ----(Angiotensin converting enzyme)---->Angiotensin II
c. Angiotensin II causes blood pressure to increase and increase GFR by
i. Stimulate vasopressin release from posterior pituitary -> increase water
reabsorption
ii. Stimulate aldosterone secretion from adrenal gland -> increase Na+, Cl-
reabsorption, which increase water retention by osmosis
iii. Increase sympathetic activity -> vasoconstriction
iv. Constrict efferent arteriole (afferent stays less constricted by PGE2) -> increase
GFR
d. By inhibiting ACE by ACEI, angiotensin II conversion is impaired -> less angiotensin II ->
decreased angiotensin II effect -> decreased blood pressure + decreased GFR
13. Renal physiology - GFR and sterling’s forces
a. GFR = glomerular capillary permeability[(glomerular capillary hydrostatic pressure -
bowman’s space hydrostatic pressure) - (glomerular capillary oncotic pressure -
bowman’s space oncotic pressure)]
b. In normal conditions, there is no protein in bowman’s space, so the equation becomes
c. GFR = glomerular capillary permeability[(glomerular capillary hydrostatic pressure -
bowman’s space hydrostatic pressure) - glomerular capillary oncotic pressure]
d. Hydrostatic pressure can be altered by constriction of afferent/efferent arteriole.
i. Constriction of afferent arteriole decreases hydrostatic pressure, decreasing GFR
ii. Constriction of efferent arteriole alone increases hydrostatic pressure, increasing
GFR

2009
MEQ
1. Neuro
a. Papilloedema - optic disc (where CNII nerve exit) swelling caused by increased
intracranial pressure
i. This causes vision disturbance on the affected side - right side
ii. As you cannot see right side well, keeps bumping into object on his right side
iii. Or
 iv. Right sided proprioception/coordination dysfunction - tumour on left hemisphere
v. Right hemineglect
b. May have lesion/disturbances (increased ICP, tumour) on the speech area of left
hemisphere - broca, wernicke’s area - causes speech impairment (receptive/expressive
aphasia)
i. Most likely wernicke’s/receptive aphasia - ‘occasionally mixing up his words’
c. Timeline of aphasia - Abrupt aphasia in patients with a stroke or head injury.
Slow/Insidious aphasia development in patients with neurodegenerative diseases or
mass lesions.
d. MRI - more sensitive than CT, can detect smaller infarct/tumour in very clear picture. Can
also screen parts of brain that are not shown well in CT
e. Does any1 know answer?
i. Midline shift can be caused by both benign low grade tumour or malignant glioma
ii. Only way to differentiate the grade of glioma is by biopsy
f. Does any1 know answer?
i. SPIKES (Setting Perception Invitation Knowledge Emotion+Exploring Summary)
ii. From AA
1. listen up m8 you are probs fuckd for life but i can't confirm until i have the
the results of the biopsy.
g. Patient with brain tumour are at higher accident risk due to significant neurodegenerative
deficit like any cognitive (vision, decision making) deficits
i. This may put passengers and bystanders in danger
ii. Grade 1-2, cannot drive for a year after treatment
iii. Grade 3-4, cannot drive for 2 year after treatment
iv. If tumour progresses/relapses - cannot drive until treated
v. Recommend to not to drive until the biopsy results come back and wait for
treatment. Or let his wife drive for him
2. MSK - inflammatory joint disease
a. Normal vs RA joint
i. Normal
1. Microscopically, fluid has not many WBC
2. (mononuclear), synovial membrane has synoviocytes, on chondrocytes
on cartilage
ii. In RA
1. Fluid has high number of WBC (multinuclear and mononuclear) forming
lymphoid follicles of CD4+ T cells and B cells
2. Synovial hyperplasia/pannus is formed with - papillary architecture,
synovium infiltrated with lymphocytes, increased vascularisation of
synovial membrane
3. There are fibrin accumulation/aggregation in synovial fluid
b. RA causes are multifactorial, they can be caused by genetic, smoking, infection, or
hormonal imbalances
i. These factors all result in inflammatory reaction in your joint fluid - synovium ->
causes bone erosion and damage in joint capsule as it becomes more inflamed
ii. MORE INFO
1. Genetic - mutation in HLA (CD4+ receptor for T helper cell), PTPN 22
(mutation allow autoreactive T cells to survive)
 2. Periodontitis - peptidylarginine deaminase convert arginine to citrulline
which is antigenic -> produces Anti-CCP autoantibodies (also can be
caused by genetics)
3. Estrogen is protective factor, increased risk during menopause
c. RA morphology
i. Pattern of joint involvement
1. Proximal interphalangeal, metacarpo-carpal, carpal joint involved
ii. Soft tissue change
1. Periarticular fusiform swelling (edema) at affected joints
iii. Joint/bone changes
1. Symmetrical and concentric bone erosion
2. Decreased joint space
3. Ankylosis if RA is severe
4. Marginal erosions by pannus
d. Arachidonic acid is converted to prostaglandins by COX 1 and 2. Prostaglandins are
hyperalgesic, chemotactic, roles in clotting and has many other properties
i. NSAIDS work by blocking COX 1 and 2, which reduces production of
prostaglandins and reducing its hyperalgesic and chemotic effect, resulting in
reduced pain and inflammation
ii. Side effects of NSAIDS comes from blocking of COX 2 (PGI2 production) and
COX 1 (PGE2 and PGI2 production) pathway
1. PGI2 is antithrombotic, reduced PGI2 production increases platelet
aggregation -> increase stroke and CVD risk
2. PGE2 and PGI2 regulates mucus production in stomach, reduced PGE2
and PGI2 causes reduced mucus production -> reduced protection of
stomach lining from gastric acid -> increase gastric ulcer risk
3. PGE2 cause afferent arteriole vasodilation to increase GFR, reduced
PGE2 impairs renal GFR maintenance
iii. Overdose of NSAIDs cause hepatotoxicity and liver damage
e. RA systematic effects
i. heart/CVS
1. Autoimmune reaction to vessels by immune complex deposition and
cross reactions -> atherosclerosis is accelerated -> leads to CVD
2. Autoimmune reaction can also cause pericarditis and vasculitis
3. Carotid bruits, chest pain, breathlessness, claudication
ii. Lung
1. Inflammation in lung membrane cause interstitial lung disease, pleural
thickening, effusion and bronchiectasis. Rheumatoid nodules may form in
lung parenchyma
2. Breathlessness, lung crackling
3. Neuro
a. Symptoms
i. Diplopia on gaze to right
1. Right abducens nerve block by tumour/lesion
ii. Ptosis on both eye
1. Myasthenia Gravis affecting levator palpebrae superioris
iii. Weakness of deltoid, triceps of both sides
1. GBS, MG, nerve root compression
iv. Voice changes
 1. Vagus nerve affected by tumour, MG
v. Fatigue
1. MG, graves disease
b. Myasthenia Gravis
i. Gait and limb is normal
ii. Coordination and reflexes are all normal
iii. Neck and pharynx is normal
iv. Visual acuity is normal
v. GBS will also show autonomic dysfunction
vi. Graves disease may present with goiter, tremor, heat intolerance
vii. Spinal cord lesion will cause level below lesion to be affected, her triceps and
deltoids are affected, but all the function below is normal.
viii. Brainstem tumour is associated with morning headaches
ix. Diplopia looking to right, maybe caused by right lateral rectus muscle weakness
x. Ptosis on both eye by levator palpebrae superioris muscle weakness
xi. Deltoid and triceps weakness
xii. Voice changes due to weakness of muscles of phonation
xiii. Generalised fatigue due to less pronounced weakness of all muscles
xiv. Affected sites suggests more peripheral nerve disease then central, with all of
her symptoms can be attributed to Myasthenia Gravis
c. Cbf explaining eye mvmt by word, just draw diagram and talk about it

i. SR - looks upwards and laterally

ii. IR - looks downwards and laterally
iii. LR - looks laterally
iv. MR - looks medially
v. IO - extorsion, elevation, abduction
1. Elevates the eye when looking medially
vi. SO - intorsion, depression, abduction
1. Elevates the eye when looking medially
vii. As she only experiences double vision when looking right, it could be either right
lateral rectus or her left medial rectus could be affected, causing each eye to
have different visual field, causing diplopia
d. Tests
i. Edrophonium/Tensilon test (anticholinesterase test)
1. Patients with MG has low AchR numbers in neuromuscular junction.
Acetylcholine is metabolised by AchE in NMJ. By inhibiting AchE, Ach
concentration at NMJ will increase. This allows the Ach remain longer in
NMJ and increase its chance to interact with its receptor. Which will only
improve muscle weakness in MG
ii. Anti AchR antibody
 1. People with MG will present with Anti-AchR antibody
4. Renal
a. Kidney ascend from pelvis to abdomen + rotates 90 degrees medially
b. Ureter derived from ureteric bud of mesonephros
i. Ureters
ii. Renal pelvis
iii. Calyces
iv. Collecting tubules
v. Ureteric bud comes from mesonephric duct, which it penetrates into the
blastemal tissue.
1. Inside it bifurcates and branches further
2. Ampulla becomes renal pelvis
3. Bifurcation coalesces to form major and minor calyces
4. The ends of calyces goes through further bifurcation and becomes
collecting ducts
c. Ureteric bud may split into 2 before penetrating into metanephric blastemal tissue ->
results in two ureter for one kidney, upper and lower pole ureters are formed
i. The lower-pole ureter integrates with the bladder earlier than expected and is
carried into a more superolateral position.
ii. The upper-pole ureter integrates with the bladder later than usual and is
inferomedially carried.
d. Duplex ureter causing incomplete voiding i.e urine is collected in upper pole ureter and is
not excreted -> overflows to renal pelvis, causing hydronephrosis -> decreasing GFR by
increasing hydrostatic pressure of bowman’s space -> decreased creatinine excretion
i. Or can be caused by her infection
e. Renal clearance - volume of plasma completely cleared of specific compound per unit
time by the kidney
i. Ability for kidney to remove substances from blood and excrete them into urine
f. Renal clearance = GFR
i. Creatinine constantly produced by body -> filtered freely in glomerulus with
minimal secretion, meaning creatinine clearance = GFR
g. Chronic kidney disease
i. Anaemia due to decreased erythropoietin synthesis from kidney as functional
kidney mass decreases
ii. Secondary hyperparathyroidism
1. Decreased number of functional nephron -> decreased phosphate
clearance -> trigger PTH release as an attempt to increase phosphate
excretion, but clearance impaired + PTH also cause bone resorption,
releasing phosphate and calcium into blood -> hyperphosphataemia
2. Decreased calcitriol synthesis as functional renal mass, so PTH
secretion is uninhibited
3. Hyperphosphataemia further stim PTH release -> prolonged stimulation
cause parathyroid gland -> secondary hyperparathyroidism
iii. Metabolic acidosis
iv. LDL VLDL increased as pth cause lipases in liver to become inactive
v. Uraemic syndrome
h. Reduce daily sodium intake, add more fiber from fresh fruits and vegetables (are
negatively charged and basic)
i. Intravenous pyelogram, MRI
 5. Mental health - Postpartum depression
a. Postpartum depression, postpartum psychosis
b. Postpartum depression criteria
i. Loss of interest or pleasure in activities
ii. Weight loss or decreased appetite
iii. Changes in sleep patterns
iv. Feelings of restlessness
v. Loss of energy
c. Postpartum depression risk factors
i. Prenatal depression or anxiety
ii. Maternity blues
iii. Birth-related psychological trauma
iv. Birth-related physical trauma
v. Previous stillbirth or miscarriage
vi. Low self-esteem
vii. Childcare or life stress
viii. Low social support
ix. Poor marital relationship or single marital status
d. Asking about self harm
i. Interview setting
1. In a quiet room where the chances of being disturbed are minimised.
2. Ideally you should meet with the patient alone but also see their
family/carers/ friends, together or alone, as appropriate.
ii. Asking about suicidal ideas
1. It should be possible to broach suicidal thoughts in the context of other
questions about mood symptoms or link this into exploration of negative
thoughts
2. Another approach is to reflect back to the patient your observations of
their nonverbal communication
3. ASK
a. Are they feeling hopeless, or that life is not worth living?
b. Have they made plans to end their life?
c. Have they told anyone about it?
d. Have they carried out any acts in anticipation of death
e. Do they have the means for a suicidal act?
f. Is there any available support?
e. Dunno the answer - see ‘overview of MI, “issues in pregnancy and postpartum”
slide”
i. If they are breastfeeding? SSRI’s and TCA’s thought to be safe since they don’t
pass into breast milk at high levels. Anticholinergic side effects may impair with
her ability to care for the child.

SAQ
1. MSK pathophysiology - Inflammatory vs noninflammatory arthritis
 a.
2. MSK pathophysiology - OA vs RA under imaging
a. LOSS (OA) or LESS (RA)
i. Loss of joint space
ii. Osteophytes
iii. Subchondral sclerosis
iv. Subchondral cysts
v. Loss of joint space
vi. Erosions
vii. Soft tissue swelling
viii. Soft bones (osteopenia)
X-ray feature RA OA

Joint space narrowing Concentric Eccentric

Periarticular erosions Present Absent

Changes to subchondral Osteoporotic Sclerotic

bone

presence/absence of Absent Present

subchondral cysts

presence/absence of Absent Present

osteophytes
3. MSK pathophysiology - RA drugs MOA
a. Anti-TNF alpha therapy
i. TNF-alpha inhibitors/Antibodies binds to TNF-alpha in circulation and synovium.
ii. It prevents its interaction with its surface TNF-alpha receptors in lymphocytes.
iii. Minimises downstream pro inflammatory effects
b. T-cell costimulatory blocking agent
i. Inhibit T cell activation by binding to CD80/86 in antigen presenting cell - blocks
its interaction with CD28 on T cells
1. This signal is required for full T cell activation
ii. This decreases inflammation as it reduces T cell activation and inhibit
progression of disease
c. Anti-CD20 antibody
i. Targets CD20 on B cells -> cause B cell depletion by growth arrest, cell lysis,
cytotoxicity, apoptosis
ii. By decreasing number of B cells -> decreased plasma cell number and overall
decreased antibody secretion
1. Plasma cells do not express CD20 -> resistant to this Ab
4. Renal physiology - GFR and sterling’s forces
a. REPEAT FROM 2008 SAQ PAPER Q13o

5. Renal physiology - RAAS and ACEI

a. REPEAT FROM 2008 SAQ PAPER Q12

6. Renal genetics - one and two hit model and ADPKD

a. DNA mutates as we age
b. For PKD development, both alleles within one cell needs to have mutation
c. Normally cells have normal chromosome makeup - normal alleles -> no PKD
predisposition
i. Needs 2 environmentally caused mutation to induce cyst formation
ii. So 2 hit is required - 2 hit model
d. With ADPKD, each cell has already one defective allele
i. Need one environmentally caused mutation to induce cyst formation
ii. So 1 is required - 1 hit model
7. Mental health - delirium or dementia

8. MSK pathophysiology - Bone cancer

a. Metastatic bone tumors
b. Primary bone tumor
c. Primary hematopoietic tumor
9. Neuro pathophysiology- brain tumour
a. A tumor’s location will largely determine the symptoms a patient experiences and will play
a major role in choosing the best course of treatment.
b. For example, brain stem gliomas are particularly difficult to treat, whatever their grade.
The brain stem is a very complicated and delicate part of the brain and completely
removing the tumour is not likely to be possible.
c. The likelihood of curing a brain tumor has to do with its location, the cell that makes it up,
and how the tumor cells look under a microscope.
10. Neuro pathophysiology - brain tumour WHO staging
a. Grade 1 - best prognosis, grade 4 - worst prognosis
b. Grade 1 (pilocytic astrocytoma)
i. Relatively circumscribed, slow growing 90%
c. Grade 2 (diffuse astrocytoma)
i. Diffusely infiltrating ill defined lesion, slow growing but have potential to grow to
grade 3 and 4 tumours 50%
d. Grade 3 (anaplastic astrocytoma)
i. Shows nuclear atypia with increased cellularity, mitosis, anaplasia 10%
e. Grade 4 (glioblastoma)
i. Necrosis/palisading necrosis, vascular proliferation, mitosis, anaplasia, increased
cellularity 1%
11. Neuro pathophysiology - dementia causes

12. Neuro pathophysiology - cerebral infarct morphology

a. REPEAT FROM 2008 SAQ PAPER Q3
13. Neuro pathophysiology and pharmacology - Dopamine antagonist + PD and Schizophrenia
a. REPEAT FROM 2008 SAQ PAPER Q5
14. Pharmacology - prescribing to elderly
a. REPEAT FROM 2008 SAQ PAPER Q6
15. Neurophysiology - proprioception
a. REPEAT FROM 2008 SAQ PAPER Q9
16. Renal physiology - Anion gap
a. The anion gap is the difference in the measured cations (positively charged ions) and the
measured anions(negatively charged ions) in serum, plasma, or urine
b. High anion gap metabolic acidosis examples
i. Lactic acidosis
ii. Ketoacidosis
iii. Chronic kidney disease

17. Mental health - anxiety disorder therapy

a. Exposure therapy
b. Acceptance and commitment therapy
c. Interpersonal therapy
d. Cognitive behavioural therapy
18. PPD - compliance and adherence
a. Limited ability to understand/speak english
b. Medication cost
c. Limited access to health care facilities
d. Frequent changes/complex medication regime
e. Personal experience - think they are getting better -> stop taking medication earlier that
specified
19. MSK pathophysiology - fracture healing
a. Early stage - hematoma
i. Ingrowth of capillaries and fibroblasts, forms granulation tissue
ii. Initially infiltrated neutrophils then macrophages -> to remove hematoma and
tissue debris
b. Weeks - soft callus
i. Chondroblasts replace hematoma with hyaline cartilage and connect the ends of
fracture
c. Months - hard callus
i. Osteoblasts replace cartilage with woven bone, lamellar bone, forming trabecular
bone
 d. Years - bone remodelling
i. Remodelling of trabecular bone by osteoblast and osteoclast activity into
compact bone
20. MSK pathophysiology - Rheumatoid Arthritis lab markers
a. REPEAT FROM 2008 SAQ PAPER Q1
21. Neuro pharmacology - paracetamol and opioids
a. Toxicity
i. Paracetamol - metabolised in liver. If overdosed, will cause hepatotoxicity and
liver failure
ii. Opioids - acts on many opioid receptors to produce analgesic effect. Because it
acts on many different opioid receptors, it has many side effects such as
respiratory depression, euphoria. Overdose will cause further respiratory
depression and decreased level of consciousness
b. Opioids mechanism
i. There is opiate receptors in brain. They are g-coupled and the main receptor is μ
ii. When opiate bind to opioid receptor - Neurons excited in periaqueductal grey
matter and projects to nucleus raphe magnus
iii. Nucleus raphe magnus neuron contain serotonin + enkephalin that run to
substantia gelatinosa in dorsal horn, which inhibit pain transmission
iv. Directly inhibit dorsal horn and peripheral nociceptive neurones
v. Also inhibit synthesis of substance P which usually trigger inflammation (PG,
bradykinin) - inhibit pain transmission
c. Paracetamol mechanism
i. Work by indirect inhibition of COX - reduce active COX -> cannot form
hyperalgesic compounds
ii. Modulates endogenous cannabinoid system
1. Is metabolised to AM404 which inhibit reuptake of endogenous
cannabinoid ligand and inhibit PG synthesis
2. Induce analgesic action by acting on cannabinoid, cox, system and alter
pain pathways
22. Neuro physiology - Ear
a. Ear anatomy
i. 1---ear canal
ii. 2---malleus
iii. 3--incus
iv. 4---stapes
v. 5---oval window
vi. 6---scala tympani or helicotrema
vii. 7---auditory nerve (cochlear nerve)
viii. 8---basilar membrane (or cochlear duct)
ix. 9---organ of corti
x. 10---scala tympani
xi. 11---round window
xii. 12---tympanic membrane
b. Sound transmission to brain
i. Sound arrives to tympanic membrane and causes vibration
ii. Vibration of tympanic membrane causes displacement of auditory ossicles
1. Malleus -> incus -> stapes
 iii. Vibration at stapes causes oval window causes pressure waves to flow through
scala vestibuli (perilymph)
iv. The pressure waves distort vestibular membrane and basilar membrane and
cause hair cells to be bend against tectorial membrane
v. Then pressure waves exit to scala tympani and to round window
vi. Bending of stereocilia towards kinocilium (highest stereocilia) opens potassium
channels and cause potassium influx -> depolarisation of hair cell
vii. Depolarisation causes calcium influx -> release of neurotransmitter to spiral
ganglion -> CN VIII
viii. Cochlear nuclei -> decussate at superior olivary complex -> ascend to inferior
colliculus by lateral lemniscus -> ascend to medial geniculate body in thalamus
-> primary auditory cortex in temporal lobe
1. (Eighth nerve -> Cochlear nuclei -> superior Olivary complex -> Lateral
lemniscus -> Inferior colliculus -> Medial geniculate body -> Auditory
cortex ECOLI MA)
c. Tactile or auditory transmission
i. Auditory transmission
1. Pressure waves only cause displacement of hair cells that represent with
sound frequency
2. The displacement cause influx of potassium and depolarise hair cell and
subsequently cause neurotransmitter release
ii. Tactile transmission
1. Initial detection of vibration by pacinian corpuscle
a. Cause displacement/movement of a disc that represent with that
vibration frequency
b. Leads to sodium influx into the middle of disc -> action potential
2. Continuous detection by merkel’s disk
a. Stimuli pops/opens vesicle with neurotransmitter and attach to
receptor -> AP
23. Neuro physiology - cortical plasticity
a. Cortical map plasticity
i. Talk about auditory cortex reorganisation/phantom limb in carl’s lecture
b. Any1 understand this question?

2010
MEQ
1. Neuro REPEAT FROM 2009 MEQ PAPER Q1
2. MSK a, b, d, e REPEAT FROM 2009 MEQ PAPER Q2
a. RA soft tissue changes
i. Fusiform and periarticular swelling at affected joints - PIP, MCP
1. Edema, tenosynovitis, joint effusion
ii. Rheumatoid nodules can be seen at elbows
iii. Indirect finding from soft tissue changes
1. Joint space space narrowing due to cartilage destruction
3. Neuro REPEAT FROM 2009 MEQ PAPER Q3
4. Mental health REPEAT FROM 2009 MEQ PAPER Q5
5. Renal
a. Creatinine
i. Renal clearance = GFR
1. Creatinine is filtered freely in glomerulus and is not reabsorbed, meaning
creatinine clearance = GFR
b. pH balance
i. Decreased functional nephron number due to past long term intake of BEX,
leading to decreased acid excretion.
ii. To balance plasma pH, bicarbonate buffer system is used to balance pH -> leads
to decreased bicarbonate concentration
c. CKD lab markers
i. Serum creatinine
ii. Hyperphosphataemia
iii. Hypocalcaemia
iv. Elevated serum PTH
d. CKD microscopy
i. Fibrotic cortex
ii. Sclerotic glomeruli
iii. Thickened arteries
iv. Lymphocyte infiltrated
v. Dilated tubules filled with pink casts
vi. LM: cortical scarring, atherosclerosis, hyalinosis, glomerulosclerosis, tubular
atrophy, interstitial inflammation/fibrosis
vii. IF: varies
viii. EM: thick/wrinkled GBM
ix. Prev three are for hypertensive renal disease
x. Chronic interstitial nephritis: interstitial scarring/fibrosis, tubular atrophy,
inflammatory infiltrate
e. CKD symptoms
i. Patients with CKD stages 1-3 are generally asymptomatic i.e remaining
functional nephron units can still can compensate for the kidney tissue damage.
ii. The damage needs to be severe to stage where the remaining functional
nephron units cannot compensate for the kidney tissue damage. Typically,
symptoms do not show until GFR<30. It is not until stages 4-5 that
endocrine/metabolic derangements or disturbances in water or electrolyte
balance become clinically manifest
f. CKD in anaemia
i. Decreased EPO synthesis
ii. Iron deficiency
g. CKD in anaemia
i. Nephrotoxicity by BEX intake
ii. Anaemia resulted from decreased EPO synthesis
iii. Decreased functional renal mass due to CKD -> decreased EPO production ->
decreased erythropoiesis -> decreased RBC in blood -> anaemia
h. CKD and ion balances
i. Phosphate clearance decreased due to decreased functional nephron unit
numbers
 ii. Increased phosphate concentration stimulates PTH in attempt to increase
phosphate excretion. But PTH also cause bone resorption which release calcium
and phosphate into blood. -> increasing serum calcium
iii. But as phosphate clearance is impaired, serum phosphate is increased

SAQ
Q1~12, 16, 18, 19, 21, 23 b ARE REPEAT FROM 2009 SAQ PAPER
Q15 is REPEAT FROM 2008 SAQ PAPER Q9
Q20 is REPEAT FROM 2008 SAQ PAPER Q1
13. Neuro physiology + pathophysiology - cortical lateralization and stroke
a. Cortical lateralization
i. Refers to how some neuronal function/cognitive function processing tends to be
more dominant in one hemisphere than the other
ii. Allows parallel processing (multitasking
iii. Left hemisphere
1. Language - broca’s and wernicke’s area
a. Reading
b. Writing
c. Speaking
d. Grammar and syntax
2. Calculation
3. Decision making
4. Right side motor
5. Right visual field on each eye
iv. Right hemisphere
1. Spatial perception
2. Emotion
3. Sensory information analysis
4. Face recognition
5. Left side motor
6. Left visual field on each eye
b. Because of this cortical lateralization, stroke on right or left hemisphere will produce
different symptoms
i. If it occurs at left hemisphere especially on wernicke and broca area, stroke
causes aphasia
ii. Depending on stroke size, it may impair other left hemisphere function
iii. If it occurs on right hemisphere, you may especially on inferior parietal lobe,
stroke causes hemispatial neglect
iv. May see other impairments such as emotionless speech, impaired recognition of
face etc.
14. MSK physiology - muscle spindle and fusimotor system
a. Muscle spindles are stretch receptors
i. Ia fibres - nuclear bag fibres - measure velocity of contraction and activated only
during contraction
ii. IIa fibres - nuclear chain fibres - measure length of muscle, stimulating is
decreased when contracted
 b. In order for Ia fibres to be firing, spindle needs to have proper tension when extrafusal
muscle fibres contracts - i.e. muscle spindle fibres are innervated by gamma motor
neuron
c. Fast alpha motor neuron innervate extrafusal muscle fibres, causing muscle to contract. It
does not innervate intrafusal fibres
d. When the extrafusal muscle fibres contracts, intrafusal fibres (muscle spindles) become
loosened and is it does not fire to CNS - have no information on muscle length
e. In order to maintain muscle spindle sensitivity, slow gamma motor neuron innervates
muscle spindles to contract intrafusal fibres when extrafusal fibres - keeping muscle
spindle fibres taught and allows Ia fibres to fire even during muscle contraction
17. PPD - health inequality and inequity
a. Inequality - observable health difference between subgroups within a population, can be
measured and monitored
i. Dies younger due to genetic mutation (non controllable factor)
b. Inequity - unjust differences in health between persons of different social groups
i. Population has lower lifespan due to lack of access to medications
22. Neuro physiology - ear sound travel course
a. Outer ear sound transmission
i. Auricle acts like antenna dish, collecting sound. Then sound travels through
external acoustic meatus and to tympanic membrane
b. Middle ear sound transmission
i. The vibration in tympanic membrane causes the ossicles to vibrate. The vibration
travels through malleus, incus, stapes then to oval window
ii. As the size of tympanic membrane is greater than oval window, the sound is
amplified when sound reaches to oval window
c. Inner ear sound transmission and neural transmission
i. From oval window, the sound travels to scala vestibuli (perilymph) -> scala
tympani (perilymph) -> exits through round window
ii. The pressure waves bends the membranes in cochlear duct at a point of
maximum vibration for a given frequency. This causes stereocilia in hair cells in
the basilar membrane to move
iii. The movement of stereocilia against tectorial membrane opens up potassium
channels -> influx of potassium ions into hair cells -> depolarisation
iv. Depolarisation -> voltage gated calcium channel open -> calcium influx ->
exocytosis of neurotransmitter, travels through spiral ganglion -> cochlear nerve
d. REPEAT FROM 2009 SAQ PAPER Q22 c.
23. Neuro physiology - cortical plasticity
a. Convergence and divergence (we didn’t learn this)
24. PPD - public health domains
a. Health improvement
i. Surveillance and monitoring of specific diseases and risk factors
b. Improving services
i. Service planning
c. Health protection
i. Emergency response
2011
MEQ
1. Renal
a. Provisional diagnosis
i.
Nephrotic syndrome caused by minimal change nephropathy, focal
glomerulosclerosis
b. Nephrotic syndrome lab markers
i. Blood test - will show hypoalbuminemia, hypercholesterolemia
1. Hypoalbuminemia as albumin is being excreted in urine and production
cannot match with excretion
2. Hypercholesterolemia as albumin is excreted, liver tries to compensate.
LDL is released to blood as consequence
ii. Urinalysis, 24 hour bedside urinary total protein estimation- will show Urinary
albumin >3.5 g/day
1. Nephrotic syndrome is represented by urinary albumin >3.5g/1.73m2/day
iii. Kidney biopsy
1. To identify type of glomerulonephritis involved
c. ??
d. Treatment
i. Limit intake of sodium, and eat food low in saturated fat and cholesterol
ii. Drugs to lower blood pressure - ACEI or ARB
iii. Statins to lower blood cholesterol
2. Renal
a. Diagnosis
i. SLE
b. SLE lab markers
i.Blood test
1. If positive - shows anti-nuclear factor, anti-double stranded DNA
2. ESR and CRP will be increased due to inflammatory reaction
ii. Kidney biopsy
1. In immunofluorescence will show IgG,A,M and complement on
mesangium and capillaries
2. On electron microscopy will show immune complex in endothelium,
subendothelium, and see tubuloreticular inclusions
3. On light microscopy will show proliferative with/without necrosis, deposits
and minimal space
iii. Urinlaysis
1. Protein, blood and specially cellular casts under microscope
c. SLE light microscopy
i. Mesangial and/or capillary immune deposits.
ii. Increase of the matrix and/or mesangial cellularity, endocapillary proliferation,
thickening of capillary walls, glomerular tuft necrosis, extracapillary
proliferation
 iii. Hyaline thrombi and “wire loop” lesions - homogeneous and “rigid”
thickening of peripheral capillary loops due to subendothelial immune
deposits
d. PPD breaking bad news
i. SPIKES mnemonics
3. Renal REPEAT FROM 2009 MEQ PAPER Q4
4. Neuro
a. Headache
i. Occipitofrontalis muscle pain
ii. Nerve compression by increased intracranial pressure
iii. MMA or superficial temporal arteries
b. History taking for headache
i. Disease onset/duration – Headache onset
1. Headache duration
2. Headache frequency ( per year, per month, per day)
ii. Core symptoms (“PUMA”)
1. Pulsatile or Not
2. Unilateral or Not
3. Moderate or severe VS. Mild intensity
4. Activities (daily) exacerbation
iii. Associated symptoms
1. Aura
2. nausea, vomiting, photophobia, phonophobia
3. Cranial autonomic symptom
iv. Severity
v. Quality
1. Throbbing/ pulsating: i.e. migraine
2. Dull/Tightness: i.e. TTH
vi. Radiation, rapid
1. gradually: i.e. migraine, tension-type headache
2. rapid in seconds: thunderclap headache
c. Cervical back pain to bifrontal headaches
i. Neck pain on C1~2 levels travel through spinal afferent to trigeminocervical
nucleus.
ii. Stimulation of trigeminocervical causes pain sensation in trigeminal nerves ->
experiences headache pain
d. Back pain red flags
i. Bladder and bowel dysfunction
ii. Past history of cancer
iii. Unexpected weight loss
e. Back pain and reflex
i. Achilles reflex checks if S1 and S2 nerve roots are intact and functioning
 ii. Reduction of achilles reflex may indicate sciatic nerve pathology i.e. nerve root
compression in spinal root S1/L5
iii. As the reflex arc is blocked by nerve root complex, reflex is impaired
f. Carpal tunnel syndrome
i. If issues in hand was caused by problem of cervical radiculopathy, it would
not just affect hand, but will affect every muscle that nerve supplies
ii. In the case of median nerve, it provides innervation to anterior forearm except
for flexor carpi ulnaris. In hand it supplies thenar muscles and lumbricals I and
II
iii. If it was a problem of nerve root blockage, will cause weakness at forearm
flexion and hand.
iv. Also it would not only affect median nerve, may affect other nerves in brachial
plexus most of the time.
v. Since the problem is only localised to right thumb which means it has
affected thenar muscles not forearm muscles.
vi. As median nerve passes through carpal tunnel, carpal tunnel syndrome will
cause median nerve entrapment, causing weakness of muscles supplied by
median nerve from wrist onwards - thenar muscle weakness -> weakness in
right thumb
5. Neuro
a. Dx
i. Transient ischemic attack
ii. Left middle cerebral artery thrombosis
iii. Tumour (stroke like symptoms)
iv. Spinal cord injury
b. CT scans
i. Stroke needs to be treated asap to prevent further damage to brain.
ii. CT scans are readily available at all hours at most major hospitals and produces
images quickly unlike MRI which has long line of wait and takes long to produce
images
iii. CT is used to rule out hemorrhagic cause of stroke, so doctors can determine
thrombolytic therapy can be used immediately or not. Thrombolytic therapy will
be used for ischemic stroke and cannot be used and worsen hemorrhagic stroke
iv. occasionally show a tumor that might mimic a stroke.
c. Facial droop
i. Left motor cortex disturbance or pontomedullary junction disturbance
ii. Lower left motor cortex innervate and represent face, efferent travels to internal
capsule and decussates and travel as contralateral facial nerve, supplying
contralateral muscles of facial expression
iii. Upper ½ of face on both side has dual innervation, meaning motor cortex
damage on one side will not affect upper contralateral ½ of face as ipsilateral
motor cortex.
iv. Lower ½ of face is innervated by contralateral motor cortex
 v. Same applies to facial nucleus at pontomedullary junction (dorsal aspect have
dual innervation, ventral aspect have contralateral innervation)
vi. (ill probs draw the facial innervation cuz i cannot be fked 2 write out description)
d. Dysphagia
i. Difficulty with swallowing (or dysphagia) happens after a stroke because the
brain doesn't activate muscle reflexes at the back of the throat quickly enough, so
that food or liquids pass down the throat into the larynx and/or lungs and may
cause blockage or aspiration
ii. nuclei of glossopharyngeal and vagus lie close to the pontomedullary junction
therefore there is reduced activity of vagus and CN IX
e. ‘Nil by mouth’
i. (cbf writing whole thing)
ii. Address that she is going through surgery and what is going to happen to
swallowing reflexes when she goes through general anaesthetics
iii. Tell her complications of drinking/eating before surgery - pulmonary aspiration
f. Ototoxicity
i. Gentamicin is aminoglycosides
ii. It has slow clearance rate in inner ear
iii. It enters and accumulates in hair cells and cause disruption in mitochondrial
protein synthesis (decline of ATP production) , ROS formation, and activates
caspases
iv. These damage and cause apoptosis of hair cells
v. Hair cell death in cochlear duct occur from high frequency to low frequency -
causes progressive hearing loss
vi. Hair cell death in vestibular apparatus cause dizziness
g. Vertigo and dizziness
i. Dizziness is feeling of being lightheaded, unbalanced - include pre-syncope,
disequilibrium and vertigo
ii. People who have dizziness may have vertigo
1. It is an illusion of motion - feel as though you are spinning despite you
are not moving
2. Can be caused by vestibular apparatus damage - peripheral vertigo
3. Or damage of brainstem - central vertigo
iii. Dunno what else to say
h. Stroke motor effect
i. Muscle spasticity - hypertonicity
ii. Joint contracture - due to abnormal tightening of muscle
iii. Hyperreflexia
iv. Weakness
v. Coordination loss
6. MSK
a. Diagnosis
i. Duchenne muscular dystrophy
b. Frameshift mutation
 i. Frameshift mutation - insertion or deletion of nucleotide, shifts the reading frame
of codons from point of mutation onwards -> change every amino acid that
follows the point of mutation -> alter protein completely -> alter its function
(unable to perform its normal function)
ii. So if there was frameshift mutation of dystrophin gene in DMD, it alters the
structure of dystrophin protein and its function is lost
c. Inheritance of DMD
i.Is x linked recessive disease, i.e. males can only be affected by disease, cannot
be carriers
d. Dystrophin function and DMD pathogenesis
i.Dystrophin found within muscle cell, is sarcolemmal cytoskeletal protein - b/w
sarcolemma and outermost layer of myofilaments
ii. Functions to mechanically link cytoplasmic actin and dystroglycan complex - link,
stabilize, provides strength to intracellular contractile proteins and extracellular
matrix (sarcolemma) during contraction
iii. With dysfunctional dystrophin, damages sarcolemma during contraction and
cause calcium influx into muscle cell - activate calcium dependent cellular
enzyme that degrade cells - muscle destruction
e. Calcium in muscle
i. Stored in sarcoplasmic reticulum
ii. Action potential from postsynaptic neuron travels through T tubule
iii. Causes conformational change in dihydropyridine receptor - cause coupling of
ryanodine receptor + dihydropyridine receptor -> opens ryanodine receptor ->
allows calcium release from sarcoplasmic reticulum to sarcomere
iv. Calcium binds to troponin C and shifts tropomyosin and exposes myosin binding
site of actin fibres - allows myosin head to bind (sliding filament theory)
f. DMD microscopy
i. Fibre size variation
ii. Internal nuclei
iii. Fibre splitting
iv. Proliferation of fat and connective tissue
v. Dystrophin is absent in immunostaining

SAQ
1. MSK physiology - articular cartilage composition
a. Is 60~80% water in gel form
b. Fibrillar collagen
i. Functions to hold proteoglycans and water gel
c. Proteoglycans
i. Is 90% aggrecan
ii. Bottlebrush appearance
iii. Attract water
d. Glycosaminoglycans
i. Has viscoelastic function
 e. Fluid changes shape within cartilage
f. Fluid spreads out throughout cartilage, acts as means to absorb the pressure of
movement
2. Renal physiology - Defence mechanism REPEAT FROM 2008 SAQ PAPER Q11
3. Renal pathophysiology - UTI
a. Upper UTI
i. Flank pain
ii. Fever
iii. Nausea
iv. Vomiting
b. Lower UTI
i. Burning with urination
ii. Urge to urinate frequently
iii. Pain above pubic bone
iv. No Upper UTI symptoms
4. MSK pathophysiology - RA lab features
a. Dunno about fasting blood sugar and protein electrophoresis
b. Your best bet is to choose 2 of “ESR CRP LFT” for your answer. It is easier to do
REPEAT FROM 2008 SAQ PAPER Q1
c. Not sure if immunoglobulin assay also include anti-CCP, RF in RA but if it does you can
talk about it
5. Mental health - delusions, illusions, hallucinations
a. What does he have
i. Illusions
b. MSE - memory and concentration test
i. Attention and concentration are assessed by
1. serial sevens test (From 100 and subtract 7 onwards)
2. By spelling a five-letter word backwards
3. Testing digit span
ii. Memory
1. Immediate registration (repeating a set of words)
2. Short-term memory
a. Recalling the set of words after an interval
b. Recalling a short paragraph
c. Digit span testing
3. Long-term memory (recollection of well known historical or geographical
facts)
6. Neuro physiology - Cortical plasticity REPEAT FROM 2009 SAQ PAPER Q23
7. Neuro physiology - Speech
a. Primary auditory cortex - brodmann area 41, 42 at temporal lobe
i. Receives auditory information and sends language information to wernicke’s
area for language comprehension
b. Primary visual cortex - brodmann area 17, at occipital lobe
i. Receives visual information and sends language information to wernicke’s area
for language comprehension
c. Wernicke’s area - brodmann area 22, at posterior superior temporal gyrus in left
hemisphere (in most)
i. Mainly involved in comprehension of language
 ii. The auditory and visual information from respective primary cortex area comes
into wernicke’s area
iii. Memorise how words look and sound
d. Arcuate fasciculus connects wernicke’s area to broca’s area
e. Broca’s area - brodmann area 44, 45, at posterior inferior frontal gyrus in left hemisphere
(in most)
i. Involved in production of language
ii. Anterior area involved in semantic function
iii. Posterior area involved in phonology
iv. Also involved in forming sentence structure with proper grammar
f. Primary motor cortex - brodmann area 4, precentral gyrus
i. Broca’s area sends information on how to control the muscle of speech
ii. Larynx control - phonation
iii. Mouth control - articulation
g. Right hemisphere associated with emotion in speech
8. Renal pathophysiology - CKD signs
a. GFR <60mL/1.73m2/day for 3 months +
b. Albuminuria >30mg/day
c. Markers of kidney damage - casts, proteinuria, hematuria
9. PPD - health domains REPEAT FROM 2010 SAQ PAPER Q24
10. Neuro physiology - depression and cingulate cortex
a. Chronically depressed patients show low activity in the perigenual ACC, electrical
stimulation of this region alleviates the depression (nowhere near enough for 6 marks,
fuck it)
11. Neuro anatomy - limbic lobe structure
a. Hippocampus
b. Cingulate cortex
12. Neuro pathology - astrocytic brain tumours
a. Pilocytic astrocytoma - grade 1
b. Diffuse astrocytoma - grade 2
c. Anaplastic astrocytoma - grade 3
d. Giloblastoma - grade 4
13. MSK pathology - fracture healing REPEAT FROM 2009 SAQ PAPER Q19
14. Renal physiology - GFR determinant REPEAT FROM 2008 SAQ PAPER Q13
15. Renal physiology - filtration barrier
a. Drug size > 70nm
b. -’ve charged substances
c. Drug weight >70kDa
16. Neuro pharmacology - blood brain barrier
a. Not lipophilic
b. charged
17. Neuro pharmacology - Benzodiazepines
a. Benzodiazepines acts to increase efficacy of GABA - decreases excitability of neuron ->
reduces communication between neurons -> calming effect on brain
b. GABAa receptors contain chloride channel across neuronal membrane, 2 binding sites
for GABA and 1 binding site for benzodiazepines
c. Benzodiazepine binding to GABAa receptor acts as allosteric modulator - changes
conformation of receptor which increases affinity for GABA neurotransmitter.
 d. Ths increases frequency of opening of GABAa chloride channel -> increased sodium
transport to neuronal cytoplasm -> hyperpolarizes neuronal membrane potential -> due to
increased difference between resting potential and threshold potential, neuron is less
likely to fire -> calming effect
18. MSK pathology - imaging
a. Bone cancers
b. Infection involving bone
c. Bone inflammation
d. Fractures that aren’t visible in traditional X-ray
e. Avascular necrosis
19. MSK pharmacology - side effects of glucocorticoids
a. Increased weight - due to increased hepatic gluconeogenesis and insulin resistance
b. Immunodeficiency - glucocorticoids work by immunosuppression, long term use will
cause further decreased function+number of WBC
c. Increased RANK-L expression, decrease estrogen secretion → increase osteoblast apoptosis,
increase osteoclast differentiation and activity → osteoporosis
d. Inhibition of hypothalamic-pituitary-adrenal function → iatrogenic Cushing’s syndrome
20. Pop health - incidence rate and types of studies
a. Incidence rate is measure of frequency with which a disease occurs in population over a
period of time
i. Number of new cases of disease/population at risk
b. Case control studies does not provide relative risk - cannot calculate incidence rate
(Cohort studies allow calculation of incidence rate)
21. Neuro pharmacology - analgesics (opioids)
a. Inhibit pain reception
b. Produce euphoria
22. MSK physiology - phosphate and calcium homeostasis
a. PTH
i. Cause bone resorption -> release calcium and phosphate into blood
1. Binds to osteoblasts - decrease osteoprotegerin and increase RANKL
expression - RANKL-RANK receptor binding without OPG inhibition lead
to increased osteoclast activity -> bone resorption
ii. Increase calcium reabsorption (DCT) + decrease phosphate reabsorption (PCT)
iii. Increase calcitriol formation
1. Stimulates 1-alpha-hydroxylase in kidney -> increased calcitriol
iv. Overall increases serum calcium and decrease serum phosphate
b. Vitamin D
i. After being converted to calcitriol
ii. Increases calcium and phosphate absorption in gut
iii. Stimulates bone resorption - release calcium and phosphate into blood
1. Increases expression of RANKL
iv. Increase calcium and phosphate reabsorption from kidney
v. Overall increases serum calcium and serum phosphate
c. EXTRA INFORMATION
i. PTH
1. Decreased serum calcium concentration is detected by Calcium
Sensing Receptor on parathyroid cells -> release PTH
2. Hyperphosphataemia is also stimulant for PTH release
 3. PTH then increases serum calcium, decreases serum phosphate by :
a. bone resorption by stimulating osteoclasts (increases calcium
and phosphate release to blood)
i. This is done by PTH binding to its receptor in
osteoblast -> increase RANK ligand (RANKL)
expression and decrease osteoprotegrin(OPG, binds
to RANKL and prevent it from binding to RANK
receptor). Binding of RANKL to RANK receptor
without any OPG inhibition will lead to increased
osteoclast formation -> bone resorption
b. Increasing calcitriol formation
c. Increasing calcium reabsorption (DCT) and decreasing
phosphate resorption (PCT) in kidney
ii. Calcitriol
1. Calcitriol production is stimulated by PTH by stimulation of 1-alpha-
hydroxylase in kidney
2. It increases serum calcium and phosphate by:
a. Increased calcium and phosphate reabsorption in kidney
b. Increased absorption of phohsphate and calcium in gut
c. Stimulation of bone resorption
i. (similar mechanism to PTH? Just upregulates RANKL
expression by osteoblast)
iii. FGF-23
1. It is produced by osteocyte and its production is stimulated by
calcitriol and increased serum phosphate level
2. It decreases serum phosphate level by
a. Inhibition of calcitriol formation (inhibition of 1-alpha-
hydroxylase)
b. Decreased reabsorption of phosphate in kidney (does this by
binding to FGF receptor in PCT, requires klotho as a
coactivator. Binding causes downregulation of phosphate-
sodium channel on the luminal side)
c. Inhibition of PTH release
iv. Calcitonin (not mentioned in lecture)
1. Produced by parafollicular cells of thyroid gland in response to
increased serum calcium
2. It decreases serum calcium by
a. Inhibition of bone resorption by binding to its receptor in
osteoclast -> decreases osteoclast activity
23. Renal anatomy - nephron structure
 PCT
Bowmans
capsule

Glomerulus
DCT
Efferent
arteriole
Afferent
arteriole

Thick Collecting
ascending duct
LoH

Thin
descending
LoH

24. Renal pathophysiology - Renal colic

a. Severe pain in lower back or sides
b. Caused by blockage of urinary tract - kidney stones, spasms, dead tissue etc.
25. Renal pathophysiology - diabetic nephropathy histology
 Nodular
lesion

GBM
expansion Hyaline
26. Neuro anatomy - spinal cord arteriosclerosis?
 Posterior horn
of grey matter

Dura and
arachnoid mater

Pia mater
Central canal

Dorsal root

Anterior horn of
grey matter

Dorsal root White matter

ganglion

Ventral root

27. Mental health - DSM axes

 a. Axis 1 - clinical syndromes
i. Mental disorders that has been diagnosed clinically
ii. Bipolar disorder
iii. schizophrenia
b. Axis 2 - personality disorders
i. Borderline personality disorder
ii. Moderate mental retardation
c. Axis 3 - general medical conditions
i. Asthma
ii. Hypertension
d. Axis 4 - psychosocial and environmental problems
e. Axis 5 - global assessment of functioning
28. Neuro pathophysiology - brain death and vegetative state
a. Brain death
i. Complete and irreversible loss of brain function
ii. Irreversible coma
iii. Absence of brainstem reflexes and motor responses
iv. Absent glucose metabolism
v. Aponeic
b. Vegetative state
i. Wakefulness without consciousness - can be permanent or reversible
ii. No evidence of awareness or environment
iii. Inability to interact
iv. No evidence of sustained/reproducible response, language, comprehension
v. Intermittent wakefulness manifested by sleep wake cycle
vi. Sufficiently preserved brainstem + hypothalamus autonomic function to survive
1. Spontaneous eye opening
2. Facial expression
3. Noxious stimulation increases activity in thalamus + cortex
4. Can breathe spontaneously
5. Decreased glucose metabolism
vii. Spinal and cranial nerves spared in random fashion
29. Neuro pathophysiology - chronic pain and associated brain changes
a. Chronic pain
i. Pain that persists beyond predicted time of recovery of > 3 months
ii. Constant pain without any real stimulus - centrally evoked pain
b. Brain structural changes
i. In chronic orofacial pain
1. Cell loss in thalamus, nucleus accumbens, putamen, primary
somatosensory cortex
2. The severity of pain directly correlates to the degree of cell loss in
contralateral thalamus
ii. In spinal cord injury
1. Reorganisation of primary somatosensory cortex occur
2. Neurons decrease in number in ventroposterior thalamus
a. Increased loss -> increased pain
3. Increased neuronal activity in primary motor cortex
 4. There is increased neuronal activity in anterior insula, dorsolateral
prefrontal cortex, premotor cortex, supplementary motor area - relates to
ongoing pain imagination
iii. In general - grey matter loss in pain processing structures

2012
MEQ
1. Renal
a. Nephritic syndrome
b. Nephritic syndrome children causes
i. IgA nephropathy
ii. Henoch-schonlein purpura
iii. Post streptococcal glomerulonephritis
iv. Hemolytic uraemic syndrome
v. MORE INFO
1. Adults
a. SLE
b. Goodpasture syndrome
c. Infective endocarditis
d. Rapidly progressing glomerulonephritis
c. AKI lab markers
i. Blood tests
1. Elevated serum creatinine
2. Hyperkalemia
3. Hyperphosphataemia
4. Azotaemia
ii. Observations ??
1. Increased blood pressure
2. Oliguria
d. Increased blood pressure in AKI
i. In intrarenal AKI
ii. As immune complexes deposit into glomerular tissue, it activates complement
system -> inflammation and podocyte damage -> damage filtration membrane
iii. This causes fluid leakage into tubule -> increased hydrostatic pressure in tubule
-> reduces pressure differences ->decreases GFR
1. Also the plug formed by dead cells that lodge into tubule can also
contribute to increased hydrostatic pressure in tubule
iv. Decrease in GFR -> excess volume not excreted as urine -> increased blood
volume -> hypertension
e. Hematuria in AKI
i. Discoloured urine due to erythrocyte leakage
ii. Inflammation in glomerulus caused by immune complex deposits results in
filtration membrane damage, especially the capillary wall
iii. The damage to capillary wall allows erythrocyte to pass through the capillary wall
into the renal tubules
 iv. As they pass through the capillary wall, mechanical damage when passing
through filtration membrane and osmotic damage from tubular fluid causes
erythrocyte damage -> dysmorphic erythrocyte in urinalysis
v. Erythrocytes may adhere to hyaline casts in tubular segment -> show up as RBC
casts in urinalysis
2. Neuro REPEAT FROM 2011 MEQ PAPER Q5
3. Neuro
a. Dx
i. Dysgraphia
1. Stroke in broca’s area
2. Peripheral motor neuron diseases - myasthenia gravis
ii. Aphasia
1. Stroke in language area
2. Brain lesion/trauma in language area
iii. Imbalance
1. Multiple sclerosis
2. Otitis media
b. MSE??
c. Workup
i. ESR
ii. CRP
iii. Leukocytosis
iv. RF
v. Protein electrophoresis
d. Imaging
i. MRI, CT, PET, fMRI, SPECT
e. PPD
i. Support groups
ii. ??
4. MSK
a. ICM - back pain history
i. Does your back pain not subside on rest?
ii. Did you have a history of any cancer? Did you experience any unexpected
weight loss?
b. Calcium and phosphate homeostasis
i. Vitamin D is converted to calcitriol in kidney by 1-alpha-hydroxylase
ii. Calcitriol acts to maintain skeletal calcium balance by
1. Increasing calcium + phosphate reabsorption in kidney
2. Increasing calcium + phosphate absorption from gut
3. Promoting bone resorption
iii. This maintains calcium and phosphate concentration of bone formation + PTH
levels to maintain serum calcium level
iv. Without vitamin D, calcium absorption and reabsorption is dramatically
decreased -> phosphate and calcium balance is disturbed -> bone formation
cannot happen
v. As calcitriol inhibits PTH secretion, inhibition is lifted + low calcium and
phosphate level -> PTH released -> stimulate bone resorption to maintain serum
calcium level -> further bone resorption causes osteoporosis
c. Knee joint anatomy
 i. Extracapsular ligament - At medial and lateral sides of knee, there is lateral
(femur and fibula) and medial collateral (femur and tibia) ligaments
1. Medial collateral ligament protect medial side of knee from being bent
open by lateral force/valgus force
2. Lateral collateral ligament protect lateral side of knee from being bent
open by medial force/varus force
ii. Intracapsular ligament - Anterior cruciate ligament (lateral condyle of femur -
anterior intercondylar area) and posterior cruciate ligament (medial condyle of
femur - posterior intercondylar area)
1. ACL prevents the tibia from being pushed too far anterior in relation to
femur
2. PCL prevents posterior deviation of tibia in relation to femur
d. OA and osteoporosis
i. Osteoarthritis is a joint disease that result from cartilage degradation of joints
ii. Osteoporosis is a porous bone disease - decreased bone strength due to
reduced bone quantity and quality
e. OA and RA on knee
i. On palpation, osteophytes may be felt
f. Articular cartilage component REPEAT FROM 2011 SAQ PAPER Q1
i. Glucosamine sulfate - inhibit collagenase, aggrecanase, phospholipase A2,
lysosomal enzymes, radical formation from macrophages
g. NSAID on COX pathway

i.
5. Neuro
a. Back pain causes
i. Muscle damage
ii. Spine fracture
iii. Spinal cord nerve root compression
iv. Intervertebral disc compression
b. Nerve root supplying right leg
i. Nerve root from L2~4
c. Dermatome of medial right calf
i. L3~4
d. Nerve root compression to back pain + paresthesia
i. Nerve innervates whatever muscles that it runs past
 ii.When nerve root exits, the roots splits into ventral and dorsal rami
iii.Dorsal rami supplies the muscles of the back
iv. Ventral rami projects laterally and supplies either body wall or limbs depending
on which level root is exiting
v. Lumbar spinal nerve root gives innervation to
1. Dorsal rami - muscles of lower back
2. Ventral rami - muscles of the lower limb
vi. As the compression blocks/interferes with innervation, will cause paresthesia of
muscle it gives innervation to, and causes pain in muscles of the back it gives
innervation to
e. Rotator cuff muscles
i. Supraspinatus
ii. Infraspinatus
iii. Teres minor
iv. Subscapularis
f. Rotator cuff tear and abduction pain
i. Supraspinatus assists abduction of upper limb with deltoid from 0~15 degrees
ii. Then deltoid takes over for the rest of the angle
iii. If supraspinatus is damaged, will have difficulty initiating abduction of upper limb
6. Neuro
a. OD history taking
i. Was it planned?
ii. What precipitated attempt?
1. Quantity of tablets
b. 8 putative current psychiatric symptoms it would be MOST important to ask about
in the history of the present complaint.
i. Hopelessness
ii. Anhedonia
iii. insomnia/oversleeping
iv. Loss of appetite/overeating
v. Depression
vi. anxiety/impaired concentration
vii. Panic attack
viii. Severe remorse
c. What aspects of this opening statement are important to include in an aetiologic
psychiatric formulation for this patient? Please explain why for each. (3 marks)
i. Family moved home
1. depression
ii. Paracetamol
1. Is painkiller - to reduce severe pain/cancer pain etc.

SAQ
1. MSK pathophysiology - arthritis type
a. Monoarthritis
i. Infection
ii. Crystal arthropathy
b. Oligoarthritis
 i. reactive arthritis
ii. psoariasis
c. Polyarthritis
i. Rheumatoid arthritis
ii. SLE
2. Neuro pathophysiology - parkinson’s disease and dopamine
a. REPEAT FROM 2008 SAQ PAPER Q5
3. MSK pharmacology - RA pharmacology Methotrexate
a. Methotrexate inhibits DHFR -> inhibit folic acid synthesis -> DNA synthesis + purine
synthesis inhibited
i. Inhibit DNA+RNA synthesis
b. Results in inhibition of proliferation of cells that are responsible for synovitis
c. Inhibits toxic compound synthesis
d. Decrease intracellular glutathione -> decrease macrophage function and recruitment
e. Increase adenosine release -> mediate anti-inflammatory effects
4. Renal genetics - one and two hit model and ADPKD
a. REPEAT FROM 2009 SAQ PAPER Q6
5. Neuro pathophysiology - agnosia
a. Prosopagnosia - cognitive disorder, inability/impaired ability to recognise faces
b. Cannot recognise faces they have seen before
i. Acquired - in adults by brain damage/head trauma in occipito-temporal lobe
ii. Developmental - in child with no signs of brain damage
c. Damage in right hemisphere fusiform gyrus + occipitotemporal cortex
6. Neuro physiology - central pattern generator
a. Neural networks that produce rhythmic patterned outputs without sensory feedback
b. Involves
i. Interneuron stimulation of protagonist muscle
ii. Stimulation of inhibitory interneuron leading to inhibition of antagonist muscle
iii. The motion repeatedly returns to its starting position
c. Generates rhythmic pattern in walking, swimming, respiration
i. Central pattern generator for locomotion in lower thoracic + lumbar spinal cord
7. Renal pathology - modifiable factors of renal disease
a. Obtain data on community’s
i. Height
ii. Weight
iii. BMI
iv. BP
v. Blood analysis results
vi. From local hospital
b. Face to face interview in local clinical research centre on
i. Education
ii. SES
iii. Activity level
iv. Diet
v. Family health history
vi. Medical history
8. Renal pathology - nephrotic syndrome
a. Nephrotic syndrome
i. Hypoalbuminemia
 ii. Hyperlipidemia
9. Renal embryology - supernumerary kidney
a. Ureteric buds penetrates the blastemal tissue to form from ureter to collecting duct of
nephron
i. Rest of kidney is formed by blastemal tissue
b. Additional kidney is due to splitting of the blastemal tissue or from separate metanephric
blastemas into duplicated/separated ureteric buds enter to form separate encapsulated
kidneys
10. MSK physiology - phosphate and calcium homeostasis
a. REPEAT FROM 2011 SAQ PAPER Q22
11. Mental health - psychiatric formulation
a. Differential diagnosis
b. Aetiology of probable diagnosis - predisposing, precipitating, perpetuating factors
c. Conclusion about diagnosis and aetiology summarised
d. Treatment plan - social measures, psychological treatments and medication
e. Prognosis
12. Neuro pharmacology - alzheimer's disease and AchE inhibitors
a. In AD, cholinergic neurons number decline -> decreased Ach release for transmission
b. AchE degrades Ach in synapse -> inactivates Ach
i. Inhibition allows Ach to stay longer within synapse - compensates for lowered
concentration of Ach due to decreased number of cholinergic neurons
13. Neuro pharmacology - heroin or morphine
a. Heroin is morphine with acetyl group attached
b. This acetyl group allows heroin to be lipophilic - able to cross blood brain barrier more
quickly than morphine - heroin is stronger than morphine
14. MSK pathophysiology - bone fracture complications
a. Injury to major vessels
i. Fractured bone may rip/block major vessels - damage them
b. Injury to muscles and tendons
i. Fractured bone may pierce/rip through nearby muscle and tendons
c. Injury to joints
i. Joints connecting bone may be ripped/snapped depending on the direction of
force that caused the bone fracture
d. Injury to viscera
i. Rib fractures endanger/may cause damage into lungs
15. Symptom or syndrome or diagnosis
a. Symptom - abnormal feeling/function that patients experiences
i. Flank pain
b. Syndrome - set of medical signs and symptoms that correlate with each other to a
specific disease
i. Nephritic syndrome
c. Diagnosis - identification of the cause of those medical signs and symptoms
i. IgA nephropathy
16. Renal physiology - reabsorption and excretion
a. Na+/K+ ATPase pumps 3 Na+ out of cell and 2 K+ into cell - resides in basal membrane
in nephron cells
b. This makes cell negatively charged - maintains low intracellular sodium concentration
 i. Allows sodium to passively get into cell in PCT from tubule through apical
cotransporter -> Allows glucose, amino acid, phosphate resorption with sodium
co-transporter
ii. Allows apical Na/K/Cl symporter + apical K pump to make tubular lumen
positively charged in Thick ascending limb of loop of Henle
1. Na/K/Cl symporter reabsorbed Na, K, 2Cl - Na (by Na/K ATPase) and Cl
(basal Cl pump) is pumped out of cell and K is pumped into tubular
lumen (by apical K pump, intracellular K from apical Na/K/Cl and basal
Na/K ATPase) - makes lumen positively charged
2. This positive charged lumen allows Mg, Ca reabsorption through
paracellular junction by repulsion of charge
c. Mediates countercurrent multiplier
i. In TAL of LoH is impermeable to water - only allows ion exchange
1. Excretes Na into medullary interstitium by basal Na/K ATPase
2. Increases medullary interstitium osmolarity
ii. In Thin Descending Limb of LoH is permeable to water but impermeable to ions
1. Due to increased osmolarity of medullary interstitium, water flows out
from tubule to interstitium due to osmosis
iii. This allows water conservation and concentrates tubular fluid
17. Renal physiology - reabsorption mechanisms
a. Passive transport - does not require energy/ATP for transport of ions
b. Facilitated transport - passive transport of molecules (AA, glucose, Phosphate) by
specific integral molecules (Na+)
c. Active transport - requires energy for transport of ions, transport against concentration
gradient
d. Osmosis - passive transport where solvent is diffused from low to high ion concentration
through a semipermeable membrane to maintain equal osmolarity in both
18. Renal pharmacology - NSAIDS
a. “Draw diagram of normal arachidonic acid pathway”
i. COX 1 constitutive in most cells
ii. COX 2 in inflammatory cells
b. NSAIDS work by blocking COX 1 and 2, which reduces production of prostaglandins and
reducing its hyperalgesic, chemotic, pyretic effect, resulting in reduced pain and
inflammation
c. Aspirin - inhibits COX 1 more - decreased TXA2 production - anticoagulant effect
d. Coxibs - inhibits COX 2 more - mediates anti-inflammatory effect as it is only produced in
inflammatory cells
19. MSK genetics - Achondroplasia
a. Is autosomal dominant, mutation in FGFR3 gene in chromosome 4
b. FGFR3 in proliferating chondrocytes, mediates differentiation of cartilage to bone
c. In Achondroplasia, FGFR3 become hyperactive - result in premature conversion of
cartilage (also growth plate) to bone
i. Decreased cartilage matrix production
ii. Decreased cellular hypertrophy
d. Results in shorter and smaller bones -> smaller and shorter limbs
20. Neuro physiology - movement of eye
a. REPEAT FROM 2009 MEQ PAPER Q3 C
21. Neuro physiology - cerebellum
a. Vestibulocerebellum
 i. Input from vestibular apparatus and vision information
ii. Output to vestibular nuclei - maintains equilibrium, movement during stance and
gait + vestibulo-ocular reflex
b. Spinocerebellum
i. Input from cerebral cortex and peripheral sensory receptors
ii. Output to interposed nuclei and fastigial nuclei - control proximal and distal
musculature
c. Vermis
i. Input from cerebral cortex
ii. Control axial musculature
1. Vermis + spinocerebellum forms feedback loop
d. Cerebrocerebellum
i. Input from cerebral cortex
ii. Output to dentate nucleus - plan movements, timing etc
22. Neuro physiology - Basal ganglia
a. Direct pathway - mediates movement
i. Inhibits Globus Pallidus internus and stimulates globus pallidus externus from
striatum -> decrease inhibitor effect of globus pallidus internus to thalamus ->
stimulate cortex -> movement
b. Indirect pathway - inhibits movement
i. Inhibits globus pallidus externus and disinhibit globus pallidus internus from
striatum -> inhibition of GPe disinhibit subthalamic nucleus which stimulates
globus pallidus internus -> increase inhibitor effect of globus pallidus internus to
thalamus -> decreased stimulation to cortex -> inhibition of movement
23. Neuro pathophysiology - anopia and visual circuit
a. Left half of visual field on both eye cannot be seen except for the centre of eye (just draw
diagram)

i.
b. Right occipital lobe damage - PCA damage etc.
24. Neuro pathophysiology - aphasia
a. Aphasia definition
i. Language impairment
b. Broca’s or wernicke’s aphasia
i.
Language aspect Broca’s aphasia Wernicke’s aphasia

comprehension preserved impaired

Fluency Decreased preserved

repetition Limited impaired

c. Broca and wernicke’s area in brain
 i. Broca’s area in inferior frontal cortex, wernicke’s area in superior temporal gyrus
of left hemisphere in left hemisphere of right handed person
25. Stats

2013
MEQ
1. Renal
a. Juxtaglomerular cells and its response
i. Secrete renin in response to decreased blood pressure
ii. More info
1. Decreased BP
a. Decrease blood flow -> decrease GFR as glomerular hydrostatic
pressure is decreased
b. Decreased sodium and chloride delivery to macula densa by
NKCC2 -> decreased macula densa activity -> release and
synthesise PGE2 to juxtaglomerular cells and smooth muscle
cells -> PGE2 in JG cells cause renin release - eff, aff arteriole
vasoconstriction
c. Afferent arteriole stays dilated as PGE2 direct vasodilator
i. -> increase GFR
2. Increased BP
a. Increased blood flow -> increased GFR -> increased sodium and
chloride in tubular lumen -> increased delivery to macula densa
by NKCC2 -> cell osmolarity increased
b. Increased cell osmolarity -> water flows into cell -> ATP leaves
basolaterally
c. ATP converted to adenosine -> binds to extragranular mesangial
cells -> release calcium to JG and smooth muscle cells of
afferent arteriole
d. Calcium influx to JG cells -> no renin release - no
vasoconstriction
e. Calcium influx to smooth muscle cells of afferent arteriole -> aff.
A vasoconstriction
b. Angiotensin 2 effects
i. Stimulate aldosterone release from adrenal cortex - act in DCT, CT
1. Increase sodium channel in apical membrane
2. Increase Na/K ATPase in basolateral membrane
3. Increased K secretion and Na reabsorption
4. Increased water reabsorption by osmosis
ii. Stimulate ADH release from posterior pituitary
1. Increased AQP2 insertion into apical membrane - increased water
reabsorption
iii. Vasoconstriction
iv. Vasoconstriction of efferent arteriole -> increased GFR
1. Decreased flow to vasa recta - decreased solute washout
 a. Favor reabsorption
v.Increased thirst sensation
vi.Increase sensitivity of tubuloglomerular feedback
vii.Increase noradrenaline release + reuptake inhibited
1. Increase sympathetic adrenergic function
viii. Add/remove if you think there is more/wrong
c. Osmolarity and sodium concentration in hemorrhage
i. Hemorrhage -> decreased blood flow -> decreased GFR -> decreased Na and Cl
delivery to macula densa -> PGE2 synthesised and released to JG and smooth
muscle cells
ii. Smooth muscle cells + PGE2 effects -> vasoconstriction of efferent arteriole ->
increased GFR
iii. Cause renin release from JG cells - Angiotensin II -> release Aldosterone from
adrenal cortex and ADH from posterior pituitary
iv. Urine sodium concentration - low
1. Aldosterone increases apical sodium channel + basolateral Na/K
ATPase -> increased sodium reabsorption in attempt to increase blood
volume
v. Osmolarity - increased
1. ADH increases apical AQP2 insertion -> increased water reabsorption to
increase blood volume -> decreased water in urine -> concentrates urine
d. ADH and hemorrhage
i. ADH release from posterior pituitary when stimulated by AT II
ii. ADH increases apical AQP2 insertion in DCT and CT -> increased water
reabsorption -> increase blood volume to increase GFR
iii. As GFR increases -> increased Na and Cl delivery to macula densa
iv. Cause water to flow into cell, ATP leaves basolaterally
v. ATP -> adenosine
vi. Adenosine binds to extraglomerular mesangial cells -> calcium released to JG
and smooth muscle cell
vii. Calcium in JG cells inhibit renin release -> decreased ATII release -> decreased
ADH release -> decreased AQP2 insertion
2. MSK
a. Dx
i. BMD - if it is muscle problem
ii. GBS - if it is PNS demyelination issue
b. History taking
i. Do you have a family history of muscle diseases (mention muscular
dystrophy)? – if yes will gravitate towards Becker Muscular Dystrophy
ii. Have you noticed any changes in your vision? Ptosis + diplopia – ?
myasthenia gravis
iii. History of heart conditions? ?angina + ?intermittent claudication
iv. Any Hx of autoimmune conditions? ?Guillain–Barré syndrome + ?
myasthenia gravis
c. Gower’s sign
i. Patients needs to use their upper limb to walk up their own body in order to stand
up from squatting position
ii. Indicates proximal muscle weakness especially at hip and thigh
d. Lower limb exam
 i. Weakness in extension and flexion of legs and thighs on both sides
ii. Muscle tenderness (if severe)
iii. Atrophy of muscles (if very late stage)
iv. Sensory perceptions are all normal
v. Reflexes should be all normal
e. Blood markers
i. Creatine Kinase
f. Calcium and muscle
i. High calcium concentration inside muscle cause calcium sensitive proteases,
phospholipases, ATPase, endonuclease to become active and increase reactive
oxygen species -> result in muscle breakdown and necrosis
ii. Because of muscle cells are damaged/dead, activate satellite cells to replace and
repair damaged muscle fibres
iii. If the muscle repair is continuing, repair by satellite cells will not be able to keep
up with rate of degeneration -> cause regenerated muscle fibres will not be in an
orderly fashion but have different size with branching fibres
1. This makes muscle fibres to be weakened -> progressive weakness of
muscle
iv. The loss of muscle is replaced by fat and fibrotic tissue -> muscle is now stiff and
contracted (appear hypertrophied)
g. Sarcopenia
i. Degenerative loss of skeletal muscle mass associated with ageing
h. Changes in aging skeletal muscle
i. Decreased fibre size
ii. Elasticity of skeletal muscle decreases
iii. Atrophy of fast twitch fibres
iv. Fat and fibrous tissue replace lost muscle mass
v. Motor Neurons are lost
vi. NMJ are degraded
1. Endurance and strength of muscle is significantly reduced
2. Muscle fatigue much more easily
3. Decreased capacity for muscle fibres to recover from injury
3. Neuro
a. Stroke mechanism
i. Hemorrhagic stroke
1. Occur when weakened blood vessel (aneurysm) ruptures -> decreased
blood supply to part of brain supplied by ruptured blood vessel -> stroke
ii. Ischaemic stroke
1. Occur when obstruction (thrombosis) happens to blood vessel supplying
brain -> decreased blood supply to brain -> ischaemia to part of brain
that is supplied by blocked artery -> stroke
b. Site of block
i. Left middle cerebral artery
c. Other symptoms
i. wernicke/broca/global aphasia
ii. Right hemineglect
d. Neuro exam
i. Hypertonia
ii. Decreased power
 iii. Hyperreflexia
iv. Decreased coordination
v. Decreased/no sensation
vi. On inspection - spastic, disuse atrophy
e. Risk for stroke
i. Do you smoke?
ii. Do you have diabetes?
iii. Do you have any previous history of heart disease or surgeries?
iv. Do you have hypertension/take drugs to treat hypertension?
v. Do you drink?
vi. Do you take fat lowering drugs (statins)?
f. Old or new stroke in MRI
i. Old stroke
1. Well demarcated
2. Very low density in stroke lesion(similar to CSF)
3. Negative mass effect
ii. New stroke
1. Less well demarcated
2. Lower density than normal brain but higher density than CSF
3. Positive mass effect

g. Course of embolus
i. Left ventricle -> aorta -> left common carotid artery -> left internal carotid artery
-> left parietal lobe
h. Ischemic penumbra
i. In acute cerebral ischemia, central core is irreversibly infarcted
1. Caused by significantly decreased blood perfusion
ii. Surrounding the infarcted core is peripheral region of stunned cells - ischemic
penumbra
1. Caused by decreased blood perfusion, but not as significant to central
core
2. Metabolism is active but blood flow is diminished
 iii. Ischemic penumbra is salvageable area of brain if perfusion is restored early - if
Mr Reid showed up at hospital early, with quick diagnosis with CT he will be
treated quickly -> further damage by embolus would’ve been prevented
iv. If perfusion is not restored, the ischemic penumbra will be converted to
irreversibly infarcted area -> infarcted region enlarges -> more severe symptoms
4. Neuro
a. Dementia test
i. MMSE
ii. Neuro exam
b. Reversible cause of dementia
i. Metabolic causes - uraemic, hepatic encephalopathy
1. LFT for hepatic
2. Renal FT - for uraemia
ii. Endocrine - hypothyroidism
1. Thyroid FT
iii. Infection/inflammation - HIV, neurosyphilis
1. ELISA for HIV
2. VDRL - for neurosyphilis
c. Investigations
i. Imaging - CT, MRI, SPECT
1. To establish subtype of dementia
2. To exclude other cerebral pathologies - hematoma, hydrocephalus,
tumours
ii. Lumbar puncture - CSF examination
1. To exclude other forms of rapidly progressive dementia (like prion
disease)
iii. Electroencephalography
1. In suspected frontotemporal dementia, or suspected seizure disorder
with dementia
iv. Brain biopsy
1. When causes suspected cannot be diagnosed in any other way/cause
cannot be identified
d. Dx
i. Alzheimer’s disease?
e. Family history + advice
i. Most likely to be inherited form AD
ii. Increased risk for his son to have AD/dementia as well - 50~60 years old
f. Frontal lobes and behaviour
i.
5. Renal
a. Syndrome
i. Nephritic syndrome
b. Causes
i. IgA nephropathy
ii. Post streptococcal glomerulonephritis
iii. SLE
c. Symptoms
i. Blood tests
1. Elevated serum creatinine
 2. Hyperkalemia
3. Hyperphosphataemia
4. Azotaemia
ii. Observations
1. Increased blood pressure
2. Oliguria
6. MSK
a. Dx for back pain
i. Back muscle strain
ii. Disk herniation
iii. Spinal fracture
iv. Tumour
b. Xray observation
i. Compression fracture
c. Osteoporosis
i. Disease of low bone density leading to increased bone fragility and increase in
fracture risk
ii. Normal bone composition
iii. Bone resorption rate > bone formation rate
iv. In T score, T<-2.5
d. Bone remodelling cycle
i. Activation
1. Osteoclast activated by RANKL and RANK
ii. Resorption
1. Osteoclasts digest old bone, with acids. release calcium and phosphate
iii. Reversal
1. Mononuclear cells appear on bone surface
2. Cover up digested surface and secrete matrix
iv. Formation
1. Osteoblasts form new bone in place of what has been resorbed
2. Osteoblasts inside bone matrix gets differentiated into osteocytes -
maintain its structure
e. T, Z score
i. Standard deviation of:
ii. T score
1. Bone density comparison between you and young healthy adult of same
sex
2. 0> T >=-1 - normal
3. -1> T >= -2.5 - osteopenia
4. -2.5 > T - osteoporosis
iii. Z score
1. Bone density expected of your age, sex, ethical origin, weight, height
2. -2> Z - abnormal bone density
f. Lab markers of bone formation/resorption
i. Formation
1. Propeptide and pro collagenase
2. ALP
3. Osteocalcin
ii. Resorption
 1. C terminal telopeptide of T1 collagen (CTX)
2. N-telopeptide of type 1 collagen (NTX)
3. pyridinoline cross-links
g. Osteoporosis treatment
i. Calcitonin agonist
1. Inhibits osteoclast activity
ii. Estrogen replacement therapy
1. Increase OPG expression, binds to RANKL and inhibits further
osteoclastic activity
iii. Bisphosphonates
1. Cause osteoclast apoptosis by binding to hydroxyapatite
h. Osteoporosis intervention
i. Weight loss
ii. Exercise
iii. Walking aid
iv. Sunlight exposure

SAQ
1. Neuro physiology - LTP + Neuro pathophysiology - Alzheimer’s disease
a. LTP
i. Strengthening of synapses due to long term high frequency stimulation, resulting
in increased signal transmission between two neurons
b. LTP changes
i. Post synaptic
1. Increased AMPA receptor expression
2. Increased dendritic spine area
ii. Pre-synaptic
1. Increased neurotransmitter release
2. Increased number of vesicle containing neurotransmitter
c. Alzheimer’s disease and amyloid beta oligomers
i. In order to form new memory, LTP is required
ii. Beta amyloids from inappropriate amyloid protein precursor excision by beta
secretase aggregate and from beta amyloid oligomers
1. Block transmission between neurons
2. Directly toxic to glial cells and neurons
3. Slow down its repair process
4. Disturb normal neuronal metabolism
a. Overall impair normal brain function
iii. Amyloid oligomers also trigger immune response - damage surrounding neuron
iv. Amyloid oligomers also trigger formation of neurofibrillary tangles from tau
protein - transmission of neurotransmitters impaired
1. Cause apoptosis
v. It disturbs transmission between neurons + destroys neurons -> LTP cannot
occur -> new memory cannot be formed
2. Neuro physiology - cortical plasticity in phantom limb
a. Works by brains priority of putting visual feedback over somatosensory/proprioceptive
feedback
b. In amputee, somatosensory area of amputated part will be invaded by surrounding area
 i. In arm amputation, will feel pain in face as phantom limb pain
c. Mirror therapy works to reorganise cortex to relieve pain by using visual stimuli - to make
brain think that amputated arm exists
i. This reorganises somatosensory cortex so that the invasion is removed ->
alleviates pain with continued practice of mirror therapy
3. Neuro physiology - proprioception
a. Muscle spindles
i. Detect static length changes (stretch receptor) + small movement and vibration
b. Golgi tendon organ
i. Detect force on tendon
c. Joint receptor
i. Detect edge of range of movement of joints
d. Cutaneous mechanoreceptors
i. Bidirectional detection (doesn’t contribute to proprioception a lot normally, but
when there is disease like HSAN where muscle spindles doesn’t function)
4. Neuro pathophysiology - locked in syndrome
a. Awake and conscious but physically immobile
b. Corticospinal and corticobulbar pathways interrupted -> no speech, limb, facial
movements, etc.
i. Only motor function affected
ii. PET scan normal
c. Most common cause - acute ventral pontine lesion
d. If acute ventral pontine lesion allows, trochlear nerve not affected
i. As only nerve coming from the dorsal aspect
5. Renal pathophysiology - Lupus nephritis and types
a. Class 1 - minimal mesangial GN
i. Normal microscopic appearance, mesangial deposits under electron microscope
ii. Nephrotic syndrome
b. Class 2 - mesangial proliferative GN
i. Mesangial matrix expansion
ii. Nephritic syndrome
c. Class 3 - focal GN
i. Sclerotic lesions in <50% of glomerulus
ii. Nephritic syndrome
d. Class 4 - diffuse GN
i. Sclerotic lesions in >50% of glomerulus
ii. Nephritic syndrome
e. Class 5 - membranous GN
i. Diffuse thickening of glomerular capillary wall
ii. Diffuse membrane thickening
iii. Nephrotic syndrome
f. Class 6 - advanced sclerosing lupus nephritis
i. Sclerotic lesions in >90% of glomerulus
ii. Nephritic syndrome
6. Renal pathophysiology - nephritic syndrome features
a. Urinalysis
i. Dysmorphic RBC
ii. RBC casts
iii. Mild proteinuria
 b. Blood test
i. Azotaemia
c. Fever
d. Fatigue
7. Renal pathophysiology - nephrotic syndrome features
a. Urinalysis
i. Proteinuria
b. Blood test
i. Hyperlipidaemia
ii. Hypoalbuminaemia
c. Kidney biopsy
8. MSK physiology - calcium and phosphate balance
a. REPEAT FROM 2012 SAQ PAPER Q10
9. Renal pathophysiology - excessive salt and water loss
a. Non renal causes
i. Vomiting
ii. Diarrhoea
iii. Blood loss
b. Compensatory mechanism
i. Blood loss
ii. Decreased blood volume -> decreased GFR -> Macula densa release PGE2 to
JG and SM cells
iii. JG cells release renin -> ATII
1. ATII stim aldosterone release from adrenal cortex -> increase sodium
reabsorption in principal cell -> increased water reabsorption by osmosis
2. ATII stim ADH release from posterior pituitary -> increase AQP2 insertion
-> increased water reabsorption
3. Vasoconstriction to maintain blood pressure
10. Renal pathophysiology - CKD and its features
a. CKD - GFR <60 for 3 months
b. In urine
i. Proteinuria
ii. Hematuria
iii. Isosmotic urea
c. In blood
i. Hypoalbuminemia
ii. Hyperlipidaemia
iii. Increased serum creatinine
iv. Decreased serum calcium
11. MSK pathophysiology - RA epidemiology
a. M>F
b. 2% of australians reported to have RA
c. Occur 45 y.o
d. In male, decrease in life expectancy by 4 years
e. In female, decrease in life expectancy by 10 years
f. Smoking increases risks
g. Unemployment
i. ⅓ are unemployed by 5 years
ii. ½ are unemployed by 10 years
12. MSK pathophysiology - RA extra articular manifestation
a. Pericarditis
i. Echocardiography, x-ray
b. Felty’s syndrome (splenomegaly and neutropenia)
i. Splenomegaly - palpation + ultrasound
ii. Neutropenia - FBC
c. Retinal vasculitis
i. Eye examination
d. Dermatitis, vasculitis, rheumatoid nodule
i. Inspection
13. MSK pathophysiology - OA reversible causes
a. High BMI - exercise and diet change
b. Post menopausal - HRT
c. Joint injury - immediate treatment + supports
14. Renal physiology - sodium co-transportation
a. Glucose reabsorption
i. Co-transported with sodium ions in PCT by SGLT2 cotransporter on apical
membrane
b. Glycosuria
i. Glucose in urine
ii. Untreated diabetes mellitus
c. Co-transportation in nephron
i. Amino acids
1. Protein synthesis
ii. HCO3-
1. Blood acid/base buffering
iii. K+, Cl-
1. Electrolyte required for neural transmission
15. Pop health - health policy
a. Primary
i. To prevent occurrence of disease - reduce/eliminate causative risk of disease
ii. Before disease
iii. Immunisation, exercise
b. Secondary
i. To decrease disease’s effect by early detection
ii. After disease has begun
iii. Blood tests
c. Tertiary
i. To minimise further effect of disease
ii. Disease is established
iii. Aspirin
16. Pop health - incidence rates
a. Incidence rate = New case/population at risk
i. Number of new cases per population in given time period -> tells information
about risk of contracting disease
ii. Population at risk = risk ratio
b. Case control studies does not allow us to calculate risk ratio (but provide odds ratio)
c. So cannot calculate incidence rate from incidence rate
d. MORE INFO
 i. Prevalence
1. Proportion of cases in the population at a given time (not occurrence of
new cases)
2. Tells how widespread the disease is
17. Renal pathophysiology - Renal colic
a. Pain at flank - hypochondrium or to groin
i. Comes in waves
b. Caused by renal stone obstruction in ureters - colicky nature due to ureteric peristalsis
18. Renal pathophysiology - diabetic nephropathy features

Nodular
lesion

GBM
expansion Hyaline
arteriosclerosis?
19. Neuro physiology - functional cerebellum organisation
a. From middle to lateral
i. Spinocerebellum (middle is vermis)
1. Contains (medial to lateral)
a. Fastigial nuclei
b. Glabose nuclei
c. Emboliform nuclei
i. Glabose + emboliform - interposed nuclei
ii. Cerebrocerebellum
1. Contains dentate nuclei, most lateral
b. Flocculonodular lobe is vestibulocerebellum
c. Vestibulocerebellum
i. Input - Vestibular apparatus and visual information
ii. Output - vestibular nuclei
iii. Maintain equilibrium, vestibulo ocular reflex, balance during movement
d. Spinocerebellum
 i. Input - cerebral cortex, peripheral sensory receptors
ii. Output - fastigial, interposed nuclei
iii. Control proximal and distal musculature
iv. Vermis
1. Input - cerebral cortex
2. Control axial musculature
v. With spinocerebellum forms feedback loop
e. Cerebrocerebellum
i. Input - cerebral cortex
ii. Output - dentate nucleus
1. Movement planning and initiation
20. MSK embryology - endochondral ossification
a. Week 4
i. FGF10 - AER – FGF8 – Stimulates growth of mesenchyme extending limb bud.
b. Week 5
i. Lateral plate mesoderm within limb bud condenses
c. Week 6
i. Condensed mesoderm chondrifies -> hyaline cartilage model formed
d. Week 7 ~ 9 - Ossification centre formation (femur and tibia)
i. Cartilaginous cells hypertrophy and dies as matrix around calcifies
ii. Blood vessels grow around edges and deliver pre osteoblastic cells -> replace
chondrocytes
1. Osteoblasts deposit bone matrix under perichondrium -> bone collar
formed
iii. Primary ossification centre
1. Bone collar deprives nutrients to cartilage in centre
2. Nutrient artery penetrates diaphysis and deliver osteoblasts to
disintegrating cartilage
a. Replaces cartilage matrix to bone matrix -> form trabecular
network
3. Fills medullary cavity with red bone marrow
4. Ossification continues - forms diaphysis
iv. Secondary ossification centre
1. Forms in epiphyseal ends of bones
2. Blood vessels enter cartilaginous epiphysis - similar process like primary
ossification centre
a. Except no formation of medullary cavity
b. Interior remains as spongy bone
e. Secondary ossification leaves layer of cartilage covering epiphysis - articular cartilage
f. Also forms plate between epiphysis and diaphysis - epiphyseal plate
i. Consist of hyaline cartilage and allow diaphysis growth - ossifies completely
around age of 20
21. Neuro embryology - neural tube cytodifferentiation
a. Derived from neuroepithelium which is derived from ectoderm
b. Wall of recently closed neural tube - neuroepithelial cells
c. Neuroepithelial cells divide to form neuroblasts - form mantle layer around neuroepithelial
layer
d. When neuroblast formation stops, neuroepithelium form glioblasts - migrate to mantle
and marginal layers
 e. When neuroblast and glioblast formation stops from neuroepithelium, neuroepithelial cells
differentiate to ependymal cells
f. Microglial cells - mesenchymal cells
i. Invade CNS in fetal period by blood vessels
g. Layer
i. Ventricular layer (innermost layer)
1. Glioblasts
2. Neuroblasts
3. Ependymal cells
ii. Mantle layer
1. Neuroblasts differentiate into neurons - form gray matter (future gray
matter of spinal cord)
2. Glioblasts - differentiates into glial cells (astrocytes, oligodendrocytes)
j. Marginal layer
i. Outermost layer
ii. Contain processes of cells from mantle zone - axons of neurons and glial
cells
iii. Future white matter of spinal cord
22. MSK pathophysiology - DMD mutation
a. Inframe mutation - deletion/insertion of codon, the reading frame is maintained
i. Only part of protein is missing, but is still functional
b. Frameshift mutation - deletion/insertion of nucleotides that is not divisible by three, shifts
entire reading frame from point of mutation onwards
i. This results in formation of completely different protein - its normal function is lost
23. Neuro pharmacology - MAOI and tyramine
a. Restriction of fermented foods
b. Fermented foods contain tyrosine
c. Tyrosine converted to tyramine in our body when consumed
i. Tyramine is catecholamine releasing agent
d. Tyramine normally inactivated by MAO-A in gut, liver, vascular endothelial cells
i. Tyramine has no effect due to MAO-A
e. When taking MAOI for depression - targeted towards MAO-A inhibition, as involved in
degradation of serotonin and noradrenaline
f. MAOI inhibitors inhibit central and peripheral MAO-A
g. When taking fermented food when MAO-A are inhibited, tyramine is not inactivated
i. Allows high amount of tyramine to enter circulation and initiates/stimulates
noradrenaline release from large number of adrenergic neurons
ii. Systematic increased release of noradrenaline -> increase blood pressure (by 30
mmHg), heart rate, etc -> hypertensive crisis
iii. If severe -> cause cerebral artery hemorrhage

2014
MEQ
1. Renal
a.

b. GFR physiological determinants

i. GFR = K * (glomerular capillary hydrostatic force - bowman’s space hydrostatic
force - glomerular capillary oncotic force)
1. K = capillary permeability*surface area
2. There should not be protein in bowman’s space in normal kidney so
bowman’s space oncotic force = 0
ii. Decreased surface area and capillary permeability due to glomerulosclerosis
c. CKD and hyperphosphatemia
i. High phosphatemia stimulates release of PTH from kidney
ii. PTH is released as an attempt for body to excrete more phosphate and reabsorb
more calcium in kidney - to maintain serum free calcium. Done by:
1. Increased calcium reabsorption (DCT) and decreased phosphate
reabsorption (PCT)
 2. Increased RANKL expression -> increased osteoclastic activity ->
increase serum calcium and phosphate
3. Increase calcitriol formation - acts to increase calcium absorption and
reabsorption
iii. However, as functional renal mass is decreased
1. Calcitriol formation decreased - PTH secretion uninhibited
2. Phosphate not excreted + calcium not reabsorbed
iv. Further increase in phosphate further stimulates PTH release - lead to secondary
hyperparathyroidism. Result in
1. renal osteodystrophy - osteitis fibrosa cystica, osteomalacia
2. Calciphylaxis
d. EPO and erythropoiesis
i. Erythropoietin produced by interstitial fibroblasts in kidney in peritubular capillary
+ PCT in response to hypoxia
ii. EPO produced and released to blood travels to bone marrow
iii. Stimulates erythropoiesis by binding to its receptor in RBC progenitors in bone
marrow
1. Stimulates RBC formation and release
2. Renal
a. Nephritic syndrome features
i. Nephritic syndrome
ii. Additional tests
1. Urine microscopy
a. RBC casts
b. Dysmorphic RBC
2. Oliguria
3. Blood test
a. Azotaemia
b. Hypertension
i. Due to inflammation in kidney - endothelial cell proliferation
1. Decreased blood flow to nephrons
ii. Decreased blood flow to nephron -> decreased GFR -> decreased sodium and
chloride delivery to macula densa
iii. Macula densa synthesise and release PGE2 to JG cells and capillary smooth
muscle cells
iv. PGE2 in JG cells cause release of renin -> converted to ATII, act to increase
blood pressure to increase GFR
1. Aldosterone released from adrenal cortex -> acts on collecting duct
principal cells
a. Increase expression of basolateral Na/K ATPase, apical sodium
channel
b. Result in increased sodium reabsorption and water reabsorption
by osmosis
2. ADH released from posterior pituitary -> acts on collecting duct principal
cells
a. Increase expression of AQP 2 on apical membrane
b. Increase water reabsorption
3. Both acts to increase blood volume
 v. By increasing blood volume -> blood pressure increased, but blood flow to kidney
still impaired due to inflammation -> ATII pathway stimulation does not stop ->
hypertension
3. Renal
a. Acid metabolism in kidney
i. In PCT
1. Reabsorption of bicarbonate in glomerulus
a. H2O in cell separated into H+ and OH-
b. H+ leaves proximal tubule cell and enters PCT by
i. Na-H antiporter
ii. H-ATPase
c. Filtered HCO3- cannot cross apical membrane of PCT cell
d. HCO3- instead combines with secreted H+ and to produce CO2
and H2O (by carbonic anhydrase)
e. CO2 lipid soluble - enters PCT cell and combines with OH- to
produce bicarbonate
f. HCO3- enters blood by basolateral Na+-HCO3- symporter
g. HCO3- in blood acts as buffer
2. Production of ammonia
a. Ammonium produced within PCT from glutamine
i. Glutamine enters cell from peritubular capillaries or
filtrate
ii. And is excreted to tubular lumen by apical Na+-NH4+
exchanger
b. Ammonia diffuses from blood to tubular fluid, combines with H+
secreted by PCT cells -> ammonium formed
i. Ammonium cannot leave tubular lumen - excreted
ii. In DCT, CT
1. Intercalated cell alpha - secrete H+ and absorb remaining HCO3-
2. Intercalated cell beta - secrete HCO3- and absorb H+
a. Acts to maintain acid/base balance
b. Anion gap
i. Anion gap = difference b/w measured cations and measured anion
ii. High anion gap metabolic acidosis
1. From accumulation of organic acids or impaired H+ excretion
2. Caused by
a. Toxins
b. Ketones
c. Lactate
d. Renal impairment
iii. MORE INFO
1. Normal anion gap metabolic acidosis
a. From loss of HCO3-
b. Caused by
i. Chloride excess
ii. Bicarb loss - GI/renal (vomiting, diarrhoea)
iii. Diuretics
4. Neuro
a. Dementia causes
 i. Infectious causes
1. Neurosyphilis
ii. Endocrine causes
1. Hypothyroidism
iii. Vascular causes
1. Multi-infarct dementia
b. MMSE sub categories
i. Repetition
1. Speaking back a phrase
ii. Attention and calculation
1. Serial sevens - count from 100 and subtract 7 each time
2. Spell ‘world’ backwards
iii. Orientation of time
1. Asking what's the time now, from broadest to most narrow (year -
minutes)
iv. Orientation of place
1. Asking where you are now, from broadest to most narrow (country -
street)
v. Language
1. Naming objects that I present/point
c. Brain changes due to AD
i. Increased ventricular size
ii. White matter atrophy
iii. Increased gyrus size
d. AD microscopic features
i. Intracellular neurofibrillary tangles
ii. Extracellular amyloid beta plaque
iii. Neuronal loss
iv. Reactive astrocytes and microglia
v. Abnormally distended and tortuous neuronal processes surrounding amyloid core
vi. Amyloid beta plaque deposition in walls of cerebral artery and arterioles
vii. Loss of synapses
viii. Lipofuscin deposit
e. AD pathogenesis
i. Genes involved
1. APP
2. ApoE 4
3. Presenilin 1
4. Presenilin 2
ii. Normally APP excised by alpha and gamma secretase, but due to mutation beta
and gamma secretase excise APP -> leads to production of excess insoluble
amyloid beta
iii. Amyloid beta accumulates -> form amyloid beta oligomers -> disturb neuronal
synapse, repair, metabolism and trigger inflammatory reactions
1. Cause apoptosis of neuron
2. Cause disturbances of neural transmission
iv. Also cause tau proteins to form neurofibrillary tangles -> microtubules
architecture destroyed, vesicles containing neurotransmitters cannot travel + lead
to apoptosis of neuron
5. MSK
a. CT image
i. Compression fracture due to osteoporosis
b. Risk factors of osteoporosis
i. Old age - bone integrity decreases as you get older
ii. Postmenopausal - estrogen decrease causes increased osteoclastic activity
iii. Physical inactivity - mechanical strains detected from osteocytes stimulate
osteoblastic differentiation
c. Osteoporosis pathophysiology
i. In normal bone, bone resorption and formation is balanced by RANKL, OPG and
other signalling pathways
ii. In osteoporosis, rate of bone resorption is greater than rate of bone formation.
Could be due to
1. Aging
a. Osteoprogenitor cell replication is decreased
b. Decreased synthetic ability of osteoblasts
c. Decreased physical activity
2. Menopause
a. Decreased estrogen lead to increased RANKL expression and
decreased OPG production -> results in increased osteoclastic
activity -> increased bone resorption
3. Decreased physical activity
a. Osteocytes detect mechanical strains and stimulate osteoblastic
differentiation to strengthen bone. Inactivity reduces osteoblastic
differentiation
iii. Could be caused by one or more of these factors and they all result in decreased
bone mass, resulting in increased fracture risk
d. Prevention
i. Cannot prevent osteoporosis completely as it comes naturally as you age
ii. However reversible risk factors can be mitigated to reduce its effects
1. Using supports/physical activity
2. HRT after menopause
3. Calcium and vitamin D supplements
e. Back pain red flag
i. history/suspicion of cancer, unexpected weight loss, appetite loss- metastatic
malignancy
ii. Fever, IV use - vertebral infection
iii. Bladder and bowel incontinence, saddle anaesthesia, lower limb
weakness/numbness - cauda equina syndrome
iv. Pain not relieved - cancer, vertebral infection
6. MSK
a. RA or OA
i. RA is chronic inflammatory disease of joints, affecting synovial membrane of
joints, and leading to marginal erosions of bones
ii. OA is more of degenerative joint disease where articular cartilage is damaged
due to reduced joint space
iii. Also RA affects MCP, PIP, carpal joints in hand whereas OA affects PIP and DIP
b. RA damage to joint, cartilage, bone
 i. RA results in pannus formation by cytokines, growth factors, vascular
proliferative factors acting on synovial membrane
ii. As they expand, villous process allow cytokines to directly act on osteoclasts -
active osteoclastogenesis and cause marginal erosion of bone
iii. Synoviocytes in pannus release proteases - metalloproteinase released to
cartilage -> mediates cartilage damage and destruction
iv. All these process damage joint structure
c. RA extra-articular manifestations
i. Heart - pericarditis
ii. Blood vessels - accelerated atherosclerosis
iii. Eye - scleritis
iv. Spleen - splenomegaly
v. Skin - dermatitis, rheumatoid nodules
vi. Blood - chronic disease anaemia
d. Goals of RA therapy
i. Goal of rheumatoid arthritis treatment is to reduce inflammation by - reducing
inflammatory cell number, interaction and to stop further damage caused by
inflammation
7. Renal
a. SLE urinalysis
i. Showed proteinuria only - nephrotic syndrome
ii. Immune complex deposit in subepithelial space - this results in podocyte damage
-> filtration slit damaged and charge barrier damaged
iii. This allows negatively charged molecules and molecules smaller than 70 nm to
pass through
1. Allow protein like albumin to pass through - proteinuria
b. Other tests on urine
i. Urine microscopy - there may be microscopic hematuria, and some casts
(maltese casts)
ii. Lipid in urine - heavy loss of protein lead to hyperlipidaemia, may pass through
filtration membrane to urine
iii. Creatinine in urine - to measure GFR, determine the extent of damage
c. Nocturia
i. Decreased GFR and
ii. Decreased nephron function - reabsorption of solutes and concentration of urine
impaired -> no decrease in urine volume (concentrating ability lost)
1. At night, tubular fluid gets concentrated to metabolic wastes due to
decreased flow to kidney allowing nephron to reabsorb all the necessary
solutes and reabsorbing more water
iii. Fills up and stretches bladder faster and stimulates voiding - nocturia
d. Glomerulonephritis
i. Inflammation in glomerulus
ii. Immune complexes like antinuclear antibodies, anti double-stranded DNA
antibodies travels in blood and is deposited in kidney
iii. In glomerulus, it may deposit in subepithelial space - affecting nephron and/or
subendothelial space, affecting capillary fenestrations
iv. Regardless of where it has deposited, it triggers complement cascade +
inflammation -> causes swelling, fibrosis of glomerulus, apoptosis of cells ->
 causes apoptosis of cells and destruction of normal filtration membrane ->
leakage of blood content
8. Neuro
a. Cerebral artery
i. Right middle cerebral artery
b. Stroke risk factor
i. Old age
ii. Cardiovascular disease
iii. High blood pressure
iv. Diabetes
v. Past history of stroke
c. Pathophysiology of stroke
i. Hypertension ruptured his aneurysm in his division of right middle cerebral artery
ii. Results in decreased blood supply to its respective area of brain it supplies, in
this case, motor cortex
iii. Decreased blood supply results in infarction of the area supplied by ruptured
artery
iv. Left facial droop due to motor cortex infarction corresponding to face, as
corticobulbar tract of facial nerve decussates, so right motor cortex infarction
results in left facial droop
v. Left hemiparesis due to motor cortex infarction corresponding to limbs, as
corticospinal tract decussates at medullary pyramid (limbs) or at the level (Axial),
so right motor cortex infarction results in hemiparesis of left body
d. Neuro exam
tone hypertonicity

power reduced

reflex hyperreflexia

Babinski reflex present

Cerebellar examination Decreased coordination

Cranial nerve 7 Weak left side muscles facial

expression except for occipitofrontalis
9. Neuro
a. Cerebellar tracts
i. Spinocerebellar tracts run ipsilaterally, so will see signs in the same side of the
lesion in the brain
b. Signs
i. Right sided
1. hemiataxia
2. Loss of coordination of the right side of body
3. Dysmetria
4. Intention tremor
5. Dysdiadochokinesia
6. Dysarthria
7. Hypotonia
8. Nystagmus
 c. Tumour interfering with neural function
i. Compresses the adjacent part of brain
ii. Proliferation of malignant cells cause disturbances of neuroarchitecture -
disturbances in neural transmission/change in electrical property
iii. Increase intracranial pressure, may shut off blood supply, also compresses brain
d. Dexamethasone
i. Is corticosteroid
ii. Acts to reduce edema caused by brain tumour - to relieve symptoms
10. Neuro
a. Dx
i. Bitemporal hemianopia
b. Visual anatomy
i. Nasal retina provides visual field to temporal half of visual field of each eye
ii. Nasal optic nerve decussates on optic chiasm, temporal optic nerve go
ipsilaterally
c. Dx
i. Pituitary tumour
ii. Anterior communicating artery aneurysm
iii. Meningioma

SAQ
1. Neuro pathophysiology - aphasia
a. Location
i. Broca’s area - left inferior frontal gyrus
1. Involved in production of language
2. Anterior area involved in semantic function
3. Posterior area involved in phonology
4. Also involved in forming sentence structure with proper grammar
ii. OR?
iii. Primary motor cortex - brodmann area 4, precentral gyrus
1. Broca’s area sends information on how to control the muscle of speech
2. Larynx control - phonation
3. Mouth control - articulation
b. Causes
i. Hemorrhagic stroke
ii. Transient Ischaemic attack
iii. Trauma
iv. All three can cause reduction/loss of function to area that it affects
2. MSK physiology - muscle spindle and fusimotor system
a. Muscle spindles are stretch receptors
i. Ia fibres - nuclear bag fibres - measure velocity of contraction and activated only
during contraction
ii. IIa fibres - nuclear chain fibres - measure length of muscle, stimulating is
decreased when contracted
b. In order for Ia fibres to be firing, spindle needs to have proper tension when extrafusal
muscle fibres contracts - i.e. muscle spindle fibres are innervated by gamma motor
neuron
 c. Fast alpha motor neuron innervate extrafusal muscle fibres, causing muscle to contract. It
does not innervate intrafusal fibres
d. When the extrafusal muscle fibres contracts, intrafusal fibres (muscle spindles) become
loosened and is it does not fire to CNS - have no information on muscle length
e. In order to maintain muscle spindle sensitivity, slow gamma motor neuron innervates
muscle spindles to contract intrafusal fibres when extrafusal fibres - keeping muscle
spindle fibres taught and allows Ia fibres to fire even during muscle contraction
3. Renal
a. GFR
i. GFR = glomerular capillary permeability[(glomerular capillary hydrostatic
pressure - bowman’s space hydrostatic pressure) - glomerular capillary oncotic
pressure]
b. Pre-renal AKI
i. Dehydration -> decreased blood volume -> decreased blood flow to kidney
ii. Initially - Tubuloglomerular feedback and myogenic relaxation
1. Afferent dilate and efferent constrict + RAAS activation - overall increase
in GFR by increasing pressure and volume
iii. If this does not restore - GF turned off
1. To maintain nephron viability and to prevent further loss of perfusion at
expense of GFR
a. As 90% of energy usage in kidney is for reabsorption
b. Also nephron sensitive to ischaemia
2. Turned off by JG apparatus
a. Due to decreased PCT function -> increased sodium delivery to
macula densa -> adenosine released -> afferent arteriole
constrict -> decreased capillary pressure -> turns off GF
iv. If this does not restore GFR -> Acute tubular necrosis
1. Further decrease in perfusion -> ischaemic tubular cell necrosis
2. GF still turned off by adenosine
3. Not all nephrons affected equally
v. If ATN sustained -> cortical necrosis - irreversible damage
c. Urinalysis
test Pre renal ATN

Urine osm High due to retention Normal as tubule not functional ->
glomerular filtrate osm = plasma osm

Urine sodium Low as PCT still functional High as PCT not functional

Urine microscopy Bland hyaline casts Broad pigmented casts

Blood in urine No, caused by decreased blood no/yes, depends on cause. Yes if GN,
flow to kidney no if by toxins or decreased blood flow
4. MSK pathology - fracture complications
a. Immediate local complication
i. Hemorrhage
ii. Infection
iii. Soft tissue injury
iv. Ischaemic bone necrosis
 b. Delayed local complication
i. Fracture union - delayed healing due to poor blood supply, body necrosis, foreign
body etc.
ii. Fracture nonunion - failure of fracture healing due to poor immobilisation, soft
tissue interposition
iii. False joint formation - due to non union fracture -> fibrous tissue formation
iv. Chronic osteomyelitis - untreated fracture leading to infection in marrow
5. Renal pathophysiology - nephrotic syndrome
a. Proteinuria
i. Damage of glomerulus and leading to abnormal permeability of GBM or
effacement of podocyte foot processes - allowing protein to pass through
b. Edema
i. Decreased blood oncotic pressure, less fluid comes back into vessels from
interstitium -> fluid buildup in interstitium
ii. Also increased sodium and water retention due to decreased blood volume and
RAAS activation
c. Hypoalbuminemia
i. Albumin able to pass through filtration membrane -> lost through urine
ii. Production cannot keep up with excretion
d. hyperlipidemia
i. Liver’s method to compensate for albumin loss and to increase oncotic pressure
of blood -> stimulate lipoprotein synthesis
6. Neuro pathophysiology - dementia types
a. Frontotemporal dementia
b. Vascular dementia
c. Dementia with lewy bodies
d. Alzheimer’s disease
7. Renal pathophysiology - diabetic nephropathy
a. GBM thickening - due to extracellular matrix accumulation due to proliferation (cytokines)
and cross linking (AGE)
b. Hyaline arteriosclerosis - due to hypertension, increased pressure force proteins to
intimal layer and builds up + AGE buildup in basement membrane
c. Glomerulosclerosis - Due to GBM thickening + podocyte effacement and apoptosis
d. Mesangial expansion - due to AGE and hyperglycaemia directly inducing mesangial
matrix production and cellular expansion
8. Neuro pathophysiology - tumours
a. WHO grading
i. Grade by microscopic features - looks at tumour growth potential and malignant
features to determine if its is curable by surgery/recurs after surgery, from I to IV,
IV being the worst prognosis
ii. Size and location cannot be used to grade tumours
1. Benign slow growing tumours can grow to size where it can cause shift of
adjacent brain structure
2. Symptoms of tumour varies with location of tumour, cannot grade from its
location
iii. Grade 1 (pilocytic astrocytoma)
1. Relatively circumscribed, slow growing, 90% survival rate
iv. Grade 2 (diffuse astrocytoma)
 1. Diffusely infiltrating ill defined lesion, slow growing but have potential to
grow to grade 3 and 4 tumours survival rate 50% (>5yr survival)
v. Grade 3 (anaplastic astrocytoma)
1. Shows nuclear atypia with increased cellularity, mitosis, anaplasia,
survival rate 10% (2~3yr survival)
vi. Grade 4 (glioblastoma)
1. Necrosis/palisading necrosis, vascular proliferation, mitosis, anaplasia,
increased cellularity, survival rate 1% (<12 month survival)
b. Glioblastoma or pilocytic astrocytoma
i. Grade 1 (pilocytic astrocytoma)
1. Relatively circumscribed, slow growing, 90% survival rate
ii. Grade 4 (glioblastoma)
1. Necrosis/palisading necrosis, vascular proliferation, mitosis, anaplasia,
in]creased cellularity, survival rate 1% (<12 month survival)
9. Renal physiology and pathophysiology
a. Glomerulus

Capillary lumen

Bowman’s
capsule

Mesangial cell

Basement
Bowman’s membrane
space
Endothelial cell
Podocyte
b. Filtration barrier
i. Endothelial cell
ii. Basement membrane
iii. Podocyte
c. Minimal change disease
i. LM - no change/mild mesangial increase
ii. IF - no immune complex detected
iii. EM - podocyte effacement and swell up
10. Renal physiology - reabsorption mechanisms
a. Passive transport - does not require energy/ATP for transport of ions
b. Facilitated transport - passive transport of molecules (AA, glucose, Phosphate) by
specific integral molecules (Na+)
c. Active transport - requires energy for transport of ions, transport against concentration
gradient
d. Osmosis - passive transport where solvent is diffused from low to high ion concentration
through a semipermeable membrane to maintain equal osmolarity in both
11. Renal physiology - ADH
12. MSK pathophysiology - BMD or DMD
a. BMD, DMD - X linked recessive disease due to mutation of dystrophin gene
b. BMD - inframe mutation of dystrophin gene
i. Results in decreased production in dystrophin
c. DMD - frameshift mutation of dystrophin gene
i. Results in no production of dystrophin/production of dystrophin gene with loss of
its original function
d. Females have 2 X chromosomes - only one X chromosome is active - occurs in
embryonic stage randomly
e. If functional X chromosome > defective X chromosome - asymptomatic
f. If functional X chromosome < defective X chromosome - manifesting carrier
i. X inactivation
13. Neuro physiology - Basal ganglia
a. Direct pathway - mediates movement
i. Inhibits Globus Pallidus internus and stimulates globus pallidus externus from
striatum -> decrease inhibitor effect of globus pallidus internus to thalamus ->
stimulate cortex -> movement
b. Indirect pathway - inhibits movement
i. Inhibits globus pallidus externus and disinhibit globus pallidus internus from
striatum -> inhibition of GPe disinhibit subthalamic nucleus which stimulates
globus pallidus internus -> increase inhibitor effect of globus pallidus internus to
thalamus -> decreased stimulation to cortex -> inhibition of movement
14. Neuro physiology - LTP
a. LTP
i. Strengthening of synapses due to long term high frequency stimulation, resulting
in increased signal transmission between two neurons
b. LTP changes
i. Post synaptic
1. Increased AMPA receptor expression
2. Increased dendritic spine area
ii. Pre-synaptic
1. Increased neurotransmitter release
2. Increased number of vesicle containing neurotransmitter
15. Pop health - outbreak
a. Outbreak
i. Sudden rise in incidence of occurrence of the disease
ii. Increase in gastroenteritis
16. MSK physiology - rotator cuff
a. Rotator cuff anatomy
i. Supraspinatus
 ii. Infraspinatus
iii. Subscapularis
iv. Teres minor
v. Acts to stabilize shoulder joint
b. Dx
i. Supraspinatus
1. Supraspinatus muscle assists in abduction (first 15 degrees) of arm
2. Insertion point at greater tubercle
ii. Teres minor and infraspinatus
1. Lateral rotation of shoulder done by these two muscles
2. Insertion point at greater tubercle
17. Neuro pathophysiology - pain response
a. 4 factors that can influence a patient's psychological response to pain and injury
i. psychological investment in affected activities and functioning
ii. personal resources e.g. coping skills, tolerance thresholds
iii. features of the injury e.g. duration, severity
iv. progress in recovery
18. Neuro physiology and pharmacology
a. Serotonin and noradrenaline
i. Serotonin
1. Mood
2. Memory processing
3. Sleep
4. Cognition
5. Acts by binding to 5-HT receptors
6. Terminated by reuptake from synapse
ii. Noradrenaline
1. Alertness
2. Arousal
3. Readiness for action
4. Acts by binding to alpha, beta adrenergic receptors
5. Terminated by reuptake from synapse or MAO-A
b. SSRI
i. In depression, lack of serotonin level in brain
ii. SSRI prevent reuptake of serotonin - stopping its termination and allows it to stay
longer in synapse for interaction - increase serotonergic transmission
iii. Also is ‘selective’, works in specific serotonergic pathways
19. Renal pharmacology - NSAIDS
a. Patient with high CVD risk
i. PGI2 is antithrombotic, reduced PGI2 production increases platelet aggregation
-> increase stroke and CVD risk
b. Patients with peptic ulcer
i. PGE2 and PGI2 regulates mucus production in stomach, reduced PGE2 and
PGI2 causes reduced mucus production -> reduced protection of stomach lining
from gastric acid -> increase gastric ulcer risk/worsen existing ulcers
c. Patients with failing renal function
i. PGE2 cause afferent arteriole vasodilation to increase GFR, reduced PGE2
impairs renal GFR maintenance
d. Patients with uncontrolled hypertension
 i.
By previous mechanism, decreases GFR -> cause RAAS activation as an
attempt to increase GFR -> hypertension
20. Neuro pharmacology - opioids
i. Inhibit pain transmission
1. Directly inhibit peripheral nociceptive neurons and dorsal horn by
endogenous opioid enkephalin in nucleus raphe magnus that run in
substantia gelatinosa
ii. Motivation, response to pain and stress, food intake control
21. MSK pathophysiology - osteoarthritis
a. Examination

inspection Swelling of affected knee joint

Quadriceps wasting

Walking aids

Valgus/varus deformity

palpation Positive grind test

Palpable osteophytes

Movement and special tests Reduced range of motion

Crepitus on knee joint movements

b. Risk factors
i. Old age
ii. obesity
iii. Inactivity
iv. Untreated joint injury
v.
MCQ (ones with ‘?’ needs clarification)
2008
1. D (memory systems)
2. E (genetics)
a. 1/60 * 1/60 * ¼
3. B (genetics)
a. Chance of father: 1/60, chance of mother: 1/1, chance of child: ¼
4. B (memory systems)
5. A (aneurysms)
6. D (vagus nerve branch courses)
7. B (SCALP)
8. E (CN exits)
9. D (spinal cord anatomy) how
10. C (brain damage)
11. D (knee l=igaments)
12. E? (PD and L-DOPA)
13. C (eye blood supply)
14. E (Pupillary reflex circuit)
15. C (spinal tracts)
16. D (UMN or LMN lesion)hb
17. E (cochlear anatomy and function)
18. B (sarcopenia)
19. E (UMN or LMN lesion exam)
20. D (MAOI and tyramine)
21. A (anti-inflammatory drugs)
22. E (cerebellum and basal ganglia)
23. A (MAOI)
24. C (embolus course)
a. Cholesterol embolism = usually a part of an atherosclerotic plaque breaks off.
Not IVC because it’s a vein, atheromatous plaques tend to deposit in places with
higher BP i.e. arteries (endothelial stress etc.), and at bifurcations where the
walls are more susceptible to damage. Not the LV as it’s the heart, also if for
some reason the heart became a place conducive to atheroma then there’d be
very serious issues e.g. heart muscle tears you have to worry about, not mitral
valve because if it happens it’s rare, not the middle cerebral artery itself because
it’s more rare than a carotid bifurcation atheroma)
b. A, wrong because atherosclerotic embolus occurs in "arteries"
c. B, embolus forms in LV most commonly in acute MI
d. D, mitral valve embolus forms commonly in A.fib
e. E, if atherosclerotic plaque was formed in left MCA, the symptoms won't be
sudden
25. C or D? (CNS drugs)
26. B (brainstem sections)
27. C (CN exit)
28. D (CSF course)
29. C (Brachial plexus)
30. E (saccades)
31. C (meninges)
32. A (spinal tracts)
33. C (brain imaging)
34. D (tongue innervation)
35. C (parasymp and symp on pupil)
36. C (organisation of visual areas and lesions)
37. C (motor neurons)
38. B (function of leg compartments)
39. C (antidepressants)
40. A? (depression and dementia)
41. A? (muscle ageing)
42. D (rotator cuff syndrome)
43. B (regional brain function)
44. D (GFR)
45. C? (radiation effect)
46. B (radiation protection)
47. C (iron homeostasis)
48. D? (COPD predictor)
49. A? (ABG)
50. C (primary pul. hypertension)
51. C (liver microscopy)
52. D (heart murmur + ECG)
53. D (heart valve pathology)
54. D (sepsis)
55. D (lung carcinoma)
56. E (RA)
57. C (rotator cuff)
58. B (brachial plexus)
59. A (thigh musculature innervation)
60. E (ICM notes on leg examination)
61. A (aspirin)
62. D (arachidonic acid pathway)
63. B (glucocorticoids)
64. D? (brain deficit diagnosis)
65. B (prescribing to elderly)
66. A (elderly and young ppl)
67. D (dementia)
68. C (sarcoma)
69. B (osteosarcoma)
70. B (tumours of bone)
71. A (meningiomas)
72. A (astrocytomas)
73. D (prion disease)
74. D (multiple sclerosis)
75. A (Wat in the actual fk is dis Q)
76. A (dopaminergic pathways)
77. C? (antipsychotics)
78. C (schizophrenia diagnosis)
79. D (MAOI and tyramine)
80. C (types of mutation)
81. C (PKD sequence)
82. E (huntington disease pathogenesis)
83. D (AD pathogenesis)
84. A (telomeres)
85. B (psychopharmacology)
86. A (prescribing to elderly)
87. C (dopamine synthesis)
88. A? (dopamine agonist side effect)
89. C (creatinine, inulin, PAH)
90. C (creatinine, inulin, PAH)
91. C (filtration in kidney)
92. D (glomerular filtrate)
93. A (cori cycle)
94. B (sensory receptor)
95. B? (sensory pathways of spinal cord)
96. D (sensory pathways of spinal cord)
97. A (DCML)
98. E (immune system)
 99. B (immune system)
100. A (immune system)

2009
1. B (renal obstruction)
2. C (aphasia and its position)
3. B (shoulder movement)
4. A? (antipsychotics)
5. D (brainstem anatomy)
6. C (dural layers)
7. D (dementia risk factors)
8. D (brain lobar function)
9. B (DMD)
10. C? (opioid tolerance)
11. B (AD genetics)
12. C (DCML)
13. A (DCML) A is incorrect as the 1st order neurons do not synapse until the
level of the cuneate and gracile nuclei in the medulla - Reading the answers Im not sure
that any are actually correct? Could C be implying pain gate theory?
14. C (creatinine, inulin, PAH)
15. A? (dopamine agonist side effects)
16. D (MAOI and tyramine)
17. A (dopamine pathways)
18. A (astrocytic tumours)
19. B (bone tumours)
20. B (prescribing to elderly)
21. D (ICM lower limb examination)
22. A (thigh musculature innervation)
23. A (CKD-MBD)
24. A (resp acidosis and ABG)
25. C (resp acidosis compensation)
26. D (frontal lobe function)
27. A (dopamine Ag and side effects)
28. D (cerebellar circuit)
29. A (antidepressants)
30. C (PKD)
31. B (achondroplasia)
32. D (BMD, DMD)
33. C (AD)
34. D (huntington’s disease)
35. B (opioid dependence)
36. D (opioids)
37. B (GFR)isnt this D as Creatinine production also declines with age,
resulting in constant Scr concentrations?
38. A (PD treatment)
39. D/B? (opioid and pain pathway)
40. A (endocytosis)
41. D (kidney stones)
42. B (universal prevention)
43. C (presbycusis)
44. C (sound localisation - time- and level-differences between both ears,
spectral information, timing analysis, correlation analysis, and pattern matching)
45. D (vestibulospinal reflex)
46. A (basal ganglia)
47. C (nocebo effect)
48. D (brain changes in depression)
49. B (OCD)
50. A (classical conditioning)
51. D (schizophrenia)
52. A? (OCD?)
53. C (rotator cuff)
54. A (elderly and young ppl)
55. D (dementia)
56. D (bone tumours)
57. C (primary CNS tumours)
58. A (WHO tumour grading)
59. D (AD)
60. D (MS)
61. C (hallucination)
62. C (PKD)
63. C (nephron genetic disease)
64. C (achondroplasia - autosomal dominant where homozygous is fatal)
65. B (HD mutation)
66. D (AD)
67. A (telomere)
68. B (psychopharmacology)
69. D (Glomerular filtrate)
70. C (cross section of brainstem)
71. C (sensory receptors)
72. A (thigh compartment function)
73. A (thigh compartment innervation)
74. C (CNS supporting cells)
75. D (CNS supporting cells)
76. C (vertical - d and horizontal gaze - c )
77. D (retinal cells)
78. C (eye fluid drainage)
79. C (retinal neural circuit)
80. D (cerebellar circuit)
81. C (prion disease)
82. A? (idea of reference?)
83. A (nonsense mutation)
84. B (titratable acidity)
85. B (struvite stone)
86. B (dopamine antagonist side effects)
87. C (optic tracts)
88. D (PD)
89. C (sporadic AD)
90. B (sensory pathways)
91. D (sensory pathways)
92. C (dopamine synthesis)
93. C (sarcomas)
94. D (Coexib side effects)
95. A (femoral bone blood supply)
96. A (calcium, phosphate homeostasis)
97. B (bone cell biology)
98. D
a. Photon hits rhodopsin -> cis-retinol changes to trans-retinol -> trans-retinol
leaves and exposes binding site in opsin
i. Opsin active site converts one subunit of GDP on transducin(3 subunit) to
GTP -> leaves and binds to alpha subunit of phosphodiesterase ->
removes alpha subunit
b. a repeats to remove second alpha subunit in PDE -> PDE converts cGMP to
GMP
c. not guanylate cyclase but PDE
99. B (aphasia)
100. B (red nucleus in midbrain)
101. D (PNS regeneration)
a. Macrophage clean up debris
b. Schwann cell assist in regeneration
c. If cell body is damaged, cell neuron cannot regenerate
d. If axon damaged, can grow back - 1mm/day
e. Wallerian degeneration seen in crush injury
i. Terminal axon will die off
f. Endoneurium damage - fair growth
g. Perineurium - slow growth
h. Epineurium - no growth
102. D (memory systems)
103. D (BZD pharmacokinetics)
104. A (pupillary light reflex)
105. C (CN functions)
 106. C (Spinal tracts)
107. D (cocaine and MAOI)
108. A (cochlear hair cells)
109. D (tongue innervation)
110. C (dilation and constriction muscle in eye - Horner’s syndrome)
111. A (HD)
112. B (anticonvulsant)
113. D (Rotator cuff syndrome)
114. D (GFR)
115. C (brachial artery course)

2017 Q (not in order) - plis add if u remember any other questions

SAQ
1. OA and OP
2. Macula densa response to loop diuretics
3. Close the gap
4. Vitamin D and bone
5. Calcium storage, release, action
6. CNS cytodifferentiation
7. Bone embryology
8. Types of diuretics and their mechanism of function
9. Polypharmacy
10. Stroke - speech areas, diagnosis
11. AKI
12. Facial muscle supply
13. Corneal reflex
14. Spinal cord lesion
15. Countercurrent multiplication and exchange
16. PD symptoms and pathophysiology
17. Retinal receptor
18. Oculomotor nerve function
19. CNS glial cell function
20. DMD and phenotypic difference in males and heterozygous female
MEQ
1. MSK
a. How to determine minimal trauma fracture
b. How does femur neck fracture cause external rotation + shortening of thigh
c. Risk factors for osteoporosis
d. Bisphosphonates MOA
e. T score
f. Bone cell types, functions and interactions
 2. Neuro - Brain area involved in depression
a. Norepinephrine and serotonin function
b. Antidepressant classes and MOA
3. Renal
a. Normal glomerulus histology
b. Components of filtration barrier
c. Membranous GN immunofluorescence and pathophysiology
4. MSK
a. RA and Gout
b. How does RA cause osteoporosis
c. How does tocilizumab (IL-6 antagonist) work and its effects
5. Renal
a. Diabetic nephropathy pathophysiology and microscopic changes
b. Potassium filtration changes in diabetic nephropathy
6. Neuro
a. Alzheimer’s disease pathophysiology
b. Macroscopic changes in alzheimer’s disease
c. Microscopic changes in alzheimer's disease
7. Neuro
a. Spinal cord lesion
b. Tracts involved
c. What level
8. Renal
a. RAAS systematic and GFR effects
b. ACEI and hypovolemia
c. NSAIDS and hypovolemia
d. High serum potassium in hypovolemia
Aphasia
MMSE components and tests
Cerebellar tracts, cerebellar damage symptoms

2019 SAQ
1. Olfactory cells in nasal epithelium (describe the 4 primary types of cells) (4 marks)
2. 2 symptoms in olfactory deficit (2 marks)
3. Explain which part of nephron damaged based on HSP symptoms (past paper
repeat)
4. Label glomerulus histo (repeat) label list provided, no labels (3.5 marks)
5. Why low threshold mechanoreceptors and nociceptors produce distinct
sensations, based on knowledge of anatomy and physiology. (5 or 6 marks)
6. Explain bifrontal headache symptoms
a. Using understanding of anatomy, why would cervical neck pain
produce/accentuate the bifrontal headache (2 marks)
b. What 3 structures could be affected to produce her headache? (3 marks)
7. Explain the Lock and Key model of enzymatic reactions
8. 4 reasons why adding more substrate to enzymatic reaction won’t always increase
reaction rate (4 marks)
9. GORD pathophys + pharm treatment (4 marks)
10. Social factors of increased risk of chronic renal disease in remote health
communities (3 marks)
11. One-hit vs two-hit hypothesis in PKD
12. Guy sees u with hearing loss/ringing after live concert
a. What do you tell him about the ringing (1 mark)
b. What advice do you give him (1 mark)
c. Describe hidden hearing loss (3 marks)
13. Pt comes into ED after episode of right leg jerking, following by 4min tonic-clonic
syncopal episode with tongue biting after staying up all night drinking and
watching sport on TV with mates. Patient has history of skull fracture 2 years ago.
Febrile, normal neuro exam
a. What is your diagnosis on first preview of this patient (1 mark)
b. Seizure triggers
14. Identify 4 causes of pathological fractures (4 marks)
15. Osteoporosis pathogenesis (4 marks) + why osteoporosis is more common in
ageing females rather than ageing males(2 marks)
16. fracture of proximal femur, what main complication does it cause? and name the
artery affected
17. The motor system is divided into 3 levels, describe the hierarchical organisation
of motor system (6 marks)
18. Meiosis vs mitosis (5 marks)
19. Ca2+ storage, release and site of action in normal muscle function (repeat
question from a previous MEQ)
20. Process of endochondral ossification and difference compared to
intramembranous (4 marks)
21. A kid skateboards and falls, breaking the fall with his hand leading to a painful
wrist and distal arm(?) what distal bones are likely to be injured as a result of this.
22. Label histological image of a healing fracture (3 marks)
23. Neural control of micturition (4 marks)
24. Explain the process of gas exchange in the lungs, which direction oxygen flows
and why it flows in that direction (4 marks
25. Haemodialysis is partial replacement for a kidney(or some shit). What functions of
the kidney does it not replace? (3 marks)
26. Patient with Stage 5 kidney failure about to undergo dialysis.
a. A patient with Stage 5 kidney failure is about to undergo dialysis, what are
the expected changes in calcium, phosphate, FGF23, PTH, active vitamin D.
(2.5 marks)
b. Explain how these changes come about.
27. Old dude has history of moderate-severe alzheimers. Increasing agitation etc
Presents with High K+ and high serum creatinine
 a. What syndrome does he have?
b. What findings would you get upon abdo exam if he has a urethral
obstruction?

There are 2017 questions in more detail on the resource hub

This can be found under Resource Hub > Year 2 Sem 2 Exam resources > Year II exam > 2017