pros Flashcards
types of dementia ( 5 types)
definition of dementia
reversible vs irreversible factors of dementia
- alzhimers
- vascular
- lewy body
- frontotemporal
- CJD
definition: acquired syndrome of decline in memory and other cognitive domains, sufficient to affect daily functioning
reversible
Drugs
Emotional (depression)
Metabolic disturbances
Eyes and ears (sensory)
Normal pressure hydrocephalus
Tumour
Infection (syphillis)
Anemia/ Alcholism (B12 def)
irreversible
5 different types of dementia
alzhimers disease
(clue: 2 hypothesis)
genes:
- chromosome 21 APP (down syndrome –> trisomy 21)
- chromosome 19 ApOE4 (homozygous)
other risk factors:
- hypercholesterol (can worsen amyloid angiopathy)
- lack of physical and mental exercise
amyloid plaques:
beta and gamma secretase cleave amyloid precursor protein (APP)
= insoluble amyloid beta peptides formed
= aggregation
= amyloid beta plaques
= disrupt neuronal communication
= microglial cells activated
= increase in inflammation
= cause further neuronal damage
+ amyloid angiopathy (blood vessel walls)
tau protein hypothesis:
tau protein is hyperphosphorylated
= misfolded tau protein
= cannot form microtubules
= NF tangles
symptoms: (4 As of alzhimers)
amnesia (hippocampus shrinkage)
aphasia
agnosia –> cannot recall (temporal lobe)
apraxia –> cannot do motor tasks (frontal lobe)
gross:
- smaller, atrophied brain
- widened sulci (FP_T) –> temporal is most affected
- hippocampal shrinkage
- primary and secondary motor cortex well preserved until later disease
histo:
- beta amyloid plaques (silver stain
- NF tangles intracellularly
- thickened blood vessel walls (amyloid angiopathy)
limbic system
- what does it do
- what are the structures involved
SR memory: hippocampus (also involved in spatial problem solving)
stress: amygdala
anterior thalamic nuclei
limbic cortex
different lobes of the brain
- their functional areas
- their functions
F
- primary motor cortex
- broca’s area (speech production)
- pre frontal cortex (decision making, problem solving, impulse control, personality changes)
P
- primary somatosensory cortex (process pain, temp, pressure, touch)
- hemispatial awareness
O
- primary and secondary visual cortex (vision)
T
- primary auditory cortex
- wernicke’s area (understanding speech)
- hippocampus (memory)
- amygdala (emotion)
anterograde vs retrograde amnesia
anterograde: hippocampal lesions –> cannot form new memories
retrograde: temporal lobe lesions –> LR memories are lost
CJD prion disease
prion protein misfolding into beta-sheet rich
= prion aggregation
= amyloid plaques
= neurodegenration
= vacuolization
= spongiform encephalopathy
= rapidly progressive dementia
= myoclonal jerks, visual disturbances, etc
MRI: hockey stick in caudate/ puatmen
familial
iatrogenic
sporadic
variant
schizophrenia (subset of delerium)
dopamine hypothesis
= excessive/too little dopamine neurotransmission
excessive dopamine neurotransmission
= too happy
= positive symptoms (mesoLIMBIC pathway)
= ADHD
- abnormal behaviour (eg. shoot people)
- delusions
- hallucinations
- disorganised thoughts
(+) symptoms: temporal lobe
mesoLIMBIC: VTA –> nucleus accumbens (emotions!)
too little dopamine
= too sad
= negative symptoms (mesoCORTICAL pathway)
= AAaa (imagine someone sighing)
= apathy, affective flattening, asociatlity cognitive impairment
(-) symptoms: frontal lobe
mesoCORTICAL: VTA –> pre frontal cortex (higher order functions)
parkinson’s (most common neurological disease, think tremors etc.)
genes: PARKIN, PINK1, alpha synuclein
genes
= degeneration of dopamenergic neurons in substantia nigra compacta
= neuronal death
= decrease dopamine (since dopamine is produced by the neurons)
= dopamine clears alpha-synuclein, so now alpha-synuclein cannot be cleared
= alpha-synuclein aggregates
= lewy body formation
= even more neuronal death
histo:
- neuronal death in substantia nigra compacta
- alpha-synuclein aggregates
- lewy body formation
symptoms: TRAPM
Tremors (pill rolling resting tremor)
Rigidity (cogwheel, leadpipe)
Akinesia/ bradykinesia (freezing)
Postural instability
Micrographia
treatment:
1. levodopa + carbidopa
- levodopa crosses BBB
= converted to dopamine via DOPA decarboxylase
2. dopamine receptor agonists
= mimic dopamine
- ropinirole
- rotigotine
3. MAO-B inhibitors
- inhibits MAO-B, which breaks down dopamine
sleep
1 cycle: 90-120 mins
N1: theta waves
- easy to wakeup, feeling drowsy
N2: theta, sleep spindles, K-complexes
- decrease HR, temp
N3: delta waves
**GH release + restorative sleep
- parasomnia
- night terrors
- bed wetting
- deep sleep
REM: mixed frequency
- sleep paralysis
- dreams
- memory consolidation
common sleep disturbances
insomnia, sleep apnea, ageing –> decrease REM and N3
narcolepsy: enter REM too quickly
depression: increase REM
drugs for better sleep:
1. melatonin
2. GABAnergics (benzodiazapine)
3. antihistamines
meningitis
common pathogens:
neonates - strep B (strep agalactiae), ecoli, listeria monocytogenes
children and adults: streptococcus pneuomoniae
teens: nisseria meningiditis (think about teens kissing, sharing food)
empirical antibiotic therapy:
- neonates: gentamicin (aminoglycoside), ampicillin
- adults: ceftriaxone, ampicillin
common viruses:
enterovirus, coxsackie, mumps, HSV
pathophysio of meningitis:
infection
= crosses BBB
= infects the meninges
= inflammed meninges
how to prevent meningitis:
conjugate vaccinations
BCG vaccination (TB meningitis)
MMR vaccination (mumps)
pneumococcal PCV13, PPSV23 (step pneumo)
prophylatic antibiotics:
- rifampin
- cipro
- ceftriaxone
encephalitis
inflammation of brain parenchynama
bacteria: meningoencephalitis (spread from meninges to parenchyma)
viral: HSV
virus directly invades the brain tissue
= neuronal destruction
= temporal lobe involvement
= seizures, memory impairment, altered consciousness
can do PCR of CSF
brachial plexus
- branches
- injuries
musculocutaneous: shoulder and elbow flexion
- biceps brachii
- BRACHIALIS
- corocobrachialis
axillary:
- deltoid (shoulder abduction)
- teres minor (lateral rotation)
radial:
- wrist extensors
- triceps brachii
- BRACHIORADIALIS
median:
- thenar muscles
- lateral 2 lumbricals
ulnar:
- FPB (deep head)
tell me about FOOSH
ADULTS:
colles’ fracture
= break distal radius
= dinner fork deformity
KIDS:
= supracondylar fracture
= triceps brachii pulls the bones together
= median nerve affected
pect minor
medial pectoral nerve (branch from the ulnar nerve)
- anterior to axillary artery, brachial plexus
origin: coracoid process of scapula (does not even touch the humerus)
insertion: 3-5 ribs
cephallic vein
runs through the deltopectoral groove (between deltoid and pect minor)
- drains the radial side of the hand
vein for venepuncture
median cubital vein
biceps brachii
short head: coracoid process of scapula
long head: supraglenoid tubercle of scapula
insertion: radial tuberousity, biciptal aponeurosis
What are the LOAF muscles? Brevis
LOAF
lateral 2 lumbricals
opponens pollicis
abductor pollicis brevis
flexor pollicis brevis
flexor carpi radialis
+ which muscles attach at the medial epicondyle
origin: medial epicondyle
insertion: base of 2nd metacarpal
muscles that attach to the medial epicondyle:
cubital fossa
lateral –> medial
RN BT BE MN
bicipital aponeurosis seprates the brachial artery and the median cubital vein (more superior)
triceps brachii
insertion: olecranon process of ulnar
lat dorsi
thoracodorsal nerve (C7)
functional decline
- definition
- how to prevent it (management)
- 8 causes of acute functional decline
- 4 important Hx taking aspects to determine cause of functional decline
- 4 health strategies to manage patient (PRCS)
health strategies:
preventing
rehabalitative
curative
supportive
**aim to preserve independence and autonomy
rehabilitation of elderly patients
- goal setting for rehab process (AEE DR)
goal setting (AEE DR)
- ascertain what is impt to patient and family
- explain likely prognosis and course of progress (acknowledge the uncertainty)
- explain what is expected/ required from the patient
- discharge planning
- review goals
healthy aging
- definition
- determinants of healthy ageing
definition: functioning at the highest level possible for as long as possible
- determinants of healthy ageing
SEE HPB
1. social
2. environmental
3. ECONOMIC
4. health
5. personal
6. behaviour
how to max PHYSICAL aging
nutrition
active lifestyle
vaccination
smoking cessation
screening (for any early impairments)
how to max MENTAL aging
- max brain reserves
- exercise the mind = do cognition exercises (IQ puzzles)
- avoid doing.3 things at once - min risk factors
- decrease stroke risk factors (e.g. eating healthier, decreasing smoking, diabetes, obesity)
how to max SOCIAL aging
- build social networks = meet new people + go out with more people!
- avoid learned dependency (don’t keep asking other people to do it for you)
how to max PYSCHOLOGICAL AGING (emotional)
- life long learning –> cooking classes
- diversity of experiences –> religion
- mindset and philosophy –> self efficacy mentality
funding for healthcare in older invidivuals
medisave: compulsory savings
medifund: govt give you a bit
medishield: covers LARGE hosp bills + outpatient (eg. chemo) (for all singaporeans)
eldershield: long term disability for elderly people
dementia
- definition
- assessment of cognitive function
definition: acquired syndrome of decline in memory + other cognitive domains
= sufficient to affect daily functioning
assessment of cognitive function (ACE)
1. AMT (abbreviated mental test)
- screening, but not a confirmatory test
-
2. CMMSE (chinese mini mental state exam)
3. ECAQ (elderly cognitive assessment questionnaire)
how to differentiate the 3 Ds (use a table)
depression
- complications that result from it
0
delerium
- how to diagnose it
diagnosis of delerium: CAM (confusion assessment method)
- acute change in mental status + fluctuating course
- inattention
- disorganised thinking
- altered LoC
4 issuees to be addressed to prevent further falls before he can be discharged home
- caregiver support
- opthalamology –> make sure that there are no vision problems
- walking aids –> improve gait
- underlying risk factors –> any medications to stop?
- occupational therapist/ podiatrist
- home environment modification
financial support services for the elderly
medisave: to build up savings
medishield: help with large healthcare bills
medifund: government gives funds to needy singaporeans
what are the 4 factors in the elderly that predispose them to ADRs
- polypharmacy
- liver failure –> affects metabolism of drugs (esp for drugs with high first pass effect)
- kidney failure –> affects the clearance/ excretion of drugs = accumulation of toxic concentration
- cognitive impairment/ poor eyesight –> patient may see and take the wrong drug
why do benzodiazepines increase fall risk?
benzodiazepines
- dose related drowsiness
- increased reaction time
- decreased motor skills
what are some barriers to medication adherence in the elderly?
HPV LM
1. hearing –> cannot hear the pharmacist’s instructions clearly
2. language impairment
3. polyharmacy
4. vision
5. memory
where is the highest number of arachnoid granulations in the brain found in
- superior saggital sinus
- transverse sinus
hydrocephalus
- 2 different types
- symptoms
- non-communicating (obstructive)
= blocked CSF flow in foramen of monroe or aqueduct of sylvius
= ventricles upstream are enlarged
= increased risk of herniation - communicating
= decrease in absorption of CSF fluid by arachnoid granulations
= all ventricles are symmetrically enlarged
= brain parenchyma is stretched, expanded and white
symptoms:
- urinary incontinence
- cognitive decline
- issues with gait
orthostatic hypotension
MS (CNS)
- pathophysio
- histo findings
chronic demylinating disease
= antibodies attack the myelin in the CNS (oligodendrocytes)
= dead oligodendrocytes present as WHITE PLAQUES
IgG antibodies present as OLIGOCLONAL bands in the CSF
GBS (PNS)
- pathophysio
acute demylinating disease
previous infection (eg. campylobacter jejuni, EBV, CMV)
= molecular mimicry
= antibodies produced which attack the axons and myelin in the PNS (schwaan cells)
= myelin destruction
= decrease nerve conduction
= LMN symptoms
MG
- pathophysio
- treatment
- what happens if there is too much medication given
AChRAb production (IgG)
= AChR gets broken down
= more free floating ACh in the synaptic cleft
= ACh gets broken down by acteylcholinesterases
treatment:
acetylcholinesterase inhibitors –> pyridostigmine
= ACh not broken down
= more ACh
what happens if too much medication:
too much ACh
= overstimualtion of muscuranic receptors
= cholingergic crisis
= diarrhoea, bradycardia, smooth muscle contractions, excessive secretions, nausea and vomiting, bronchospasms, bronchorrhea
(think of organophosphates, and what happened to the north korean president’s brother)
depression
- definition
- diagnosis
- ABCs
definition: MENTAL HEALTH disorder characteristed by low mood, low interest, which can cause problems with physical, cognitive, ,and affective symptoms
diagnosis: GDS-15 (geriatric depression scale)
ABCs:
- affective
- behaviour
- cognitive devline
delirium
- definition
- why it is impt to treat
- causes (DELEIRIUM+SS)
- pharmaco (what are the 2 classes of drugs, which one causes EPS?)
- what are the EPS
definition: acute, non-specific neuropsych manifestation of disorder of CEREBRAL METABOLISM + NEUROTRANSMISSION
why impt: potentially reversible and preventable
causes:
Drugs
Environment
Little water (dehydration)
INTERNAL BLEEDING
Restraints
Infection
Urine or fecal retention –> pain
Metabolic disturbances
Sleep
SAH
treatment: antipsychotics
- typical vs atypical (ROCQ)
EPS:
1. tardive dyskinesia
2.
seizure
- definition of seizure vs epilepsy
- causes
- pre, during, and post event symptoms
- investigations
- pharmaco
- differential diagnosis
seizure: sudden, uncontrolled electrical disturbance in the brain, leading to abnormal movements, behaviour, sensations, or LoC
epilepsy: chronic condition, predisposed to spontaneous seizures
what is the muscle most active when climbing stairs
and what is it innervated by
gluteus maximus
INFERIOR gluteal nerve
what muscle dorsiflexes the foot, but also inverts it?
tibialis anterior
when standing with both feet on the ground, the body will tilt forward
which muscle stops this
what is it innervated by
triceps surae
tibial nerve
which muscle is used the most when standing from a squatting position
- what is it innervated by
quadriceps femoris (knee extension)
femoral nerve
what does inversion of the foot involve?
subtalar joint
anterior and posterior tibial muscle
flexor digitorium & brevis longus
tell me about the knee jerk reflex
L2-4
what is the blood supply of head of femur
child vs adult
adult: medial circumflex A (femoral A)
child: acetabular branch of obturator A
femoral triangle
- boundaries
- contents
- importance
- medical procedure
boundaries
- inguinal ligament
lateral: sartorius
medial: adductor longus
contents: NAVL (lateral –> medial)
femoral nerve
femoral artery
femoral vein
lymph nodes
importance: site for femoral nerve palpation
medical procedure: aim medially to prevent femoral artery puncture
nerve that passes lateral epicondyle (lateral side of leg)
common fibular nerve (which comes from the sciatic nerve, S4-L3)
layers of the plantar side of the foot
PCL vs ACL job
PCL: prevent femur from moving too far forward
ACL: prevent tibia from moving too far forwards
ligaments of the hip joint
front V: iliofemoral –> prevent hyperextension
midddle: pubofemoral –> prevent lateral dislocation
posterior: ischiofemoral –> prevent hyperflexion
rmb
ILIUM –> ISCHIUM –> PUBIS
sciatic nerve
- course
L4-S3
exit lumbosacral plexus
= greater sciatic foramen (below piriformis)
= between lesser trochanter of femur and ischial tuberousity (**ischial tuberousity is where people sit on the floor)
=
arteries of the leg
femoral artery
= passes through adductor hiatus
= turns into poplitheal artery
=
2 drugs for HYPOthyroid
T3: lio|thyroNine
T4: levo|thyroXine
3 drugs classes for HYPERthyroid and their MoAs
thioamides (agranulocytosis)
- carbimazole (cholestatic jaundice)
- propyluracil (hepatoxotic)
radioactive iodine
i131 (may cause hypothyroid later on)
iodides
- lugols solution
- potassium iodide tablets
T3/4
- full name
- which is the active form, which is more abundant
- process of thyroid hormone synthesis
T3: triiodothyronine
T4: thyroxine
active form: T3, but T4 more abundant due to longer half life
process of thyroid hormone synthesis:
1. iodine oxidation
2. organification (aka. iodination)
3. coupling
drugs for thyrotoxicosis
- thioamides
= intefere with organification and coupling
= no conversion of T4 –> T3
- carbimazole
- PTU - cholestyramine
- bile acid sequestrant
= decrease reabsorption of bile
= decrease T4 reabsorption - beta blockers
= prevents additional sympathetic activity due to excessive T3/4
- propanolol - glucocorticoids
= supress the immune response
primary HYPERthyroid pathologies
- graves
- non-toxic & toxic multinodular goiter
- de quervains thyroditis
- follicular adenoma
- follicular carcinoma
- oncocytic adenoma
graves disease
- primary/ secondary // hyper/ hypo?
- genetics
- pathophysio
- gross
- histo
- clinical triad
genetics: HLA-DR3, B8
autoimmune disease
= TSI pdtn (thyroid stimulating immunoglobin)
= overstimulate thyroid
= high T3/4, low TSH
gross:
1. hypervascularised
= red meat cut
- hyperplasia
= diffused symmetrical enlargement
histology:
1. thyroid hyperplasia
= tall columnar crowded pseudopapillae
- colloid used up
= pale scalloped colloid
clinical:
1. goiter
2. exopthalmos
3. pretibial myxedema
4. staring gaze, lidlag
5. bruits
6. diffused goiter
non toxic –> toxic MNG (hyperthyroidism)
- how non toxic leads to toxic
- pathophysio
- gross
- histo
chronic iodine deficiency
= decrease T3/4 synthesis (since iodine is needed in iodinification)
= increase TSH produced
= asymmertrical follicular growth, since some TSH receptors are more receptive than others
= thyroid enlargement
toxic MNG:
after time, the hyperplasia results in a genetic mutation of the TSH receptors
= constituitive activation of TSH receptors
= too much T3/4 produced
= hyperthyroid
= asymmetrical enlargement of thyroid
= compress recurrent laryngeal nerve
= hoarseness of voice
gross:
1. assymetrical enlargement of thyroid
2. nodules of diff sizes
histo:
1. large follicles WITH NO TRUE CAPSULE
2. cystic changes
de quervains thyroiditis
- pathophysio
- histo
viral infection
= virus enters bloodstream
= enters follicular cells in thyroid
= CD8+ recognises follicular cells as infected
= inflammation
= T3/4 spills out from follicular cells
= thyrotoxicosis
= HYPERthyroid
= damaged thyroid can no longer produce T3/4
histo:
1. inflammation
= macrophages, multinucleated giant cells around colloid (trying to clear up the colloid)
- follicular cell destruction
gross:
1. thyroid enlgargement (inflammation)
2. patchy pale yellow parenchyma (due to lymphocytic infiltrate)
follicular adenoma
- benign/ malignant
- pathophysio
benign
RAS mutation
= constuitive activation of MAPK pathway
= uncontrolled proliferation of uniform cubodial follicular cells
= well encapsultaed fibrous capsule
= thyroid enlargement
= press on recurrent laryngeal nerve
= hoarseness of voice
follicular adenoma –> follicular carcinoma
- benign/ maligant
- pathophysio
- histo
malignant
starts off with follicular adenoma
= other gene mutations
= tumour breaks through the capsule
= hematogenous spread (capsular + vascular invasion)
= cellular stress
= oncocytic changes
histo: (think: cancer histo)
1. salt and pepper chromatin
2. oncocytic changes
3. microfollicles
what does colloid contain?
- and what is the importance of the substace it contains?
thyroglobulin
follicular adenoma –> hurthle cell (oncocytic) adenoma
follicular adenoma
= extra inflammation and oxidative stress
= to compensate for energy deficit, cells proliferate mitochondria excessively
= follicular cells accumulate mitochondria –> granular
= acidic proteins stain H&E stain pink
= mitochondrial damage accumulates
= follicular cells lose their original function
= cells undergo metaplasia
= become hurthle cells
primary HYPOthyroid causes
- hashimotos thyroditis
- iodine deficiency
hashimoto’s thyroditis
- genetic predisposition
-
genetic: HLA DR3 , 5
autoimmune disease
= molecular mimicry
= immune system identifies thyroid antigens as foreign
= attacks thyroid
= IFN-gamma recruited
= follicular cells undergo ADCC (antibody dependent cellular cytotoxicity)
= B cells produce anti TPOs
= inflammation
= follicular cells destroyed
= hypothyroid
gross:
1. chronic inflammation = fibrosis
2. pale and diffusely enlarged
3. lymphocytic infiltrate
histo:
1. destroyed thyroid follicles
2. dense lymphocytic infiltrate
3. later: oncocytic changes
thyroid carcinomas
- list the types
- spread
P(o)FMA
1. papillary (lymphatic spread)
2. follicular (hematogenous)
3. medullary (familial MEN 2)
4. anaplastic
papillary thyroid carcinoma
- important facts to know
- route of spread
- mutation
- pathophysio
- histo
**MOST COMMON thyroid carcinoma
- lymphatic spread
BRAF or RET mutation in thyroid follicular cells
= MAPK pathway constituitively activated
=
- uncontrolled cell division
- inhibition of apoptosis
- no cellular differentiation
- disrupted cellular architecture
1. chromatin pushed to the side
= orphan annie eye effect
2. nucleus envelope folds inwards
= chromatin dumbing along grooves
= coffee bean nuclei
3. portion of the cytoplasm pushes into the nucleus
= cytoplasm trapped in the nucleus
= pseudoinclusion
follicular thyroid carcinoma
- important facts to know
- route of spread
- mutation
- pathophysio
- histo
**second most common thyroid carcinoma
- hematogenous spread
RAS mutation in follicular cells
= MAPK contituitively active
= loss of cell cycle regulation
= uncontrolled cell proliferation and differentiation
= tumour breaks through capsule
= hematogenous spread
= BBL (bone, brain, lungs)
= cellular stress
= oncocytic changes
histo: (think: cancer histo)
1. salt and pepper chromatin
2. oncocytic changes
3. microfollicles
medullary thyroid carcinoma
- important facts to know
- route of spread
- mutation
- pathophysio
- histo
neuroendocrine tumour (since C cells function as neuroendocrine cells)
- hematogenous + lymphatic spread
MEN-2
= RET mutation
= hyperactive parafollicular C cells
= excessive calcitonin production
= protein overload
= misfolded calcitonin
= abnormal aggregates of calcitonin
= amyloid deposits
= congo red stains
histo:
1. amyloid deposits, congo red stains
2. loss of E cadherin = spindle shaped cells
anaplastic thyroid carcinoma
**rarest, but most lethal
long standing PTC/ FTC
= TP53 mutation (or literally any mutation)
= rapid proliferation and necrosis
= tumour outgrows its blood supply
= local invasion of trachea and esophagus, CAROTID ARTERY
= spread via hematogenous and lymphatic spread
what is the blood supply to the brain
ICA –> ACA + MCA
vetebral artery –> basillar + pontine –> PCA
right side:
aortic arch
= brachiocephallic branch
= subclavian artery
= CCA
= ICA
= ACA + MCA
from subclavian artery
= vetebral artery
left side:
aortic arch
= CCA
= ICA
=
aortic arch
= subclavian artery
what are some of the important landmarks
C4: thyroid cartildge, carotid canal, CCA bificurates
C6: cricoid cartildge, trachea and oesophagus start, larynx and pharynx end
RA
- predisposing factors
- pathophysio [PPOC]
- X ray findings [SUB]
- drugs
predisposing factors:
1. RF (rheumatoid factor)
2. anti citrullinated peptide Ab
3. HLA DR 1, 4
APC recognise self antigens
= self antigens brought to lymph node
= inflammatory attack
= pro inflammatory cytokines go to joints
= attract macrophages
= synovial membrane inflammation
= PPOC
1. proteases released by synovial cells = break down articular cartildge
2. pannus (abnormally thickened granulation tissue)
3. osteoclast activation
4. chondrocytes release MMPs
(1. proteases -
synovial cells secrete proteases
= break down articular cartildge
- pannus -
chronic inflammation
= abnormally thickened synovial tissue
= pannus formation - osteoclast activation
- chondrocytes (cartildge cells)
= release matrix melloproteineases (in ECM)
= destroy cartildge)
++ RF and ACPAb target Fc portion of IgG
= immune complexes formed
= immune complex accumulates in synovial fluid
= joint inflammation
X ray findings
1. Swan neck deformity
2. Ulnar deviation
3. Boutonniere deformity
drugs:
1. synthetic csDMARDs
- methotrexate
= inhibit DHFR
= no DHF –> THF conversion
= no DNA synthesis
= decrease inflammation
+ inhibit AICAR transformylase
= decrease purine synthesis (nucleotide)
= decrease DNA synthesis
= decrease inflammation
- NSIADS
- diclofenac
- indomethacin
OA
- common joints
- X ray findings [LOSS]
- nodules
- features of inflammation
X ray findings:
1. Loss of joint space
2. Osteophyte formation
- destruction of articular cartildge
= osteophyte formation
- Subchondral cyst formation
exposed subchondral bone with gaps
= SYNOVIAL FLUID LEAKS THROUGH THE GAPS
= intraosseous accumulation of synovial fluid - Subarticular sclerosis
= constant friction
= eburnation (smooth bone surface)
= thickening of bone to fill the space
nodules:
PIPJ: bouchard’s nodes
DIPJ: herbeden’s nodes
thumb = carpometacaarpal = saddle joint
GA (tested already though, for CA1, but might test again)
bone cancers
- types
- age group
- X ray findings
- histo findings
- ewing’s sarcoma
<10yo, but can also be 10-20yo
- diaphysis
- t(11,22) EWS + FLI1 fusion
- onion skin
- swelling at night
- CD99 - osteosarcoma (most common malignancy of osteoblasts) –> OSTEO = bone
10-25yo
- metaphysis
- hematogenous spread to lungs
- sunburst pattern
- codman’s triangle
- lace like pattern of osteoid - chondroSARCOMA –> CHONDRO = cartildge
- 40-60yo
- uncontrolled proliferation of cartildge producing chondrocytes
= cartildge matrix production
BENIGN:
4. OSTEO|CHONDROMA
displaced growth cell cartildge
= cartildge capped bony outgrowth (exostosis)from metaphysis of long bones
specifics of the menstrual cycle
- LH surge = ovulation
LH binds to theca cells
= theca cells stimulated to produce androgens
= androgens are transported to granulosa cells
= FSH binds to granulosa cells
= granulosa cells produce aromatase
= andogen is converted to estriadol by aromatase
= follicles release estrogen
= higher estrogen sends positive feedback to AP
= increase FSH and LH (increase FSH to mature follicle)
= LH surge
= ovulation
after ovulation:
ruptured follicle becomes corpus lutheum
= cholesterol becomes progestrone
= increase progestrone signals to body that there is no need for LH and FSH anymore
= progesterone maintains the uterine lining
= if no fertilisation, CL degenerates
= drop in hormones
= menstruation
course of the pudendal nerve
S2-4 sacral plexus
= greater sciatic foramen
= posterior to sacrospinous ligament, which attaches to ischial spine –> GIVE PUDENDAL NERVE BLOCK HERE
= lesser sciatic notch
= perinerium
= enters the pudendal canal (which is the fascia of the obturator internus)
= give off 3 major nerves
1. inferior rectal/ anal nerve
2. perineal nerve –> perineal muscles, EUS
3. dorsal nerve of clit
innervation of the detrosur muscle (bladder)
- pelvic sphlanic
- hypogastric
innervation of EUS
CONTRACT DETRUSOR MUSCLE = urinate = PNS (rest and relax)
pelvic sphlanic nerve (S2-4)
= ACh
= contracts detrusor muscle
RELAX DETRUSOR MUSCLE = fill urine = SNS (fight or flight) = cannot pee when stressed
hypogastric nerve (T11-L2)
= NE
= relax detrusor muscle + contract internal urethral sphinccter
somatic control of EUS: pudendal nerve = continence
breast carcinomas
- 2 groups
non-invasive: DCIS, LCIS
1. DCIS
mutation in TSG in epithelial cells in lactiferous duct
- comedo
= microcalcifications
- no breach of basement membrane
pagets disease:
DCIS
= malignant ductal carcinoma cells spread to lactiferous ducts
= invade epidermis
= spread within epidermis
= nipple erosion, ulceration, scaling, and crusting
invasive: TMML
1. tubular (low grade)
- best prognosis
- well formed tubules, well differentiated
- minimal atypia
- prominent nucleoli
- mucinous
- tumour cells floating in mucin
- 70yo women - medullary
- lymphocytic infiltrate
- pleomorphic cells
- BRCA 1/2 mutation - lobular (high grade)
- loss of E cadherin
- signet ring cells
- cocentric layering –> diffuse infiltrative pattern with minimal desmoplaia
what are the different gene mutations involved in breast cancer?
DNA repair: BRCA 1/2 –> checkpoint
TSG: p53, PTEN –> promote apoptosis, chceckpoint regulation
Oncogene: HER2, ER –> disrupt cell growth and survival
what are the benign neoplasms of the breast
- intraductal papilloma
benign proliferation of epithelium in lactiferous ducts
= central fibrovascular stalk growth
= stalk is prone to rupture
= rupture causes bloody nipple discharge - fibroadenoma (breast mouse)
- benign, fibrous growth
= compress ducts - phyllodes tumour (leaf like tumour)
hypercellular overgrowth
- INTRAlobular stromal hyperplasia
- increased mitotic activity, high cellularity
- fibroepithelial tumour
- hematogenous, NOT lymphatic spread
treatment: wide local excision
pupil pathways
- compare affrent vs efferent
- affrent vs efferent pathologies
affrent:
(all the stuff i already know)
efferent:
pre tectal nucleus
= EWN
= ciliary ganglion
= short ciliary nerves (post ganglionic)
= pupil: sphincter pupillae (constrict)
lens: ciliary muscle (accomodation reflex)
pathologies:
affrent:
1. RAPD
2. visual field defects
3. retinal detachment
efferent:
1. agryll robertson
- neurosyphillis
- lesion at pre tectal nucleus
- adie’s tonic pupil
- ciliary ganglion lesion
- slow accomodation
- have light reflex - CN3
- no accomodation - horner’s syndrome
3 types of brain herniation
- cranial nerve
- uncal: uncus herniates through tentorial notch
- compress PCA
- compress CN2, 3 - subfalcine: cingulate gyrus herniates below falx cerebri
- compress ACA
- obstruct foramen of monroe - tonsillar: cerebral penduncles herniate through foramen magnum
- compress MO
- coning = compress pons and medulla = cardiorespi arrest
- CN6
2 types of syncope
- cardiac
- arrhythmias
- cardiomyopathy
- defects - vasovagal
- emotions
- reflex mediated
3 CNS infections
- clinical exam
- diagnostic tests
- abcess
bacterial/fungal
= localised infection
= compress surrounding structures
= focal neurological deficits - meningitis
- bacterial
nesseria meningities (younger adults)
streptococcus pneumoniae (elderly, neonates)
- viral
echovirus, cocksackie, mumps, HSV - SAH
test for meningitis
(A) brudzinski’s sign (bend head towards chest, patient likely to move legs up as well)
(B) kernig’s sign (point leg straight up) ==> Knee Extension is painful
- encephalitis (inflammation of parenchyma)
- bacterial
spread from meninges to parenchyma
- viral (HSV)
HSV directly invades brain tissue
= neuronal destruction and inflammation
= temporal lobe involvement
2 types of stroke
- TOAST classification
- ICF
- treatment for ischemic vs haemorrhagic stroke
- how do statins work
- ischemic (WTEL) ==> windsor TEL
- watershed
= border zone between 2 major arteries
- thrombotic
chronic plaque formation in cerebral arteries
= clot formation
= vessel occlusion - embolic
AFib/ endocarditis/ carotid plaque rupture
= clot travels to ACA/ MCA/ PCA - lacunar ==> occlusion of smalll penetrating arteries that provide blood to deep brain structures
(A) HTN = lipohyaloinosis
(B) artheroscleosis = microarethoma
(C) A Fib/ carotid sternosis = small emboli
- hemorrhagic
- ICH (**LAH)
(A) Lobular
elderly have beta amyloid deposits in small vessels
= cerebral amyloid angiopathy
= fragile vessels
= vessel rupture at cortical areas
(B) AVM
no capillary bed between artery and vein
= high pressure flow
= veins enlarge over time
= prone to rupture
= supratentorial FPT
(C) HTN
= lipohyalinosis
= weak small arteries
= microaneurysms (charcot bouchard aneurysm)
- SAH (berry anneurysm)
= at bificuration of major arteries in the circle of willis
TOAST: (ACL)
- atherosclerosis
- cardioembolic
- lacunar
ICF: [BAP]
body function and structure
activity limitations
participation limitations
ischemic: statins, tPA
haemorrhagic: antihypertensives, beta blockers, ACEInhibitors
how do statins work:
inhibit HMG-CoA reductase
= liver removes LDL from blood
= lower LDL, higher HDL
= improve atherosclerosis, prevent risk of future clots
4 sinister headaches
- causes
- histo
- treatment
- temporal artheritis
- genetic: HLA DR4 / B1
genetic/ environmental triggers
= activate DENDRITIC CELLS
= recruit macrophages
= multinucleated giant cells, granulomatous inflam
= DISRUPT INTERNAL ELASTIC LAMINA
= thickened INTIMA
= lumen narrowing of middle-large arteries
= decrease blood flow
= jaw claudication + BILATERAL BLINDNESS
**be careful of skip lesions when doing biopsy
- carotid artery dissection
Hx of head manipulation
= tear in intima
= TEARING NECK PAIN + neurological defiicts
= give antiPLATELET - venous sinus thrombosis
virchow’s triad
= thrombus formation
= venous congestion
= increase ICP
= thunderclap headache, seizures, neuro deficits
- empty delta sign at superior saggital sinus (on VENOGRAPHY)
- papilloedema
increase ICP
= compress central retinal vein
= venous congestion
= capillary engorgenment
= microhaemorrhage of fragile retinal artery
= disrupted vasculature, micrphaemorrahages
= disrupt endothelial integrity
= fluid leaks into retina
= optic disc has blurred margins
headache red flags
antiplatelet vs anticoagulant
congenital repro patho
- turner’s syndrome (XO) 45 X ==> ovarian failure = high levels of estrogen
non dysfunction during meiosis/ mosaic
= decrease estrogen pdtn
no SHOX gene
= decrease GH sensitivity
= decrease skeletal growth
= short stature
- klienfelter’s syndrome (XXY male) 47 XXY ==> testicular failure = low levels of testosterone
non dysjunction in males
= extra X chromosome
= increase FSH, LH
= low levels of testosterone
= small penis, gyanecomastia
extra SHOX gene
= tall stature
patho of male repro
- AIS
androgen recpeotrs are insensitive
= testosterone has nowhere to bind
= no wolffian duct , no DHT conversion
= no internal or external male structures
= blind ended vagina, appears female (but actually male) - 5 alpha reductase deficiency
testosterone produced
= no alpha reductase to convert it to DHT
= no external structures
= externally appears female, but actually male structures inside - kallman’s syndrome (can be male, can be female)
**plus impaired smell
impaired GnRH neuronal migration
= no GnRH
= no LH and FSH
= low levels of testosterone/ estrogen
= poor sexual development
UL patho
1. brachial plexus lesions
2. shoulder and elbow dislocations
3. common fractures
4. carpal tunnel vs cubital tunnel
5. rotator cuff injuries
colles vs smith’s fracture
(both caused by FOOSH)
smith’s: fall on flexed wrist
colles: fall on outstretched wrist
= distal radius fracture
= dinner fork deformity
=
radial artery
- course
- where is it best felt
best felt: lateral to FCR (artery runs superficial and lateral to FCR)
cephallic vein
parts of the axillary artery (SLTSub)
- superior thoracic
SPLIT BY TERES MINOR
2.
- lateral thoracic
- thoracoacromial
- subscapular
- ant and post circumflex
parts of a bicep tendon jerk
borders + contents of the axilla
anterior: pect minor and major
posterior: scapularis, teres major, lat dorsi
medial: serratus anterior, thoracic wall
lateral: humerus
contents:
axillary nerve and artery
long head of biceps vs triceps attachment point
biceps: supraglenoid tubercle
triceps: infraglenoid tubercle
cords of the brachial plexus (M(M)UAR)
lateral: musculocutaneous
medial: ulnar
post: axillary, radial
median: both lateral and medial
abduction of the arm
0-30: supraspinatus (suprascapular nerve)
30-90: deltoid (axillary)
90-180: trapezius and SA (long thoracic)
which artery accompanies the radial artery at the back of the arm?
profunda brachii artery
what are the 2 innervations of the pect major?
sterncostal head: medial pectoral nerve (C8-T1)
clavicular head: lateral pectoral nerve (C5-7)
extensor hood
made of the tendons of extensor digitorium muscles
blood supply to the head
ECA and ICA
ICA –> circle of willis
ECA –> face and scalp
muscles of HnN + their CNs
SCM - CN11
trapezius - CN11 (shrugging)
what is the action of the trapezius muscle
shrugging shoulders
if damaged, will have drooped shoulders
suprahyoid muscles
- elevate hyoid
- for swallowing
digastric (CN 5, 7)
mylohyoid (CN V3)
geniohyoid (hypoglossal nerve)
infrahyoid muscles
C1-3 ansa cervicalis
sterno~
- thyroid
- hyoid
omohyoid
thyrohyoid
muscles of the pharynx
~pharynx:
nasal (CNV2)
oro (CN 9)
laryngo (CN10)
muscle for screaming
cricothyroid (CN 10) –> external laryngeal nerve
tenses vocal cords
what are the larynx muscles and the CN
cricoid muscles
recurrently laryngeal nerve
= hoarseness
muscles of mastication
MMTL (mom makes tasty lagsana)
masseter
MEDIAL PTERYGOID
temporalis
lateral pterygoid
CN V3
borders of the infratemporal fossa
- muscles of mastication
- V3
- maxillary artery
what is the parotid gland supplied by
(gag reflex) CN9
salivatory nucleus –> otic ganglion
CN12 lesion
does the tongue deviate towards or away from it
towards
anterior vs post triangle of neck
course of CN7
PCF
= IAM
= facial canal
= stylomastoid foramen
= enters parotid gland
= splits into 5 branches (two zebras bit my cock)
cranial nerves exit from where
cerebreum 1, 2
midbrain 3, 4
pons 5, 6, 7
pontomedullary junction 8
medulla 9-12
SLE
type 3 hypersensittivity
dsDNA, ANA
complement activation
= inflammation and tissue damage
= loss of self tolerance
= increase B cell activation
INF alpha, TNF alpha
bullous pemphigoid
type 2
IgG targets hemidesmosomes (BP 180, 230) in basement membrane
= complement activation
= inflammation
= blister formation
C3 deposition on basement membrane
tense blisters, subepidermal bullae
treatment: corticosteroids
dematomyositis
dermomyositis
type 1 inteferon driven
anti Mi2
anti Jo 1
muscle inflammation
acne vulgaris
C acne proliferation
- comedomees (open - blackheads, closed - white heads)
horner’s syndrome
CN3 sympathetic pathway disruption
= loss of sweat gland innervation, unilateral ptosis, miosis, anhidrosis
do coccaine test
bells palsy CN7
entire face affected
- HSV related
- need to differentiate from stroke
‘FACE’
Facial droop (entire half of face)
Absent forehead movement
Closing eye is difficult
Eyes & mouth droop
CN3 palsy
down and out pupil
ptosis
diplopia (double vision)
pupil involvement
