mskderm 2 Flashcards

(387 cards)

1
Q

in which regions are the primary and secondary curvatures seen respectively?

A
  • primary curvatures (kyphoses):
    1. thoracic
    2. sacral
  • secondary curvatures (lordoses):
    1. cervical: forms when infant lifts head
    2. lumbar: forms when infant sits and walks

  • primary curvatures are seen in foetus and they persist all the way
  • secondary curvatures are extensions from the flexed foetal position,
    and allows for balance of body weight during upright posture and movement

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2
Q

zygapophysial joints:
* found bet (…)
* type of joint
* function

A
  • found bet articular processes
  • plane synovial joints
  • their orientation determines the type and range of movements possible in each region
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3
Q

Which of these is NOT a listed side effect of colchicine?

  • Muscle weakness
  • Skin rash
  • Diarrhoea
  • Unusual bleeding
A

Skin rash
=> more associated with allopurinol hypersensitivity syndrome

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4
Q

Hyperuricemia is defined by a serum uric acid level greater than
6.8 mg/dL.
True or False?

A

True

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5
Q

In gout, what can high concentration of uric acid lead to the formation of?

A
  • monosodium urate CRYSTAL deposition in joints
  • kidney stones
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6
Q

which part of the immune system is the main component involved in gout

A

phagocytes

pathogenesis
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7
Q

management of gout:
* acute gout attack
* urate lowering therapy

principles + drugs

A
  • acute gout attack:
    principle is to treat and resolve acute attack,
    thus use colchicine, NSAIDs and steroids
  • urate lowering therapy:
    principle is to solve root problem and prevent future attacks,
    thus use allopurinol, febuxostat and probencid
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8
Q

MOA of colchicine

A
  • main MOA: binds to tubulin
    -> preventing its polymerization into microtubules
    => thereby inhibiting leukocyte migration
  • other MOA: inhibits leukotriene B4 and prostaglandin (PG) production
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9
Q

main A/E of colchicine
(i.e. dose limiting A/E)

A

GI-related symptoms:
diarrhoea + gastritis

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10
Q

precautions for colchicine:
* which drug should it NOT be paired with?
* in which patient group should it be avoided?

A
  • statins
    bcos both drugs independently can cause myopathy and marrow suppression
    ⇒ increased risk of myopathy and pancytopenia
  • patients with renal failure
    ← renal excretion
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11
Q

when should NSAIDs vs steroids be used in acute management of gout attacks

A
  • NSAIDs: 1st-line
  • steroids: used in patients where NSAIDs are contraindicated

if prednisolone is used, should give ≤30 mg/day

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12
Q

Management of gout has 2 components:
1) treating acute gout attack
2) urate lowering therapy
What are the indications of urate lowering therapy?

A
  • when gout has chronic CHRONIC presentation
    1) frequent gout attacks (≥ 2 /year)
    2) tophaceous gout
    3) clinical or radiographic findings of gouty arthropathy
  • when gout has CHRONIC underlying cause:
    1) CKD gout
    where CKD
    → persistent decreased uric acid excretion
    ⇒ persistent hyperuricaemia
  • when gout has CHRONIC-related complications:
    1) urolithiasis gout
    since formation of stones is a long-term process
    ← long-term hyperuricaemia
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13
Q

Timeline for management of gout:
do we start ULT at the same time as an acute attack?

A
  • NO
  • but if patient is alr on ULT and acute attack happens,
    continue ULT

why not?
1. ULT decreases plasma [uric acid]
increase uric acid gradient from joint to plasma
→ increase mobilisation of crystals out of joint and into plasma
→ increasing immune recognition
positive feedback loop
⇒ attack is exacerbated
2, uricosuric agents increase amt of uric acid being excreted
→ kidney unable to handle it
⇒ increase risk of kidney stones

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14
Q

precautions when taking probenecid
to minimise formation of kidney stones

A
  • take plenty of fluid
  • keep urine pH > 6.0

can increase urine pH by administering alkaline (e.g. potassium citrate)

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15
Q

MOA of allopurinol and febuxostat

A

xanthine oxidase inhibitors
=> reduce uric acid production

note: allopurinol is 1st-line,
while febuxostat is used when allopurinol is contraindicated

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16
Q

what is the main A/Es for XO inhibitors
and what are their risk factors

A
  • main A/Es:
    allopurinol hypersensitivity syndrome (AHS),
    severe cutaneous adverse reactions (SCAR)
  • risk factors:
    1) renal impairment
    (specifically creatinine clearance < 60ml/min )
    ← allopurinol is ELIMINATED renally
    2) thiazide therapy
    decrease allopurinol clearance
    3) HLA-B*58:01

  • how do thiazides decrease allopurinol clearance?
    1) certain transporters in proximal tubule help to clear urate and oxypurinol (active metabolite of allopurinol)
    2) thiazides compete for these transporters
  • this gene is most common in han chinese, thai and koreans

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17
Q

example of uricosuric agent
(i.e. increase uric acid excretion)
and its MOA

A
  • probenecid
  • MOA: inhibits PROXIMAL tubule anion transport
    -> inhibits uric acid reabsorption
    => increases uric acid excretion
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18
Q

diff bet
anulus fibrosus vs nucleus pulposus

parts of the interverterbral disc

A
  • nucleus pulposus: inner, gelatinous core
    that acts as a shock absorber and provides elasticity
  • anulus fibrosus: thick outer ring of fibrous cartilage
    that contains the NP
    and resists excessive torsion and force
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19
Q

parts of a typical vertebral body
AND function of processes

A
  • articular processes has 4 facets:
    (2 on superior end, 2 on inferior end)
    => form the synovial joints between adjacent vertebrae
    (zygapophyseal joints)
  • spinous and transverse processes are for attachments of muscles/ligaments
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20
Q

unique features of cervical vertebral bodies

A
  • small body
  • uncinate process (on body): provides stability
    and limits side bending
  • foramen transversarium: allows passage for vertebral arteries and veins
  • bifid spinous process

ONLY cervical vertebrae have foramen transversarium
<- vertebral arteries and veins enter cranial cavity to supply brain

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21
Q

atlas:
* which part of vertebrae
* unique features

A
  • C1
  • features:
    1. no vertebral body or spinous process
    2. superior articular surfaces articulate with occipital condyles
    => nodding YES
    inferior articular surfaces articulate with axis
    => shaking head NO
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22
Q

axis:
* which part of vertebrae
* unique features

A
  • C2
  • odontoid process (dens)
    which projects upwards from body
    -> act as a pivot around which atlas and head rotate
    => shaking head NO
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23
Q

intermediate extrinsic back muscles:
* function
* which ones + actions

A
  • accessory muscles of respiration
  • serratus POSTERIOR superior: elevate UPPER ribs
    serratus POSTERIOR inferior: depress LOWER ribs
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24
Q

intrinsic back muscles:
* function
* which ones

A
  • move the vertebral column
  • superficial: splenius capitis and cervicis
    intermediate: erector spinae muscles
    (Iliocostalis, Longissimus, Spinalis)
    deep: semispinalis

for the erector spinae muscles,
can rem by “I Love Spine” from lateral to medial

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25
actions of splenius capitis and splenius cervicis (superficial intrinsic back muscles)
* when acting unilaterally: **lateral flexion** of NECK and **rotation** of HEAD to *side of active muscles* * when acting bilatrally: **extension** of HEAD and NECK
26
actions of erector spinae (intermediate intrinsic back muscles) ## Footnote erector spinae = I Love Spine = Iliocostalis, Longissimus and Spinalis
* when acting unilaterally: **lateral flexion** of VERTEBRAL COLUMN to *side of active muscles* * when acting bilaterally: **extension** of VERTEBRAL COLUMN
27
actions of semispinalis (deep intrinsic back muscles)
* when acting unilaterally: **rotation** of HEAD *contralaterally* * when acting bilaterally: **extension** of HEAD and NECK
28
innervation of intrinsic back muscles
**posterior** rami of spinal nerves ## Footnote extrinsic back muscles are NOT, they are supplied by **anterior** rami
29
diff bet conus medullaris (= medullary cone) vs cauda equina
* conus medullaris: **tapering** **INFERIOR end** of spinal cord * cauda equina: collection of nerves that **extend below end** of spinal cord
30
filum terminale
* **vestigial** remnant of spinal cord * descends from conus medullaris to coccyx * function: **anchors** spinal cord in place -> preventing its movement **within vertebral column**
31
what are the 3 layers of the spinal meninges?
superficial -> deep: * dura mater * arachnoid mater * pia mater
32
dura mater: * description * function * runs from foramen magnum and attaches to (...) via (...) (and thus ends at (...) level) * relevant space
* **tough**, fibrous, **protective** sheath * anchors spinal cord * runs from foramen magnum and attaches to **coccyx** via **filum terminale** (and thus ends at **S2** level) * **EPIdural** space (= above dura mater): contains internal vertebral venous plexus and epidural fat => site for epidural **anesthesia**
33
arachnoid mater: * description * how is it connected to pia mater * relevant space
* **thin** middle layer * connected to pia mater via arachnoid **trabeculae** * **SUBarachnoid** space (= below arachnoid mater): filled with **cerebrospinal fluid (CSF)** => site for **lumbar puncture**
34
where does the subarachnoid space end
S2
35
pia mater: * description * how it is attached to dura mater * function
* **delicate** innermost layer * attach to dura mater via **denticulate** ligaments (pierces arachnoid mater to do so) * functions: 1. rich in **blood vessels** => supply **nutrients** 2. helps to **anchor** spinal cord in place
36
ligaments in spinal column and their functions
* ligaments @ anterior side: limit **extension** of spine * ligaments @ posterior side: limit **flexion** of spine * ligaments @ lateral side: limit **lateral flexion and rotation** of spine ## Footnote nuchal ligament (external occipital protuberance -> C7) is continuous with supraspinous ligament (C7 -> sacru,), and is formed via its thickening
37
why is posterior herniation of intervertebral disc more common than anterior herniation?
posterior longitudinal ligament is **weaker** than anterior longitudinal ligament
38
for lower back pain, what does it mean if these actions exacerbate the pain? 1. flexion 2. extension
1. injury to intervertebral **disc**: lumbar **flexion** → increase disc pressure → hernation ⇒ pain 2. pathology related to **facet joints** of the vertebral column (e.g. OA): lumbar **extension** (and rotation) → **more loading** of facet joints ⇒ more pain
39
degenerative disc disease: * stages (4) * mechanism of symptoms (2)
* stages: a. normal disc b. **degeneration** (= *annulus* WEAKENS) c. **prolapse** (= *nucleus pulposus* PUSHES OUTWARD, annulus still intact) d.**extrusion** (= *nucleus pulposus* BREAKS THROUGH *annulus*) and **sequestration** (= *nucleus material* free fragment in canal) * mechanism of symptoms: a. **posterior** herniation ⇒ compression of **spinal cord** (i.e. myelopathy) b. **posterolateral** herniation ⇒ compression of **nerve roots** (i.e. radiculopathy)
40
identify the diff parts of proximal femur
## Footnote note: intertrochanteric **line** is found on **anterior** side while intertrochanteric **crest** is found on **posterior** side
41
significance of linea aspera
serves as attachment point for **muscles**
42
what is the arterial supply of the **head** of femur and what is its clinical significance
* medial circumflex artery * **FRACTURE** of *neck* of femur → **avascular necrosis** of *head* of femur ## Footnote * bcos medial circumflex artery has a **retrograde** blood supply (i.e. blood travels "backwards" from distal end to proximal end) * does NOT occur in children as **obturator** artery provides significant blood supply to head in childhood
43
factors contributing to stability of hip joint: * bony factors * ligamentous factors * muscular factors
* *head of femur* **fits nicely** into *acetabulum*, which is **deepened** by acetabular **labrum** * ligaments: **ilio**femoral ligament, **pubo**femoral ligament, **ischio**femoral ligament * muscles: muscles around hip joint
44
comment on the ligaments of the hip joint: * functions of each * strongest one
* iliofemoral (anterior): prevents hyper**extension** of hip pubofemoral (more inferior): prevents over**abduction** of hip ischiofemoral (posterior): also prevents hyper**extension** of hip * strongest = **iliofemoral**
45
hip joint: * type of joint * movements
* synovial **ball-and-socket** joint * flexion/extension, abduction/adduction, external/internal rotation ## Footnote think of the **FABER** test, which involves putting patient's tested leg in "figure 4" position, which involves **F**lexion, **AB**duction and **E**xternal **R**otation
46
sensoy innervation of leg and dorsum of foot: * The terminal branch of the femoral nerve is the (...) nerve * This nerve only has (...) function, and travels with the (...)
* The terminal branch of the femoral nerve is the **saphenous** nerve * This nerve only has **sensory** function, and travels with the **great saphenous vein** ## Footnote note: sural nerve is formed by union of 2 branches, a branch from the tibial nerve and a branch from the common fibular nerve
47
venous drainage of lower limb: * The **great** saphenous vein ascends (...) to the (...) malleolus, and drains into the (...) vein. * The **small** saphenous vein ascends (...) to the (...) malleolus, and drains into the (...) vein.
* The **great** saphenous vein ascends **anterior** to the **MEDIAL malleolus**, and drains into the **femoral** vein. * The **small** saphenous vein ascends **posterior** to the **LATERAL malleolus**, and drains into the **popliteal** vein.
48
pathway of femoral artery: * becomes femoral artery from (...) artery upon passing (...) * into (...) where it divides into (A) and main femoral artery * (...) and (...) arteries branch out from (A) * while main femoral artery continues as (B) upon passing (...) * (B) divides into (C) and (D) after passing lower border of popliteus * (C) continues as (...) artery
pathway of femoral artery: * becomes femoral artery from **external iliac** artery upon passing **inguinal ligament** * into **femoral triangle** where it divides into **profunda femoris** and main femoral artery * **medial and lateral circumflex arteries** branch out from profunda femoris * while main femoral artery continues as **popliteal** artery upon passing **adductor hiatus** * popliteal artery divides into **anterior and posterior tibial arteries** after passing **lower border of popliteus** * **anterior** tibial artery continues as **dorsalis pedis artery**
49
comment on the gluteal muscles: * function * innervation
1. gluteus maximus: **EXTENDS** and **externally rotates** hip, **inferior** gluteal nerve 2. gluteus medius and gluteus minimus: **ABDUCT** and **internally rotate** hip, **superior** gluteal nerve ## Footnote to understand action, think abt *origin* and/or *insertion* of each muscle! * gluteus maximus *originates* at **POSTERIOR** surface of body in general, and mostly ends in **iliotibial tract** which *inserts* at **LATERAL tibial condyle** * gluteus medius and minimus *originate* at **POSTERIOR** surface of body in general, but *insert* at **LATERAL and ANTERIOR surface of greater trochanter** respectively
50
Trendelenburg test: * instructions * positive test * principle behind it
* get patient to **raise one leg** off the floor * muscles on the *side of the foot on the ground* holds the pelvis ⇒ **prevents pelvis from sagging** on *side of raised leg* * (+) test: **pelvis falls** on the *side of the raised limb* ← hip **ABDUCTORS** (**gluteus medius and gluteus minimus**) on *other side* are **not functioning**
51
which muscles are involved in external rotation of hip and their innervation
* piriformis, obturator internus, quadratus femoris: **nerve to** (...muscle name...) * obturator externus: **obturator** nerve ## Footnote think of it as obturator *externus* = *outcast* = thus *diff* innervation *from the rest*
52
muscles in medial compartment of thigh and their function & innervation
* **hip ADDUCTORS** 1. **pectineus**: *obturator* **AND femoral** nerves 2. adductor brevis and adductor longus: *obturator* nerve 3. **adductor magnus**: *obturator* nerve (for adductor pt) **AND tibial portion of sciatic nerve** (for hamstring pt) * weirdo: 1. **gracilis**: hip ADDUCTOR **and knee FLEXOR**, *obturator* nerve ## Footnote * technically it is the muscles that are most proximal (pectineus) and most distal (adductor magnus) * from superficial → deep: adductor magnus, adductor brevis, adductor longus
53
patella: * found in (...) tendon * dislocates (...): due to upward (...) pull by (...)
* found in **quadriceps** tendon * dislocates **laterally** ← due to **upward lateral pull** by **quadriceps**
54
identify the diff parts of the distal femur
55
what is the main group of lymph nodes which drain the lower limbs?
inguinal
56
borders of tarsal tunnel
* floor: medial side of **tibia, talus and calcaneus** * roof: flexor retinaculum
57
contents of tarsal tunnel
* **medial** compartment of LEG: tendons of **T**ibalis posterior, flexor **D**igitorum longus and flexor **H**allucis longus ("**Tom, Dick and Harry**") * NAV in posterior LEG: **posterior tibial** artery and vein, **tibial** nerve
58
branches of **lumbar** plexus relevant to lower limb
* lateral femoral cutaneous nerve * **obturator** nerve (anterior division, **L2-L4**) * **femoral** nerve (posterior division, **L2-L4**) ## Footnote lateral cutaneous nerve only comes into play for **sensory** innervation, where it takes over **lateral** side of THIGH
59
branches of **sacral** plexus relevant to lower limb
* superior and inferior **gluteal** nerves * **sciatic** nerve (**L4-S3**)
60
tarsal bones
"**Tiger Cubs Need MILC**" * **T**alus * **C**alcaneus * **N**avicular * cuneiforms (**M**edial, **I**ntermediate, **L**ateral) * **C**uboid
61
what bones form the medial arch of the foot
* talus * calcaneus * navicular * cuneiforms (medial, intermediate, lateral) * **medial 3** metatarsals
62
medial arch: * keystone * intersegmental ties * tiebeams * slings
* keystone: *talus* → **receive body's weight** from tibia and **distributes it** along both sides of arch * intersegmental ties: plantar *calcaneonavicular* (*spring*) ligament → ties inferior edges of bones tgt and **maintain alignment** * tiebeams: *plantar aponeurosis* and *intrinsic muscles of foot on medial side* (e.g. abductor hallucis) → resists outward thrust of arch and **keep bones** in arch **from spreading apart** * slings: *tibialis* anterior and posterior, *flexor hallucis longus* → **INVERT and plantarflex** foot when they contract ⇒ **pull arch upwards**
63
lateral arch: * keystone * tiebeams * slings
* keystone: *cuboid* → **midpt** → thus **receives downard body weight** and **distributes it** along both sides of arch * intersegmental ties: *SHORT plantar* (*calcaneocuboid*) and *LONG plantar* ligaments → ties inferior edges of bones tgt and **maintain alignment** * tiebeams: *plantar aponeurosis* and *intrinsic muscles of foot on lateral side* → resists outward thrust of arch and **keep bones** in arch **from spreading apart** * slings: *fibularis* brevis and longus → **EVERT and plantarflex** foot when they contract ⇒ **pull arch upwards**
64
what bones form the lateral arch of the foot
* calcaneus * cuboid * **lateral 2** metatarsals
65
functions of medial and lateral arches of the foot
* medial arch: **weight** bearing * lateral arch: walking and **propulsion**
66
what bones form the transverse arch of the foot
"tiger cub needs **milcc**" * (**m**edial, **i**ntermediate and **l**ateral) **c**uneiforms * **c**uboid * metatarsal bases
67
what is plantar fasciitis
inflammation of **plantar aponeurosis** due to compressive and tensile forces **at insertion** ## Footnote * plantar aponeurosis: thick band of **connective tissue** on the sole of the foot that connects the heel bone to the toes, providing **structural support** * compressive force = **standing** too long tensile force = prolonged **push-off** motions
68
what is piriformis a landmark for ## Footnote hint: gluteal nerves and sciatic nerve
* **superior** gluteal nerve emerges **above** the piriformis * whilst the **inferior** gluteal nerve emerges **below** the piriformis * sciatic nerve also emerges from **below** the piriformis muscle, appearing as a wide 2cm band ## Footnote all 3 pass through the GREATER sciatic foramen!
69
actions of the sartorius muscle ## Footnote the **exception** in muscles in anterior compartment of thigh!
bring person into **cross-legged** position * flexion of BOTH hip and knee joints * **abduction** of THIGH
70
All muscles in the **posterior thigh** are innervated by the (...), except for the (...), which is innervated by the (...)
All muscles in the **posterior thigh** are innervated by the **tibial portion** of the *sciatic* nerve, except for the **SHORT head of the biceps femoris**, which is innervated by the **common fibular portion** of the *sciatic* nerve ## Footnote posterior thigh muscle are the **hamstring** muscles, which include biceps femoris (short and long head), semitendinosus and semimembranosus
71
pathway of sciatic nerve: * emerges from pelvis through (...) * (...) and (...) components run together inside a single sheath in thigh * then divides into the terminal branches, (...) nerve and (...) nerve at (...) * common fibular nerve runs down fossa, giving rise to (...) nerve of CALF before winding around (...) * it then pierces the fibularis longus muscle (thus going into the ANTERIOR compartment) and divides into the terminal branches, (...) and (...) nerve
* emerges from pelvis through **greater sciatic foramen** * **tibial** and **common fibular** COMPONENTS run together inside a single sheath in thigh * then divides into the terminal branches, **tibial** and **common fibular** NERVES at **upper end of popliteal fossa** * common fibular nerve runs down fossa, giving rise to **lateral cutaneous** nerve of CALF before winding around **neck of fibula** * it then pierces the fibularis longus muscle (thus going into the ant compartment) and divides into the terminal branches, **superficial** fibular and **deep** fibular nerve ## Footnote note: fibular = peroneal
72
what structures do you see when you make an incision into the neck (superficial -> deep)?
1. skin 2. superficial fascia 3. deep cervical fascia 4. strap muscles 5. viscera of neck (including thyroid gland)
73
what do the strap muscles consist of ## Footnote 4 muscles!
* omohyoid * sternothyroid * thyrohyoid * sternohyoid
74
what do you call muscles anterior to cervical vertebrae and what is their function
* **pre**vertebral muscles * **flex** cervical spine => allow head to **nod forward** ## Footnote muscles posterior to cervical vertebrae = **post**vertebral muscles fn is to extend cervical spine => allow head to **extend backward**
75
what are the contents of the carotid sheath
* carotid artery * **internal** jugular vein * **vagus** nerve (= cranial nerve X) ## Footnote **internal** jugular vein is **deep** to SCM while *external* jugular vein is *superficial* to SCM
76
what are the important nerves relating to the prevertebral muscles ## Footnote 2 nerves!
* brachial plexus: bet scalenus anterior and scalenus medius * phrenic nerve: anterior to scalenus anterior
77
what are the layers of the deep cervical fascia
* investing * prevertebral * pretracheal ## Footnote ALL 3 contribute to formation of carotid sheath!
78
important vertebral levels in neck: * where are they located * what significance do they have
1. C**4**: at **superior** border of **thyroid cartilage**, where **bifurcation** of common carotid artery occurs and where carotid **baroreceptors and chemoreceptors** are found 2. C**6**: at **inferior** border of **cricoid cartilage**, where larynx ends and trachea begins and pharynx ends and oesophagus begins
79
where do external and internal carotid artery give rise to their respective branches
* **external** carotid artery: **neck** * internal carotid artery: inside cranial cavity
80
ECA runs upwards towards parotid gland, where it splits into 2 terminal branches: (...) and (...)
* superficial temporal artery * maxillary artery
81
ansa cervicalis: * found around (...) * arise from (...) * give off branches which supply (...) muscles
* found around **carotid sheath** * arise from **CERVICAL plexus** * give off branches which supply **strap** muscles
82
what nerves do the sup and inf thyroid arteries run close to and thus must be careful of ligating during surgery
* STA runs close to **external** laryngeal nerve * ITA runs close to **recurrent** laryngeal nerve ## Footnote both nerves supply the **larynx**
83
Where is the somatosensory cortex located
post-central gyrus ## Footnote which is in parietal lobe of cerebral cortex
84
differences bet spino-thalamic (antero-lateral) and dorsal column medial lemniscus (DCML) pathways ## Footnote * modalities * location of 2nd order neuron * where 2nd order neuron decussates
* modalities: spino-thalamic: **N**on-discriminative (Crude) touch, **T**emperature, **P**ain DCML: **F**ine touch, **V**ibrations, (conscious) **P**roprioception * 2nd order neuron: spino-thalamic: located at spinal cord, *decussates at spinal cord* also DCML: located at medulla oblongata, *decussates at brainstem* ## Footnote * spino-thalamic pathway = "***N**ot* **T**hat ***P**atient*" * DCML = **F**eeling **V**ery ***P**atient*
85
What is the corpus callosum?
**commisural** fibres that connect both hemispheres ## Footnote in fact the BIGGEST commisural fibre!
86
what are the different neuroglial cells of CNS and their functions
* astrocytes: form part of **BBB** * *oligodendrocytes*: form **myelin sheath** in CNS * microglia: **phagocytic** role (i.e. "policeman" of CNS) ## Footnote in PNS, *schwann* cells form the myelin sheath!
87
what type of gland are each of the salivary glands ## Footnote AND thus how to differentiate them
* parotid: pure **serous** gland => **darkest**/most purplish staining * submandibular: **mixed** gland * sublingual: pure **mucinous** gland => **lightest**/least purplish staining ## Footnote serous = watery secretions
88
which nerve innervates parotid gland
CN IX (Glossopharyngeal gland) ## Footnote provides **parasympathetic** fibers that stimulate saliva production
89
clinical significance of pterion
* **thinnest** part of skull * **middle meningeal** artery runs underneath * thus trauma will result in intracranial **haemorrhage** ## Footnote anatomically, it is the meeting point of the 4 skull bones
90
layers of scalp (from outermost -> innermost)
* **S**kin * **C**onnective tissue * **A**poneurosis * **L**oose areolar tissue * **P**ericranium
91
position of parotid gland
recall: parotid gland looks like an inverted pyramid! * base (superior) is against zygomatic arch * apex (inferior) is behind angle of mandible
92
describe pathway of facial nerve (CN VII) and its unique feature
* general pathway: *UMN* originates in **motor cortex** → descends and synapses on *LMN* in **facial motor nucleus** → LMN then exits brainstem and its branches innervate **muscles of facial expression** * majority receive UMN input from BOTH cerebral hemispheres (**bilateral**) except for the part supplying **muscles of lower face**, which receives only **contralateral** input
93
How do patients w/ UMN and LMN lesion of CN VII present differently
* UMN lesion: **CONTRALATERAL lower face** weakness, upper face spared * LMN lesion: **IPSILATERAL entire face** weakness ← all LMNs to upper and lower facial muscles **travel together in the same peripheral nerve** ## Footnote since LMN lesion affects all the fibres traveling tgt in CN VII, * also affects parasympathetic fibres to lacrimal gland ⇒ decrease in **lacrimation** * and also special sensory fibres to ant 2/3 of tongue ⇒ loss of **taste** in ant 2/3 of tongue
94
blood supply to face and scalp: * mainly supplied by branches of (...), with some suppplementation from branches of (...) * MAIN supply is by (...) artery, which is a branch of (...)
* **mainly** supplied by branches of **ECA** with some **suppplementation** from branches of **ICA** * MAIN supply is by **facial** artery, which is a branch of **ECA**
95
most common type of **lacunar** stroke: * often caused by occlusion of (...) artery * results in interruption of blood flow to **posterior** limb of (...) * presents with (...)
* often caused by occlusion of **lenticulostriate** artery * results in interruption of blood flow to **posterior** limb of **internal capsule** (which is where corticobulbar and corticospinal fibres pass through) * presents with **CONTRALATERAL hemiparesis** of **(lower) face, arm and leg**
96
what are the 2 groups of muscles in muscles of facial expression
* sphincteric: functions to **CLOSE openings** (e.g. orbicularis) * levator: functions to **OPEN openings** (e.g. levator, depressor)
97
describe sensory innervation of face and scalp: * can be divided into 2 areas by the (...) line * anterior to the line is supplied by (...) nerve while posterior to the line is supplied by (...) * these 2 areas can be further divided into smaller areas: which division it is (..., ... or ...) OR which rami it is (... or ...)
* can be divided into 2 areas by the **vertex-ear-chin** line * anterior to the line is supplied by **trigeminal** nerve (CN V) while posterior to the line is supplied by **cervical plexus** (C1-C4) * these 2 areas can be further divided into smaller areas: which division it is (**opthalmic (V1), maxillary (V2) or mandibular (V3)**) OR which rami it is (**ventral or dorsal**)
98
skull bones
99
veins in face and scalp: * (...) veins connect intracranial space and extracranial space (scalp) * as (...), (...) from (...) can spread into (...) -> inflammation -> increase in ICP => compress brain
* **emisary** veins connect intracranial space and extracranial space (scalp) * as they have **NO valves**, **infections** from scalp can **spread into cranial cavity** -> inflammation -> increase in ICP => compress brain
100
pathway of arterial supply of brain: * ICA enters skull through (...) * and then divides into (...) and (...) * vertebral arteries enter skull through (...) * and merge to form (...) * which ascends and eventually divides into the 2 (...)
* ICA enters skull through **carotid canal** * and then divides into **anterior** and **middle cerebral arteries** * vertebral arteries enter skull through **foramen magnum** * and merge to form **basilar artery** * which ascends and eventually divides into the 2 **posterior cerebral arteries** ## Footnote vertebral arteries ← subclavian arteries
101
what are the 3 important grooves in the brain ## Footnote * groove = sulcus * **deep** groove = fissure * fold = gyrus
102
where are the visual cortexes ## Footnote function: see AND process visual information
both are in the **occipital** lobe * primary visual cortex (VC1) is at area 17, on both banks of the **calcarine sulcus** * visual association area (VC2) is at areas 18 and 19, **adjacent** to VC1 ## Footnote note: both have **BILATERAL** representation
103
difference bet 1º visual cortex (VC1) and visual association area (VC2)
* VC1: basic, low-level visual processing (i.e. it **sees** but does not understand) * VC2: higher-level visual processing, (i.e. it **UNDERSTANDS**) via 2 visual pathways: 1. ventral visual pathway: processing of **form and colour** info ('**WHAT**') 2. dorsal visual pathway: processing of **spatial** relationships and **motion** info ('**WHERE**')
104
where are the speech areas
* Broca's **motor** speech area: frontal lobe, at areas 44 and 45 * Wernike's **sensory** speech area: temporal lobe, at area 22 ## Footnote note: both are mainly "found" in **ONE** hemisphere only, the **dominant** one!
105
difference bet Broca's motor speech area and Wernike's sensory speech area
* motor speech area: responsible in **expressing/producing** language * sensory speech area: responsible in **understanding** language
106
where is the primary auditory cortex
* **temporal** lobe * areas 41 and 42, surrounded by Wernicke's sensory speech ara ## Footnote note: it has **BILATERAL** representation
107
important bones and fissures of cranial cavity
108
the cranial cavity can be divided into 3 fossa, of which the anterior cranial fossa (ACF): * is formed mainly by (...) and (...) bones, and partly by (...) bone * is where the (...) lobe of the brain sits * contains many small openings known as the (...), which the (...) pass through
* is formed mainly by **frontal** and **ethmoid** bones, and partly by **LESSER wings of sphenoid** bone * is where the **frontal** lobe of the brain sits * contains many small openings known as the **cribiform plate**, which the **olfactory** nerve (= CN I) pass through to supply the roof of the nose
109
the cranial cavity can be divided into 3 fossa, of which the middle cranial fossa (MCF): * is formed by (...) bone, as well as (...) bone * is where the (...) and (..) lobes of the brain sit * has a depression on the body of sphenoid known as the (...), where the (...) sits * and lateral to the body of the sphenoid is occupied by the (...) sinus on each side
* is formed by **greater wings and body of sphenoid** bone, as well as **part of temporal** bone * is where the **temporal** and **parietal** lobes of the brain sit * has a depression ON the body of sphenoid known as the **hypophyseal fossa**, where the **pituitary gland** sits * and LATERAL to the body of the sphenoid is occupied by the **cavernous** sinus on each side
110
important openings in MCF: * two round openings anterior and lateral to the depression, known as the (...), which the (...) nerve and (...) artery pass through * long-ish opening bet lesser and greater wings of sphenoid bone, known as the (A), which CNs (...), (...), (...) and (...), as well as (...) vein pass through * round opening posterior to A, known as foramen (B), which CN (...) pass through * opening posterior and lateral to B, known as foramen (C), which CN (...) pass through * smaller opening slightly posterior to C, known as foramen (D), which (...) artery pass through
* two round openings ANTERIOR and lateral to the depression, known as the **optic canal**, which the **optic** nerve (= CN **II**) and **opthalmic artery** pass through * long-ish opening bet lesser and greater wings of sphenoid bone, known as the **superior orbital fissure**, which CNs **III, IV, V1 and VI,** as well as **opthalmic vein** pass through * round opening POSTERIOR to SOF, known as foramen **ovale**, which CN **V2** pass through * opening POSTERIOR and lateral to foramen ovale, known as foramen **rotundum**, which CN **V3** pass through * smaller opening slightly POSTERIOR to foramen rotundum, known as foramen **spinosum**, which **middle meningeal artery** pass through
111
the cranial cavity can be divided into 3 fossa, of which the posterior cranial fossa (PCF): * is separated from MCF by (...)
* is separated from MCF by **PETROUS part of temporal bone**
112
important openings in PCF: * opening which IJV passes through, known as (...) foramen, which CNs (...), (...) and (...) also pass through * opening which sits on **posterior** side of petrous part of temporal bone, known as (...), which CNs (...) and (...) pass through * **pair** of openings slightly anterior to foramen magnum, known as (...) canal, which CN (...) passes through
* opening which IJV passes through, known as **jugular** foramen, which CNs **IX, X and XI** also pass through * opening which sits on **posterior** side of petrous part of temporal bone, known as **internal acoustic meatus**, which CNs **VII and VIII** pass through * **pair** of openings slightly anterior to foramen magnum, known as **hypoglossal** canal, which CN **XII** passes through
113
which artery supplying the brain is most commonly affected in stroke
middle cerebral artery
114
function of dural folds
occupy fissures/grooves -> prevent brain from moving too much => protection of brain
115
In which space (bet the meninges) does the circle of Willis reside
subarachnoid space => any rupture/aneurysm results in subarachnoid haemorrhage | a type of intracranial haemorrhage! ## Footnote aneurysm commonly occurs in circle of Willis and arch of aorta
116
In which space (bet the meninges) does the middle meningeal artery reside
epidural space => any rupture results in epidural haemorrhage | a type of intracranial haemorrhage!
117
flow of dural venous sinuses
118
where does CSF from the subarachnoid space go before emptying into IJV?
Superior Sagittal Sinus via arachnoid granulations ## Footnote arachnoid granulations = projections of arachnoid layer into SSS
119
what is CSF produced by and where
**choroid** plexus (= modificed capillaries) on the WALLS of **ventricles**
120
match the cerebral ventricle with its description: 1. lateral ventricles 2. cerebral aqueduct 3. 4th ventricle 4. 3rd ventricle a. located bet cerebellum and brainstem b. connects 3rd and 4th ventricles c. located bet the 2 halves of thalamus d. connects to 3rd ventricl via interventricular foramen
1d, 2b, 3a, 4c
121
characteristics and functions of CSF
* **clear** fluid resembling blood plasma, but **less protein** * found in subarachnoid space, ventricles and central canal of spinal cord * functions: 1. support and **cushion** CNS 2. **nourish** CNS 3. **remove waste** metabolites
122
how is the cavernous sinus more prone to infections
2 routes for spread of infection: 1. **emissary veins** connect them to extracranial venous plexuses 2. **opthalmic vein**, which drains face and scalp, also drain into them
123
clinical significance of infection of cavernous sinus
CS is **CLOSELY** related to multiple **cranial nerves** and the **ICA** ⇒ infection in CS can easily affect these structures ## Footnote the cranial nerves are the ones which pass through * SOF (CNs III, IV, V1, VI) * foramen rotundum (V2)
124
Both CSF and blood drain into dural venous sinuses (e.g. SSS) before returning to venous circulation. How does blood do so?
**bridging** veins * found in **subdural** space * allow for communication bet **cerebral veins** (in subarachnoid space) and **SSS**
125
clinical significance of bridging veins
* **subdural** space **increases** w/ AGE <- due to shrinkage of brain * **bridging** veins (which are in subdural space) are **more easily injured** during movements within cranial cavity => leading to **subdural hemorrhage**
126
sensory innervation of tongue: * general * special (taste)
* general: anterior 2/3 — mandibular div (= CN **V3**) posterior 1/3 + circumvallate papillae — glossopharyngeal (= CN **IX**) * special (taste): anterior 2/3 — facial (= CN **VII**) posterior 1/3 + circumvallate papillae — glossopharyngeal (= CN **IX**) ## Footnote circumvallate papillae is **located in anterior** 2/3 area, but has **same innervation as posterior** 1/3 due to it being originally from posterior 1/3 area but migrating forward during development
127
what epithelium lines the paranasal sinuses
respiratory epithelium (pseudostratified ciliated columnar) ## Footnote same as rest of nasal cavity
128
parts of nasal cavity NOT lined by respiratory epithelium
* vestibule: lined by **skin** (stratified squamous epithelium) * olfactory mucosa: contains **nerve endings of CN I** (= olfactory nerve) for smell
129
what structure opens into inferior meatus | space below the inferior concha!
nasolacrimal duct
130
what structure opens into the middle meatus | space below the middle concha!
* mainly **maxillary** sinus * but also **frontal** sinus and part of **ethmoidal** sinus
131
what structure opens into the superior meatus | space below the superior concha!
part of **ethmoidal** sinus
132
what structure opens into the sphenoethmoidal recess
sphenoidal air sinus
133
which paranasal air sinus is most prone to infection and why
1. **big distance** from floor of sinus to opening -> **accumulation** of e.g. mucus => infection 2. **close** proximity to **upper teeth** => infections can **spread** from there
134
describe sensory pathways (general sensory) in head: * name of tract * modalities * locations of 1st and 2nd order neurons
* **trigemino**thalamic tract * crude and fine touch, temperature, pain, vibration, conscious proprioception, pressure * 1st order neuron: **trigeminal** ganglion (PNS), 2nd order neuron: **brainstem** (CNS) (decussates there too) ## Footnote recall that for rest of body: * *spino*thalamic and *DCML* tracts * spinothalamic: crude touch, temp, pain DCML: fine touch, vibration, pressure * both have 1st order neuron in DORSAL horn of*spinal cord* (PNS) but for 2nd order neuron, spinothalamic: *spinal cord* (decussates there too) DCML: *brainstem* (decussates there too)
135
describe somato-motor pathways in head: * names of tract in **pyramidal** system * modalities * pathway
* cortico**bulbar** / cortico**nuclear** tract * **voluntary** control of movements which are **discrete** and **skilled** * LMNs located in **motor nuclei** in **brainstem** <- receive cortiocobulbar fibres from UMNs in **one OR both** cerebral hemispheres ## Footnote recall that for rest of body: * cortico*spinal* tract * also *voluntary* control of movements which are *discrete* and *skilled* * LMNs located in VENTRAL horn of *spinal cord* <- receive corticospinal fibres usually from UMNs in *contralateral* cerebral hemisphere after they decussate at pyramids of medulla
136
what are the movements of the eye ## Footnote given the reference points: * pupil * 12 o'clock
* elevation and depression: PUPIL moves **upwards or downwards** * abduction and adduction: PUPIL moves **laterally or medially** * intorsion and extorsion: 12 O'CLOCK of eye **internally or externally rotates**
137
match the following muscles of the tongue with their primary actions: 1. Palatoglossus 2. Genioglossus 3. Hyoglossus 4. Styloglossus a) Brings tongue backwards (retraction) b) Elevates tongue c) Depresses tongue d) Brings tongue forwards (protrusion)
1(b), 2(d), 3(c), 4(a)
138
which nerve innervates most of the muscles of the tongue and what is the exception
* hypoglossal nerve (= CN XII) * palatoglossus -> also considered a soft palate muscle => same innervation (Vagus, CN X)
139
effects of lesion to hypoglossal nerve (= CN XII)
tongue deviation to **ipsilateral** side when sticking out tongue ## Footnote * muscle responsible for protrusion of tongue = genioglossus * does so by BOTH (L and R) muscles working tgt * thus if e.g. R hypoglossal nerve is paralysed -> R genioglossus not working -> only L pushes forward unopposed => swings tongue over to opp side
140
which parts of the oral cavity has a frenulum | hint: 3 parts!
* frenulum of **upper lip**, frenulum of **lower lip**: connects respective lip to *gingiva* -> limit movement of lip * frenulum of tongue: connects **tongue** to *floor of oral cavity* -> provide stability to tongue and support its movements ## Footnote `
141
is the anterior 2/3 and posterior 1/3 of the tongue located in the same cavity?
No * **ant** 2/3 is located in **oral** cavity * **pos** 1/3 is located in oro**pharynx**
142
what type of gland is the lacrimal gland
pure **serous** ## Footnote recall! serous = watery secretions which makes sense cos u cry water not mucous
143
Facial nerve (= CN VII) carries taste sensation from anterior 2/3 of tongue via (...), which hitchhikes through the infratemporal fossa by staying within (...). Note that it also has (...) component, and carries preganglionic fibres which travel into the (...) ganglion (parasymp), where it synapses with postganglionic fibres which then supply the (...).
Facial nerve (= CN VII) carries taste sensation from anterior 2/3 of tongue via **chorda tympani**, which hitchhikes through the infratemporal fossa by staying within **lingual nerve** (a branch of mandibular nerve (= CN V3). Note that it also has **secretomotor** component, and carries preganglionic fibres which travel into the **submandibular** ganglion (parasymp), where it synapses with postganglionic fibres which then supply the **submandibular and sublingual glands** in the floor of the mouth.
144
what are the 3 tonsils and where are each located
* *lingual* tonsil: OROpharynx, dorsal surface of **posterior 1/3 of tongue** * *palatine* tonsil: OROpharynx. **bet palatoglossal and palatopharyngeal folds** * *pharyngeal* tonsil: NASOpharynx, on posterior slope of **pharynx**
145
what does the TMJ consists of
* temporal bone: mandibular fossa and articular tubercle * mandible: condyle
146
what type of joint is the TMJ (relate to its movements) | TMJ = Temporo-Mandibular Joint
synovial modified hinge joint * hinge = depression and elevation * modified = protrusion and retraction AND lateral movement
147
The articular disc divides the TMJ into upper and lower compartments. What types of movements does each compartment facilitate? | TMJ = Temporo-Mandibular Joint
BOTH facilitate **lateral** movements but * Upper facilitates **sliding** movements (i.e. protrusion, retraction) * Lower facilitates **hinge** movements (i.e. elevation and depression)
148
which muscles are responsible for movements of TMJ joint
* muscles of mastication * suprahyoid muscles
149
Maxillary artery is the MAIN artery in the infratemporal fossa. Describe its pathway (origin + subsequent route) and branches.
* terminal branch of ECA which enters infratemporal fossa **AFTER the split at parotid gland** * gives off many **branches** while within infratemporal fossa, such as **MMA**, branches to **muscles of mastication**, **parotid gland**, etc * subsequently enters **pterygopalatine fossa**
150
where is the infratemporal fossa
* deep to **zygomatic arch** and ramus of **mandible** * anything in face at level of zygomatic arch or below
151
Which of the following ligaments is considered a 'direct' ligament of the TMJ? A) Mylohyoid groove ligament. B) Stylomandibular ligament. C) Lateral ligament. D) Sphenomandibular ligament. | ligaments help to stabilise the joint!
C) Lateral ligament * both capsular and lateral ligaments are direct ligaments * while stylo**mandibular** and spheno**mandibular** joints are **indirect** ligaments
152
Match the TMJ movement with the primary muscles involved: 1. Elevation 2. Protrusion 3. Depression 4. Retraction a) Temporalis, Masseter (anterior fibres), medial pterygoid b) Lateral pterygoid c) Masseter (posterior fibres), digastric and geniohyoid d) Gravity, digastric, geniohyoid, and mylohyoid muscles
1a), 2b), 3d), 4c)
153
what important structures does the hypoglossal nerve pass by
* ECA * and some of its branches (e.g. lingual, facial, ...)
154
which part of the oral cavity does the submandibular ducts open into
sublingual **papilla**, which is a pair of openings just **beside frenulum** of tongue
155
what are the 2 segments the oral cavity can be divided into
1. oral cavity **proper**: bet upper and lower lips, **behind teeth** 2. oral **vestibule**: bet teeth and lips + bet teeth and cheeks
156
what passage separates the oral cavity from oropharynx and what are its boundaries
oropharyngeal isthmus * superior: soft palate * inferior: posterior 1/3 of tongue * lateral: palatoglossal fold ## Footnote both the palatoglossal and palatopharyngeal folds each consists of a mucosa covering the underlying muscle!
157
what separates the anterior 2/3 of the tongue from the posterior 1/3
sulcus terminalis, which is a V-shaped groove
158
what are the 2 common sites in the pharynx where foreign objects (e.g. fishbone) commonly gets stuck
1. vallecula: space bet **epiglottis** and posterior 1/3 of **tongue** 2. piriform recess: long, vertical fold bet **laryngopharynx** and tube of **larynx**
159
what makes up the outermost layer of the eye
* sclera * cornea
160
what makes up the intermediate layer of the eye
* choroid * ciliary body <- formed by expansion of choroid * lens <- suspended from ciliary body
161
what makes up the innermost layer of the eye
retina
162
name this area and describe it
* optic disc * where optic nerve **exits** orbit
163
name these areas and describe it
* larger area: macula pinpoint area: fovea centralis * macula = area with **high concentration of cones**, responsible for **visual acuity** and **colour vision** * fovea centralis is just the area with the **HIGHEST** concentration of cons
164
The nervous layer of the retina contains 3 important cell types: (...), (...) and (...). (...) receive and transduce light energy to action potentials -> (...) which then transmit info to => (...), of which their axons will form converge to form (...)
The nervous layer of the retina contains 3 important cell types: **photoreceptors**, **bipolar** cells and **ganglion** cells. Photoreceptors receive and **transduce** light energy to action potentials -> bipolar cells **transmit info** => ganglion cells, of which their **axons** will form converge to form **optic nerve**
165
recall the actions of each intra-ocular muscle (IOM)
1. medial rectus only ABducts and lateral rectus only ADducts 2. "**SIN** *RAD*": * **S**uperior ... = **IN**torsion * ... *R* ectus (except MR and LR) = *AD* duction
166
which nerves innervate the IOM
* ALL by CN **III** (= occulomotor nerve) * except **superior oblique**, which is innervated by CN **IV** (= trochlear nerve) * and **lateral rectus**, which is innervated by CN **VI** (= abducens nerve)
167
clinical features of CN III palsy
since it innervates the majority, easier to think abt what it does NOT innervate * rest: ptosis, pupil dilation, **downward and out** affected eye * diplopia: all directions EXCEPT **lateral** gaze to **affected side** ## Footnote * ptosis bcos CN III also innervates LPS muscles * pupil dilation bcos CN III also innervates sphincter pupillae muscle
168
clinical features of CN IV palsy
* rest: **elevation** of affected eye * diplopia: worsens on **adduction** AND on head **tilt** to **affected side** ## Footnote * when eye is adducted, strongest depressor = SO ↔ when eye is abducted, strongest depressor = IR * tilting your head to one side => eye on that side intorts AND eye on other side extorts as compensatory mechanism to keep the world upright
169
clinical features of CN VI palsy
* rest: **adduction** of affected eye * movement: FAILURE of **abduction** of affected eye * diplopia: **lateral** gaze to **affected side**
170
are LPS and Müller's muscle part of the same muscle?
NO Müller's is an **extension** of LPS but they are funtionally distinct * LPS: supplied by CN **III**, *voluntary* and **complete elevation of eyelid** * Müller's: supplied by sympathetic fibres from **superior cervical ganglion**, *baseline* tone to keep eyelid **slightly elevated**
171
diff bet CN III palsy and Horner's syndrome
172
does Horner's syndrome always lead to anhidrosis
NO * 1º neuron: from hypothalamus to spinal cord → anhidrosis of both IPSILATERAL **arm and face** * 2º neuron: apex of lungs to superior cervical ganglion → anhidrosis of **face** only * 3º neuron: along ICA and into skull to eye → **NO** anhidrosis | IPSILATERAL ← no decussation in sympathetic pathway! ## Footnote recall: triad of ipsilateral ptosis, miosis, anhidrosis
173
what are the openings in the roof of the oral cavity | 3!
1. incisive fossa: carries nasopalatine nerve and sphenopalatine artery from *nasal cavity* to **anterior hard palate** 2. greater palatine foramen: carries greater palatine nerve and artery from *pterygopalatine fossa* to **posterior hard palate** 3. lesser palatine foramen: carries lesser palatine nerve and artery from *pterygopalatine fossa* to **soft palate**
174
significance of tubal elevation in nasopharynx | J-shaped elevation just posterior to soft palate
contains opening of the **eustachian tube**, which helps to communicate bet nasopharynx and middle ear
175
which epithelium(s) line the epiglottis
* surface facing oral cavity is lined by **stratified sq** epithelium <- in contact with external envt * surface facing larynx is lined by **respiratory** epithelium (pseudostratified columnar) <- in contact with air only
176
what are the 2 groups of muscles in the pharynx
* longitudinal => elevates pharynx during swallowing (-> shorten distance bolus has to travel) * circular => peristalsis ## Footnote * longitudinal musles: stylopharyngeus, salpingo-p and palato-p * circular muscles: superior, middle and inferior constrictors
177
walls of orbit
* roof: floor of **ACF** * floor: **maxilla**, *maxillary SINUS* * medial: **nasal** cavity, *ethmoidal AIR CELLS* * lateral: **temporal** fossa * posterior: **MCF** ## Footnote recap! * ACF = mainly **frontal** bone, but also lesser wing of sphenoid bone * nasal cavity includes **lacrimal** and **ethmoid** bones
178
layers of eyelid
from superficial to deep: 1. skin and connective tissue 2. orbicularis oculi 3. tarsal plate: dense fibrous connective tissue containing tarsal glands 4. conjunctiva
179
what are the conjunctiva and conjunctival fornix
clear membrane covering **sclera** and **INSIDE of eyelids**
180
what are tarsal glands (= Meibomian glands)
* modified **sebaceous** glands found in tarsal plates * produce **meibum**, an oily substance that **prevents evaporation** of eye's tear film
181
secretomotor innervation of lacrimal gland
preganglionic **parasympathetic** fibers arise from the superior salivatory **nucleus** in the pons -> travel in **CN VII (facial nerve)** -> joins with sympathetic fibres to form another nerve -> reaches **pterygopalatine ganglion** and **synapses** => joins zygomatic nerve (from **V2**) to lacrimal nerve (from **V1**) to reach the gland ## Footnote sensory innervation of the gland is by lacrimal nerve (from V1)!
182
how to differentiate bet UMN vs LMN lesions
UMN: - brisk reflexes - hypertonia LMN: - no reflexes - hypotonia - denervative changes: muscle wasting, **fasciculations**
183
You see a patient which has absent reflexes in one part of the body (e.g. biceps) but brisk reflexes in a lower part of the body (e.g.triceps, quadriceps, gastrocnemius). How is that possible?
* lesion in **spinal cord** * take out **LMN at at level** but takes out passing **UMN** also, resulting in **everything at level below lesion** having UMN signs
184
Lesions at/above which level will result in difficulty breathing. “(…), (…), (…) keeps the diaphragm alive”
C3-5 “3, 4, 5 keeps the diaphragm alive”
185
Lesions at/above which level will result in sphincteric problems “(…), (…), (…) keeps the shit off the floor”
S2-4 “2, 3, 4 keeps the shit off the floor”
186
in what type of lesion would you see glove and stocking in all 4 limbs (i.e. distal weakness which ascends)
peripheral neuropathy
187
which nerve roots is biceps jerk
C5-6
188
which nerve roots is knee jerk
L2-4 (mainly L3 and L4)
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* cervical nerves exit (above/below) cervical vertebrae * thoracic nerves exit (above/below) thoracic vertebrae * lumbar nerves exit (above/below) lumbar vertebrae * sacral nerves exit (above/below) sacral vertebrae
* cervical nerves exit **above** cervical vertebrae * thoracic nerves exit **below** thoracic vertebrae * lumbar nerves exit **below** lumbar vertebrae * sacral nerves exit **below** sacral vertebrae
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innervation of muscles in larynx
* all supplied by **RLN** * except for **cricothyroid**, which is supplied by **ELN** ## Footnote RLN = recurrent laryngeal nerve ELN = external laryngeal nerve
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what is the action of the cricothyroid muscle
contraction -> brings thyroid cartilage forwards -> **stretch/tense vocal folds** => produce **high-pitched** sounds
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do muscles of the larynx result in abduction or adduction of vocal cords ## Footnote abduction = bring vocal folds AWAY from e/o adduction = bring vocal folds TOWARDS e/o
* all help in adduction * except for posterior **cricoarytenoid**, which rotate arytenoid cartilages away from e/o, thus bring vocal folds away from e/o
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are the ears formed by bone or cartilage
* **lateral 2/3** of **external** ear is made out of **cartilage** * rest of ear (medial 1/3 of external ear + middle ear + inner ear) is made out of bone, and housed in **petrous part of temporal bone**
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arterial suppy of ears
* external and middle ear: branches of **maxillary** artery * inner ear: **labyrinthine** artery (← basilar artery) ## Footnote * branches of maxillary artery include ext auditory artery, tympanic artery, etc
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# think of a cube! relations of middle ear * roof: 1 component, 1 relation * floor: 1 relation * lateral wall: 1 component, related to 1 cavity content * medial wall: 3 components * anterior wall: 2 components * posterior wall: 2 components, 1 relation | middle ear = tympanic cavity
6 surfaces * roof: formed by petrous part of temporal bone ⇒ superior relation: cranical cavity (MCF) * floor ⇒ **inferior** relation: **IJV** * **lateral** wall: formed by **tympanic membrane** ⇒ inside cavity, **chorda tympani runs across** wall * **medial** wall: can find promontory, which carries tympanic plexus (CN IX) **oval window** and round window * **anterior** wall: can find opening of **eustachian tube** and **tensor tympani** muscle ⇒ anterior relation: **ICA** * **posterior** wall: can find opening to **mastoid air cells** and **stapedius** muscle ⇒ posterior relation: **facial** nerve (CN VII)
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components of inner ear
* cochlea * vestibular system: semicircular canals, vestibule (utricle + saccule)
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names of the 3 ossicles in middle ear
* malleus * incus * stapes
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auditory pathway: * receptors * 1º neuron * 2º neuron * 3º neuron * where it ends
* receptors: **hair** cells in **Organ of Corti** * 1º neuron: **cochlear nerve** (CN **VIII**) in **cochlear/spiral GANGLION** at *base of cochlea* * ENTERS CC through *internal acoustic meatus* * 2º neuron: **cochlear NUCLEUS** in *pontomedullary junction* (brainstem) * 3º neuron: **medial genticulate NUCLEUS** in *thalamus* * ends off at 1º auditory cortex ## Footnote bilateral representation!
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vestibular pathway: * receptors * 1º neuron * 2º neuron * 3 neuron
* receptors: **hair** cells (**maculae** in vestibule, **cristae ampullaris** in semicircular canals) * 1º neuron: **vestibular nerve** (CN **VIII**) in **vestibular (Scarpa's) GANGLION** at *base of ganglion* * ENTERS CC through *internal acoustic meatus* * 2º neuron: **vestibular NUCLEUS** in *pontomedullary junction* (brainstem) * 3º neuron: depends on which pathway (many diff pathways) ## Footnote bilateral representation!
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diff bet what receptors in vestibule vs semicircular canals sense
* vestibule: **static** equilibrium (i.e. position of head when **head and body are NOT moving**) * semicircular canals: **dynamic** equilibrium (i.e. balance when **head IS moving**, e.g. rotation of head)
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conductive hearing loss: * simple pathophysio * common causes * Rinne and Weber's tests
* sound waves are **blocked** from efficiently traveling through the **outer or middle ear** to the inner ear * mechanical obstruction (e.g. ear wax), otitis media, perforated eardrum * Rinne: **bone > air** conduction ← air conduction ends at affected outer/middle ear while bone conduction bypasses lesion Weber: **louder** at (i.e. localises to) **affected ear** ← background noise is blocked out by affected outer/middle ear
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sensorineural hearing loss: * simple pathophysio * common causes * Rinne and Weber's tests
* problem in **inner ear** or CN **VIII** * **age-related** hearing loss, **noise-related** hearing loss, tumours/infections of inner ear * Rinne: **air > bone** conduction ← both conduction ends at affected portion but air conduction benefits from amplification Weber: **louder** at (i.e. localises to) **normal ear** ← just signal in affected side ending at affected portion
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Romberg's test: * procedure * what it tests for * (+) sign
* ask patient to stand erect with **feet tgt** + **arms by side** and **eyes closed** for **1 min** * assess for **vestibular function** and **proprioception** * (+) sign: **swaying** observed ## Footnote * recall that balance requires at least 2 out of the 3 senses involved: 1) vision 2) vestibular function 3) proprioception * (+) sign = **sensory** ataxia **NOT cerebellar** ataxia which results in (-) sign as patient is unstable EVEN with eyes open
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significance of tibial tuberosity (on proximal tibia)
serves as attachment point for **patella ligament** ⇒ connects patella to tibia
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stability of knee joint: * bony factors * ligamentous factors * muscular factors
* bony factors: articular surfaces **do NOT fit nicely**: **massive femoral** condyles vs **small and shallow tibial** condyles, **shallow** articular surfaces of **femur and patella** * ligaments: medial and lateral **collateral** ligaments, **cruciate** ligaments * muscles: surrounding muscles and tendons ## Footnote articular surfaces: 1. femorotibial articulations: femoral **condyles** with tibia **condyles**, with **menisci** in between 2. femoropatellar articulations: **patellar surface** of femur with patella
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identify parts of the tibia and fibula ## Footnote recall: **TUMFLR** * **T**ibia is more **M**edial, * **F**ibula is more **L**ateral
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knee joint: * type of joint * movements * innervation (which nerves + what type)
* modified **hinge** joint * flexion/extension, medial/lateral rotation * **capsule, synovial membrane, menisci and ligaments** have innervation in terms of proprioception and **pain sensation** * innervated by **femoral, obturator, tibial and common fibular** nerves
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organisation of knee joint
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locking and unlocking of knee joint: * to lock the knee joint, *knee* has to be *fully extended* with the *foot on the ground*, then femur (...) on the tibia ("screw home" mechanism) => results in knee being stable and suited for (...) * to unlock the knee joint, (...) muscle contracts, and femur (...) on the tibia => allows (...) of knee to occur
* to lock the knee joint, *knee* has to be *fully extended* with the *foot on the ground*, then femur **medially rotates** on the tibia ("screw home" mechanism) ⇒ results in knee being stable and suited for **weight bearing** * to unlock the knee joint, **popliteus** muscle contracts, and femur **laterally rotates** on the tibia ⇒ allows **flexion** of knee to occur ## Footnote femur medially rotating on tibia = tibia externally rotating on femur
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function of collateral ligaments
* medial (tibial) collateral ligament (MCL): prevents **abduction** * lateral (fibula) collateral ligament (LCL): prevents **adduction** ## Footnote MUST UNDERSTAND THAT abduction → **tibia** moving away from midline → knee will collapse inwards as a result → medial joint space opening ⇒ MCL has to become taut and work hard to resist it
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function of cruciate ligaments
* anterior cruciate ligament (ACL): prevents **POSTERIOR displacement of femur** on tibia (= anterior movement of tibia relative to femur) and **hyperextension** of knee joint * posterior cruciate ligament (PCL): prevents **ANTERIOR displacement of femur** on tibia (= posterior movement of tibia relative to femur) and **hyperflexion** of knee joint ## Footnote think of their origins and insertions: * ACL originates at **ANTERIOR intercondylar** area of **tibia** → inserts at **POSTERIOR** part of **LATERAL femoral condyle** * PCL originates at **POSTERIOR intercondylar** area of **tibia** → inserts at **ANTERIOR** part of **medial femoral condyle** to understand extension/flexion, think of it this way! e.g. **extension** → **femur pushes tibia forward** slightly (= anterior movement of tibia relative to femur) ⇒ pulls on ACL
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tests to check integrity of cruciate ligaments
* ACL: anterior drawer test * PCL: posterior drawer test
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why does medial meniscus get torn more often
1. **medial** meniscus is firmly **fixed to tibial collateral ligament** → lesser excursion during rotatory movements (i.e. lesser movements when flex/extend knee) ⇒ more likely to be crushed or torn 2. while **lateral** meniscus is **separated from fibular collateral ligament** by **popliteus** muscle AND **popliteus pulls** lateral meniscus **backwards** ⇒ preventing crushing bet articular surfaces 3. **medial** meniscus is **broader at the back** while lateral meniscus is more circular
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unhappy triad: * when does it occur * what ligaments does it involve
* foot is planted, **knee** is slightly **flexed**, external rotation of tibia, boom **valgus force** (i.e. abduction of knee joint) applied **to lateral knee** * ligaments: 1. **MCL**: bcos of overabduction of knee joint 2. **ACL** 3. **medial meniscus**: bcos firmly attached to MCL
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muscles in anterior compartment of thigh and their function(s) and innervation
* **hip FLEXORS**: 1. iliacus: innervated by *femoral* nerve 2. **psoas major**: innervated directly by anterior rami of **L1-L4** * **knee EXTENSORS**: all innervated by *femoral* nerve 1. vastus medialis 2. vastus intermedius 3. vastus lateralis 4. **rectus femoris**: also doubles up as **hip flexor** * weirdo: 1. **sartorius**: **knee AND hip FLEXOR**, innervated by *femoral* nerve ## Footnote * hip flexors collectively known as iliopsoas * knee extensors collectively known as quadriceps femoris "the quads" * superficial to deep: sartorius, rectus femoris, rest of quadriceps femoris (vastus ...), iliopsoas
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muscles in posterior compartment of thigh and their function(s) and innervation
**hip EXTENSOR** and **knee FLEXOR** * semimembranosus and semitendinosus: innervated by **tibial portion of sciatic nerve** * bicep femoris (short and long head): **long head** innervated by **tibial portion of sciatic nerve**, **short head** innervated by **common fibular portion of sciatic nerve** ## Footnote collectively known as hamstring muscles
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origin of hamstring muscles | 1 exception!
* ischial tuberosity * except short head of biceps femoris, which originates from **linea aspera**
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pes anserinus: * what is it * where is it * clinical significance
* shared **insertion** point just **below medial condyle** of **tibia** * for **tendons** of these 3 muscles: **sartorius, gracilis and semitendinosus** * pathologies (e.g. bursitis) can **mimic MCL/medial meniscus** pain ← MCL lies just deep to it
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femoral triangle: * boundaries * contents (from lateral → medial)
* superior: inguinal ligament medial: adductor longus lateral: sartorius * femoral **N**erve, femoral **A**rtery, femoral **V**ein ## Footnote * **most medial** actually is femoral **canal**, which is lymphatic vessels and inguinal lymph nodes * artery, vein and canal are actually in a femoral **sheath**
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ankle joint: * type of joint * movements * articular surfaces
* synovial **hinge** joint * *flexion* (= *plantar*flexion) / *extension* (= *dorsi*flexion) * distal end of **tibia** and **fibula** with **trochlea of talus** ## Footnote * the part of the tibia and fibula involved is also known as tibiofibular mortise * TMI, but posterior tibiofibular ligament is also actually part of the articular surface
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stability of ankle joint: * bony factors * ligamentous factors * muscular factors
* bony factors: tibiofibular mortise and pulley shaped trochlea of talus are fairly **congruent** * ligaments: 1. medial and lateral **collateral** ligaments, 2. **syndesmosis**, particularly the inferior transverse tibiofibular ligament * muscles: muscles surrounding the ankle which attach to bones of the foot ## Footnote ITTFL **deepens** the ankle mortise **posteriorly** and **prevents posterior translation** of the talus ⇒ contributes to stability of ankle joint
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joints bet tibia and fibula | 3!
* TOP: proximal tibiofibular joint, which is a** synovial plane** joint, consisting of head of fibula articulating with lateral condyle of tibia * MIDDLE: **interosseous membrane** * BOTTOM: tibiofibular **syndesmosis**, which is a **fibrous** joint consisting of tibiofibular ligaments (AITFL, PITFL, ITTFL) and interosseous ligament, and contributes to **stability of ankle joint**
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subtalar joint (= talocalcaneal joint): * articular surfaces * movements
* inferior surface of **talus** with superior surface of **calcaneus** * **inversion** (= **sole** of foot faces **inwards**) / **eversion** (= **sole** of foot faces **outwards**)
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muscles in anterior compartment of leg and their function(s) and innervation
**dorsiflexors**, innervated by **DEEP peroneal** nerve "**Tom, Dick, Harry ... and Terry**" * **T**ibialis anterior: **inverts** foot * extensor **D**igitorum longus: extends 2nd-5th toes * extensor **H**allucis longus: extends big toe * fibularis/peroneus **TER**tius: **everts** foot ## Footnote * **dorsi**flexion = **extension** of ankle joint * MAIN dorsiflexor = tibialis anterior
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muscles on dorsum of foot and their function and innervation | just name 1!
**extensor** *digitorum* brevis * **extends** *toes* * innervated by DEEP peroneal nerve
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muscles in lateral compartment of leg and their function(s) and innervation
responsible for **eversion of foot** (and minorly **plantarflexion**), innervated by **SUPERFICIAL peroneal** nerve * fibularis/peroneus longus * fibularis/peroneus brevis ## Footnote note: tendons of these muscles run **posterior** to lateral malleolus
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muscles in posterior compartment of leg and their function(s) and innervation ## Footnote can be divided into 2 groups: superficial and deep
**plantarflexors**, innervated by **tibial** nerve * superficial 1. gastrocnemius: plantarflexes when **leg is straight**, **flexes knee** 2. soleus: plantarflexes when **leg is bent** 3. plantaris * deep 1. popliteus: **NOT** involved in **plantarflexion**, just unlocks knee 2. flexor hallucis longus: flexes big toe 3. tibialis posterior: also **inverts** foot 4. flexor digitorum longus: flexes 2nd-5th toes ## Footnote for deep muscles in posterior compartment, almost same as muscles in anterior compartment, * "Tom, Dick, Harry ... and Terry" → "Tom, Dick, Harry ... and Pops" * tibialis anterior inverts foot → tibialis posterior inverts foot
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what is the Knot of Henry
* **FDL** starts medially and ends laterally while **FHL** starts laterally and ends medially ⇒ point of **crossover** is Knot of Henry * allows **big toe** (FHL), which is the **primary propulsive** digit, to **distribute force to lateral toes** (via FDL) → enabling **coordinated push-off and stability** across the whole foot
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triceps surae * muscles it consists of * insertion * actions * consequences of rupture
* gastrocnemius and soleus * insert at posterior surface of calcaneus via their **common tendon** — **calcaneal (Achilles)** tendon * majority of **plantarflexion** force * rupture (e.g. Achilles rupture due to sudden strong pull) can result in loss of plantarflexion ⇒ cannot **stand on tiptoe** AND **gait** impaired (as cannot propel body forward)
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low ankle sprain: * usually an (...) injury, involving a sprain of the (...) ligaments * symptoms: pain at (...) ankle, (...) * signs: +ve (...) test * treatment: 1. acute pain relief 2. (...) 3. strengthen, esp (...) muscles 4. (...)
* usually an **inversion** injury, involving a sprain of the **lateral** ligaments (commonly ATFL) * symptoms: pain at **lateral** ankle, **swelling** * will see +ve **anterior drawer** test * treatment: 1. acute pain relief 2. restore **ROM** ⇒ prevents stiffness 3. strengthen, esp **evertor** muscles as strain was likely due to **weak evertors** AND evertors need to **take over ligament function** post-strain 4. **proprioception** exercises (e.g. balance exercises) → retrains **neuromuscular control** after ligament injury ⇒ prevents recurrence ## Footnote * anterior drawer test of ANKLE: (+) test indicates excessive anterior translation of **talus** relative to **tibia** ⇒ **AFTL tear/laxity**
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high ankle sprain: * usually an (...) injury, involving a sprain of the (...) * symptoms: pain at (...) ankle, (...) * treatment: 1. (...) required 2. may require surgery
* usually an **eversion** injury, involving a sprain of the tibiofibular **syndesmosis** (commonly AITFL) * symptoms: pain at **SUPERIOR lateral** ankle, **NO swelling** * treatment: 1. **offloading** required 2. may require surgery
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ankle jerk: * how to elicit reflex * results in contraction of which muscle * giving rise to which action * root levels, plexus and nerve tested
* tap **calcaneal** (Achilles) tendon * contraction of **triceps surae** * resulting in **plantarflexion** * **S1-S2**, lumbosacral plexus, **tibial** nerve ## Footnote * recall: triceps surae consists of gastrocnemius and soleus muscles * sciatic nerve has root values of L4-S3
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knee jerk: * how to elicit reflex * results in contraction of which muscle * giving rise to which action * root levels, plexus and nerve tested
* tap **ligamentum patellae** * contraction of **quadriceps femoris** muscle * resulting in **extension of knee** joint * **L2-L4**, lumbosacral pelis, **femoral** nerve ## Footnote ligamentum patellae is BELOW the patella! the one about the patella is quadriceps tendon
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common causes of compartment syndrome
* acute: **fractures**, reperfusion injury, external compression, bleeding disorders * chronic: repetitive high-impact **activity** ## Footnote chronic: results in exercise-induced **increased muscle volume** that fascia cannot accommodate
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pathophysiology of compartment syndrome
* **muscle groups** are enclosed by inelastic fascia and thus **cannot expand** * pressure INSIDE compartment increase → **compartment pressure >> perfusion pressure** → ischaemia of muscles and nerves → which then results in **endothelial damage** → more **oedema** → **higher compartment pressure** → worse **ischaemia** ⇒ **positive feedback loop**
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signs and symptoms of compartment syndrome
* early signs: pain **out of proportion**, pain on **passive stretch** of affected compartment * late signs: "6 Ps" 1. pain out of proportion 2. paresthesia (= tingling and numbness) 3. paralysis 4. pallor 5. poikilothermia (= cool limb) 6. pulselessness ## Footnote late signs: * (2) and (3) are due to nerve ischaemia * (4), (5) and (6) are due to compression on arteries
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how to distinguish bet shortening affecting soleus vs affecting gastrocnemius ## Footnote context: * injury to triceps surae → fibrosis ⇒ shortening / contracture of 1 or both muscles * shortening **restricts opposite movements** of muscles ⇒ usually tested via opposite actions
* **gastrocnemius crosses BOTH knee and ankle joints** while soleus only crosses ankle joint * **dorsiflexion** (opp action) when **KNEE IS BENT** tests ONLY **soleus** ← **gastrocnemius** is **slackened**
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which part of gluteus maximus should you administer an intramuscular injection at?
**upper outer** quadrant in order to **avoid sciatic nerve**, which runs diagonally (downwards, medially -> laterally) right under gluteus maximus
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functional loss due to injury of sciatic nerve: * motor * sensory
* motor: 1. paralysis of hamstrings ⇒ NO hip extension but **weak flexion of knee** 2. paralysis of all muscles below knee ⇒ NO dorsiflexion/plantarflexion of foot, inversion/eversion of foot. moving of toes AND **footdrop** * sensory: loss of sensation **below knee** EXCEPT medial side of leg and medial border of foot up to ball of big toe ## Footnote * all hamstring muscles carry out hip extension **AND knee flexion**, weird muscle in anterior compartment (**sartorius**) carries out hip flexion **AND knee flexion**, weird muscle in medial compartment (**gracilis**) carries out hip adduction **AND knee flexion**, THUS weak flexion of knee possible * footdrop occurs due to **weight of foot** and **gravity** * medial side ... still has sensory innervation as they are supplied by **saphenous** nerve (← branch of femoral nerve) * common causes of injury to sciatic nerve: 1. IM injection at wrong site of gluteus maximus 2. posterior dislocation of hip joint
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functional loss due to injury of common fibular/peroneal nerve
* motor: paralysis of all muscles in anterior and lateral compartments of leg → unopposed actions of opposing muscles ⇒ plantarflexion of foot (**foot drop**) and **inversion** of foot * sensory: loss of sensation over **lateral side of leg** and **dorsum of foot and toes** EXCEPT medial border of foot up to ball of big toe and **lateral border** of foot ## Footnote * medial border of foot up to ball of big toe is innervated by saphenous nerve ← femoral nerve * lateral border of foot is innervated by sural nerve ← common fibular AND tibial nerve * common cause of injury to common fibular/peroneal nerve: fracture (or other injuries) at upper end of fibula
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how does body discourage formation of varicose veins
**perforating veins** connect superficial and deep veins → **valves** in them results in blood flowing in only 1 direction (**superficial vein -> deep vein**) → discourage **pooling** of blood **in superficial** veins ⇒ prevent **dilatation **of superficial veins (i.e. varicosity)
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causes of varicose veins | have both pathological and physiological! ## Footnote think in terms of: 1) superficial veins 2) perforating veins 3) deep veins
* superficial veins: **congenital weakness** of venous WALL * perforating veins: **incompetency** of venous **valves** ⇒ blood flowing in opp directioin * deep veins: **obstruction of deep** veins → prevents upwards flow of blood → **increased pressure** of **deep** veins ⇒ **pressure transmitted** to superficial veins a) physiological: **pregnancy** (baby compresses deep veins) b) pathological: **tumours**, DVT, ...
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treatment for varicose veins
2 diff treatments for 2 diff phases * **chronic** varicose veins: polidocanol * **acute** bout of **inflammation** in **pre-existing** varicose veins: mucopolysaccharide polysulphate
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MOA of polidocanol
"basically destroying veins so that better blood pathways can be used" * induce **endothelial damage** -> inflammation and fibrosis * formation of **thrombus** within vein -> ischaemia -> fibrosis and sclerosis => **obliteration of vessel**
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A/Es of polidocanol
* MAIN: **thromboembolism** * "allergic" side effects: e.g. redness, pruritus. anaphylaxis
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MOA of mucopolysaccharide polysulphate
* **anti-thrombotic** * *anti-inflammatory* * improves *microcirculation* * *analgesic* * fibroblast modulation ## Footnote * think abt the **cause** of the inflammation (could be **formation of thrombus**) AND the cardinal *signs* of acute *inflammation* (redness, *swelling*, warmth, *pain*, loss of fn) * fibroblast modulation = influence fibroblasts to take on anti-inflammatory role (instead of pro-inflammatory)
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A/Es of mucopolysaccharide polysulphate
* "allergic" side effects: mild skin irritation, contact dermatitis, hypersensitivity
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Which nerve provides sensory innervation for each of the following: 1. Ear 2. Nasal cavity 3. Nose 4. Parotid 5. TMJ joint
1. V3 2. V2 3. V1 4. V3 5. V3
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A specific modality of a specific tract has their **1st order neuron** in a sensory **nucleus** instead of a ganglion. Which one is it?
* **trigeminothalamic** tract (proprioception) * 1st orer neuron found in **mesencephalic** NUCLEUS instead of trigeminal ganglion
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3 soft palate muscles have the same function of depressing the soft palate. What is their difference in function? ## Footnote hint: tensor palatini, palatopharyngeus, palatoglossus
* palatoglossus: depresses soft palate (and elevate tongue) → **closing oropharyngeal isthmus** ⇒ sealing oral cavity during **chewing** * tensor palatini: tenses and depresses soft palate ⇒ **pushing bolus** backwards during **swallowing** * palatopharyngeus: depresses soft palate and elevates pharynx ⇒ **further propulsion of bolus** during **swallowing**
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which muscle is responsible for blinking ## Footnote hint: muscle of facial expression!
orbicularis oculi ## Footnote to be exact, it is the **palpebral** part of OO which gently closes eyelids for **blinking** while **orbital** part is the outer portion that **tightly closes** the eyelids
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lesion in which area would result in homonymous hemianopia w/ macular sparing AND what is the cause
* **1º visual cortex** (in occipital lobe) * **PCA** infarct ← macula spared due to **dual blood supply (PCA + MCA)**
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what is the minimum and maximum score you can get on the glasgow coma score (GCS): * components * minimum score * max score * cutoff for concern ## Footnote 3 components: 1) eye-opening response 2) verbal response 3) motor response
* **E**ye-opening response (4), **V**erbal response (5), **M**otor response (6) * min: **3** (= no eye-opening response, no verbal response and no motor response) * max: **15** (= spontaneous eye-opening response, orientated verbal response and obeying commmands) * cutoff for concern is **< 12** | min is NOT 0!
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clinical features of stroke affecting the **cerebellum** | hint: **DDAS**H**ING**
* **D**ysdiadochokinesia * **D**ysmetria * **A**taxia (ipsilateral) * **S**canning / Staccato speech * **I**ntention tremor (= tremor that worsens as **target is approached**) * **N**ystagmus (= rhythmic, uncontrolled eye movements(esp gaze-invoked)) * **G**ait disturbance (= **broad-based**, unsteady, drunk-like gait)
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cause and types of syncope
* cause: cerebral **HYPOPERFUSION** * types: a) **NEUROgenic** 1. **vasovagal**: (where increased vagal tone → bradycardia + vasodilation) **hot, closed, crowded** areas w/ poor ventilation, prolonged **standing**, **painful** stimuli, **fear** or **shock** 2. reflex-mediated **situational** syncope: increased vagal stimulation due to e.g **straining (micturition/defecation)** 3. **orthostatic**: occurs **upon becoming upright** b) **CARDIOgenic**: (where there is sudden reduction in cardiac output) cardiac **arrhythmias**, cardiac **defects** and **cardiomyopathy** ## Footnote hypoglycaemia ≠ cause of syncope since it does NOT cause cerebral hypoperfusion!
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features of syncope vs seizure
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investigations for syncope
* **postural BP** measurement ⇒ to rule out **orthostatic** syncope * **ECG** ⇒ to rule out **cardiogenic** syncope
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is seizure = epilepsy?
NO * seizure: results from an **acute** systemic metabolic disturbance, or an **acute** disturbance of brain structure or metabolism * epilepsy: **chronic** condition characterised by a predisposition to **recurrent**, usually spontaneous **seizures**
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what investigation can you use for neuropathies | e.g. bet demyelinating and axonal neuropathies
nerve conduction study * involves stimulating nerve at 1 point and measuring response at another point ⇒ measure **velocity** and **amplitude** of signal * **demyelinating** (e.g. GBS): decreased **velocity** (← myelin = insulation for fast conduction) * **axonal** (e.g. diabetic neuropathy): decreased **amplitude** (← axon loss = fewer signals transmitted)
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what is the key feature of **poly**neuropathy | also known as **peripheral** neuropathy
**glove and stocking** pattern, where **distal** nerves are affected **before proximal** ones
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pathophysiology of GBS
**molecular mimicry**! **C. jejuni** proteins resemble **axolemma** → cross-reactive **antibodies** ⇒ immune-mediated segmental **demyelination** and axonal degeneration ## Footnote axolemma = plasma membrane of axon
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what is a serious consequence of GBS
**Type II resp failure** cos GBS results in demyelination of muscles needed for respiration → hypoventilation ⇒ **CO2** builds up ## Footnote type **II** cos **high CO2** but normal (or low) O₂
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why can't patients with GBS lie flat
weak **diaphragm** → **lying down** will result in **abdominal contents compressing** diaphragm ⇒ **breathless** (esp since **NO accessory muscles** to compensate) ## Footnote * diaphragm affected ← demyelination of phrenic nerve * accessory muscles affected ← demyelination of nerves supplying them
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clinical features of GBS
* ASCENDING **numbness** * ASCENDING **flaccid paralysis** later on * **NO muscle wasting** ← too **acute**
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clinical features of Charcot-Marie-Tooth disease
* DISTAL **sensory loss** * foot drop, pes cavus and hammer toes (← DISTAL **motor** loss) * DISTAL **muscle wasting** ("inverted champagne bottle legs") ← very **chronic** ## Footnote * leg: **dorsiflexors** and *evertors* tend to be affected first ⇒ **foot drop** and *pes cavus (= high arches)* * foot: **intrinsic mucles (interossei, lumbricals**) affected before extrinsic muscles (mainly FDL and FHL) ⇒ **hammer toes** (= hyperextension of metatarsophalangeal joints and flexion of PIP joints)
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what maneouvre can be done to accentuate tendon reflex
we all know to get patient to **clench their teeth**, and flex both sets of fingers into a **hook-like** form, and **interlock those sets of fingers** together... but what is this called? **JENDRASSIK** maneouvre
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features of myopathies: * what kind of weakness? (motor/sensory/both) * where is the weakness? * reflexes? * any abnormal labs
* **motor** weakness ONLY * **proximal** > distal weakness * **normal reflexes** * **increased creatine kinase** levels ← **breakdown of muscle membrane** results in **release** of CK from muscle cells
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what investigation can you use for myopathies
**electromyography** (EMG) * records electrical activity of **muscles**
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pathophysiology of myasthenia gravis | NMJ pathology
**AUTOantibodies** bind to **postsynaptic** nicotinic ACh receptors (**AChRs**) → **competitive inhibition** of ACh binding, AChR **internalisation** and **complement activation** resulting in **damage** to postsynaptic membrane and muscle fibres themselves → poor **neuromuscular transmission** ⇒ **FATIGABLE skeletal muscle weakness**
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clinical features of myasthenia gravis
* HALLMARK: **fatigable weakness** (worsens w/ **repeated activity**, and at **end of day** — diurnal variation) * **ocular**: ptosis (asymmetric), diplopia * **bulbar**: dysphagia, dysarthria * **respiratory** weakness (during MG **crisis**) * **PROXIMAL** *limb* **weakness** ## Footnote NO **sensory** loss NORMAL **reflexes**
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investigations for myasthenia gravis
* anti-**AChR** antibodies * **repetitive nerve stimulation** test: decremental response seen
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what condition is myasthenia gravis commonly associated with
thymoma
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how does pyridostigmine help in management of myasthenia gravis
**inhibits acetylcholinesterases** (AChE) → increased **conc of AC**h at NMJ → increased **neuromuscular transmission** ⇒ **symptom** control
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pathophysiology of Duchenne Muscular Dystrophy (DMD)
**X**-linked mutation → **absence of dystrophin** (dystrophin usually links actin to ECM, thus making muscle fibre structurally stable) → **sarcolemma** becomes **vulnerable during contraction** → micro **tears** → **muscle fibre necrosis** and subsequently being **replaced by fat and connective tissue** ⇒ **weakness** AND **pseudoHYPERtrophy** ## Footnote * DMD is a XL**R** disorder * sarcolemma = **membrane** of a muscle fibre
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clinical features of Duchenne Muscular Dystrophy
* **PROXIMAL weakness** (starting from *pelvic girdle*) => (+) **Trendelenburg** sign, lumbar loidosis, **Gowers** sign * **cardiac** involvement ## Footnote Gowers sign = pushing up along thighs to stand
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clinical features of dermatomyositis
* symmetrical **PROXIMAL weakness** * **skin** manifestations: heliotrope rash, gottron papules, shawl / V-sign ← **dermal vessels** are also attacked * **perifascicular atrophy** ← **outer edges** of muscle fascicles are poorly perfused, resulting in **ischemia** and thus **atrophy** ## Footnote pathophysiology: **AUTOantibodies** attack **capillaries and arterioles** supplying muscles
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what is the most common brain tumour
**METASTASES** (i.e. 2º brain tumour) ## Footnote but otherwise most commo 1º brain tumours are meningiomas and gliomas
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common brain tumours in children ## Footnote 1 from almost every component of brain (EXCEPT meninges): *ventricles*, *midline structures*, brain parenchyma (*neurons* and *glial cells*)
* **ependymoma**: from ependymal cells lining *ventricles* * *germ cell tumours*: from primitive germ cells that migrate along the body's *midline* during fetal developmen * medulloblastoma: immature *neurons* in cerebellum * **pilocytic astrocytoma**: from *astrocytes*
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# CNS tumours meningioma * gross and histo appearance * associations
* gross: **whorled** cut surface histo: **whorl** formation * associated with **children**, associated w/ **NF-2** syndrome
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# **ventricular** brain tumour histological features of ependymoma
* rosettes * pseudorosettes
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other than pituitary adenoma, what is one other pituitary tumour? (name + gross appearance)
craniopharyngioma * formed from embryonal remnants * contains yellow, viscou fluid resembling **'engine oil'**
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# immature neuronal tumour medulloblastoma: * brain region affected * histo * association
* affects **cerebellum** * **sheets** of **small round blue** cells, "**carrot** shaped" nuclei, rosettes * associated w/ **children** ## Footnote * histo: 1. similar to **medullary** IDC (breast cancer) which also has tumour cells arranged in **sheets** 2. must NOT confuse w/ **Ewing** sarcoma, which also has **small round uniform blue** cells * in contrast, **mature** neuronal tumours (e.g. central neurocytoma) are associated w/**adults**
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why is genetic profile important in brain tumours involving glial cells ## Footnote glial cells = supporting cells in CNS includes astrocytes, microglia and oligodendrocytes
* **IDH** mutation determines **prognosis** * IDH **mutant** > wild type
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glioblastoma: * IDH mutation? * gross appearance * histological features
* IDH **wild-type** => **very poor** mean survival * gross: haemorrhage, *necrosis* * histo: **palisading** *necrosis*, microvascular proliferation
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oligodendroglioma: * mutation (hint: not IDH!) * histological feature
* whole arm **deletion** of **1p** and **19q** in **chromosomes** => responsive to **chemotherapy** * histo: uniformed round cells with **'FRIED EGG'** appearance
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what are the inheritance patterns for these neurocutaneous syndromes, NF1, NF2, tuberous sclerosis and Von Hippel-Lindau syndrome?
all **AD**
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Bilateral vestibular schwannomas are characteristic of: A. NF1 B. NF2 C. VHL D. Tuberous sclerosis E. Ataxia telangiectasia
B. NF2 | recall: schwannomas are **benign**! ## Footnote NF2 also associated with other neural tumours like **meningioma** while NF1 is more associated ith neural tumours like **neurofibroma**
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Which neurocutaneous syndrome carries a high risk of renal angiomyolipomas? A. NF1 B. NF2 C. VHL D. Tuberous sclerosis E. Sturge–Weber
D. Tuberous sclerosis ## Footnote other clinical features of TS are * **cortical tubers** in the brain * **SKIN lesions**: Shagreen patch, Ungual fibromas, Ash leaf patches
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Multiple renal, pancreatic, and adrenal cysts are most associated with: A. NF1 B. NF2 C. Tuberous sclerosis D. VHL E. Ataxia telangiectasia
D. VHL ## Footnote other clinical features of VHL are * haemangioblastomas (usually retinal) * renal cell carcinoma * pheochromocytoma * endolymphatic sac tumour (in inner ear)
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how can **cerebral** tuberculosis present itself | 2 ways!
a) tuberculous **meningitis** - involves **base of brain** - eventually lead to tuberculoma formation, seen GROSSLY as **white granules** b) **tuberculoma**: - from infection of brain parenchyma - seen as a **ring-enhancing lesion** on IMAGING
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most common congenital CNS **malformation**
spina bifida
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relations of parotid gland: * anterior * posterior * medial * lateral
* anterior (superficial -> deep): masseter, ramus of mandible, medial pterygoid * posterior (superficial -> deep): **SCM**, mastoid process, **digastric muscle**, styloid process * medial: styloid process * lateral: skin, superficial fascia (containing platysma)
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contents of parotid gland (superficial -> deep) | 3!
**N**e**VA** * facial **N**erve * RETROMANDIBULAR **V**ein * EC**A** and its terminal branches
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signs of Parkinsonism
TRAP * (resting) **T**remor * (lead pipe) **R**igidity * **A**kinesia * **P**ostural instability ## Footnote * can also have pill-rolling tremor, which is a type of resting tremor. and looks like a rhythmic, circular motion of rolling a small object, like a pill, between the thumb and forefinger * understand that dopamine: a) activates the direct pathway → facilitates movement b) Inhibits the indirect pathway → suppresses unwanted inhibition → excessive inhibition without dopamine → weak postural reflexes → body cannot realign quickly ⇒ imbalance
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how does bradykinesia present in a patient with parkinsonism | hint: face, upper limb lower limb!
* face: **hypomimia** (mask-like facial expression), paucity of blinking, hypophonia * upper limb: **decremental** bradykinesia (reduced **arm swing** when walking, **micrographia**) * lower limb: **shuffling/festinant gait**, turning in numbers ## Footnote decremental = decrease in amplitude and frequency w/ repeated movements
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rigidity in Parkinsonism vs UMN lesions
* Parkinsonism: **lead pipe** rigidity, where resistance is the **same regardless of joint position** * UMN rigidity: **clasp knife** rigidity, where resistance **varies** depending on joint position, with there being a sudden release of resistance towards the end ## Footnote notr: cogwheel rigidity = lead pipe rigidity + tremor
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what type of posture do you observe on inspection in UMN lesions
**pyramidal** * normal: corticospinal tract (**pyramidal**) **inhibits** reflexes and tone while **extrapyramidal** tracts **increase** tone * **corticospinal tract damaged** in UMN lesion → extrapyramidal tracts are now **unopposed** → **increased tone** (esp in flexors in UL and extensors in LL) and **overactive stetch reflex** ⇒ **involuntary** muscle **contractions** (= spasticity) ## Footnote **increased tone** in flexors in UL and extensors in LL => pyramidal pattern of weakness (**UL flexed** posture + **LL extended** posture) * can think of it as "anti-gravity" muscles are stronger and thus not as weak when lesion occurs, since: a) flexors in UL raise forearm and hand against gravity b) extensors in LL help you get up from sitting/squating position
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parkinsonism caused by **toxins**: * caused by anti-(...) agents, such as (...) and (...) * tends to have more (...symmetrical/asymmetrical...) involvement initially
* caused by anti-**dopaminergic** agents, such as **antipsychotics** (e.g. haloperidol, risperidone) and **metoclopramide** (anti-emetic) * tends to have more **symmetrical** involvement
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what is a possible **metabolic** cause of parkinsonism
**Wilson**'s disease * **AR** disease * **defect** in biliary **copper excretion** → **deposition** of copper in **basal ganglia** ⇒ parkinsonism ## Footnote * could also have deposition in: 1) **liver** ⇒ cirrhosis 2) eyes ⇒ **Kayser Fleischer rings** * diagnoised via 1) low levels of **caeruloplasmin** (copper transporter) 2) high **urinary** levels of **copper** * treatment: **penicillamine** → sequesters copper for **urinary excretion**
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what kind of presentation does **idiopathic** parkinson's disease have initially? symmetrical or asymmetrical?
more **asymmetrical**
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# sen what are the symptoms of idiopathic parkinson's disease
* motor symptoms: resting **T**remor, lead pipe **R**igidity, bradykinesia (**A**kinesia) * mood/psychiatry: **depression** and psychiatric symptoms (e.g. psychosis, hallucination) * cognition: cognitive impairment/deficits (e.g. dementia) * sleep/fatigue: severe fatigue, insomnia, excessive daytime sleepiness * autonomic: dysautonomia, **constipation**, sialorrhoea, **postural hypotension** * others: **anosmia**, pain ## Footnote general timeline of symptoms: 1. **anosmia** 2. **motor** symptoms 3. non-motor symptoms (e.g. autonomic symptoms)
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treatment for idiopathic PD and rationale
**L**-DOPA w/ DOPA **decarboxylase inhibitor** * principle: to address **dopamine deficit** * L-DOPA used instead of dopamine as dopamine is **too large** to cross the **BBB** → will **remain in circulation** ⇒ **ineffective**, as well as create various **side effects** * DOPA decarboxylase inhibitor (e.g. **carbidopa**) used to inhibit DOPA decarboxylase and **prevent L-DOPA conversion** while it is still **periphery** ← works as **inhibitor** is **too large** to cross **BBB**, and thus **canot follow L-DOPA** into brain and prevent its conversion in CNS ## Footnote side effects include positive inotrope and chonotrope effects on heart, effects on BP and effects on kidney
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is L-DOPA + carbidopa (= DOPA decarboxylase inhibitor) the **1st-line** treatment option in **young** patients with PD
NO! **alternative** agents (e.g. **dopamine agonists**) are preferred as the **efficacy** of L-DOPA + carbidopa **diminishes over time** and thus should be saved for when there is no choice
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dementia vs mild cognitive impairment (MCI)
both involve cognitive impairment but **ADLs** are affected in **dementia**
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what are the 2 most common causes of dementia
1. **Alzheimer**'s disease — most most common! 2. **vascular** dementia: caused by multiple strokes (multi-infarct dementia) or chronic small vessel disease
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what imaging can be done to find out the cause of dementia
**MRI** * Alzheimer's: **atrophy** of medial temporal lobe * vascular: white matter **hyperdensities** ## Footnote note: white matter, not grey matter! white matter (deeper, inner part of brain) is supplied by **small vessels** (e.g. lenticulostriate arteries) ↔ most common cause odf dementia is chronic **small vessel** disease
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primary headache: * cause? * common types: 1. (...): **most common**, often in **females**; (...uni/bilateral...); associated with **nausea and vomiting**, (...), (...), (...) 2. (...): (...uni/bilateral...); **tight band** around head 3. (...): affects **males** more; associated with (...)
* **NO** underlying cause * common types: 1. MIGRAINE: **most common**, often in **females**; **unilateral**; associated with nausea and vomiting, **photophobia, phonophobia, aura** 2. TENSION: **bilateral**; **tight band** around head 3. CLUSTER: affects **males** more; associated with **IPSILATERAL autonomic** symptoms (e.g. tearing, nasal congestion, ptosis, miosis) ## Footnote miosis = **CONSTRICTED** pupil while mydriasis = dilated pupil
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features of temporal/giant cell arteritis: * patient grp? (hint: part of SNOOP10) * accompanying features: 1. (...) 2. associated with (...) * complications if untreated
* **new onset** headache in **elderly** * accompanying features: 1. **temporal** tenderness / **jaw** claudication 2. associated with **polymyalgia rheumatica** * complications: **BILATERAL blindness** ## Footnote * jaw claudication = pain and fatigue in the jaw muscles during chewing, which resolves with rest * definitive test: temporal ARTERY biopsy * treatment: high dose **steroids**
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what condition is saccular (berry) aneurysm associated with? | unexpected LOL
autosomal dominant polycystic kidney disease (ADPKD)
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treatment for meningitis
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differentials of thunderclap headache (3) and how to tell them apart
* SAH * cerebral VENOUS sinus THROMBOSIS: may present with **seizures**; risk factors: **coagulation** disorders, **pregnancy**, **OCP**; diagnosis: CT/MR **venography** where **empty delta sign** is seen due to **filling defect** * carotid artery DISSECTION: may present with **tearing neck pain** and **Horner's** syndrome ## Footnote in this Horner's syndrome, NO anhidrosis
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definition of anxiety vs Generalised Anxiety Disorder (GAD)
* anxiety: response to **ANTICIPATED threat** * GAD: **excessive, uncontrollable** worry which interferes w/ **daily functioning**, and is present for **at least 6 months**
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general principles for effects of CNS depressants: * low dose * high dose * even higher doses
* low dose: **anxiolytic** and **sedative** effects * high dose: **hypnotic** effects * even higher doses: **anaesthetic** effects ## Footnote * sedative = **relaxed** * hypnotic = **drowsy**, sleepy
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what kind of symptoms are seen in schizophrenia
* **positive** symptoms (= **added** abnormal stuff): delusions, hallucinations, ... * **negative** symptoms (= **subtracted** normal stuff): withdrawal from social interactions, flattening of emotional responses, ... * anxiety/depression * aggression * cognitive symptoms ## Footnote comparing positive vs negative symptoms, **(-)** symptoms are generally **more dominant**
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If **benzodiazepines** are taken with alcohol, patients can experience ACUTE TOXICITY/OVERDOSE and RESPIRATORY DEPRESSION. What can we treat this with?
flum**AZE***NIL* ("think of it as *NO MORE* benzodi**AZE**pines") * benzodiazepine receptor **antagonist**
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give examples for diff classes of benzodiazepines: * short acting * intermediate acting * long acting ## Footnote recall that benzodi**AZE**pines in general all have "**AZE**" (or "AZO") in their names
"*T*o*M* the *LO*nely *CAT* from *DC F*ilms" * short acting: 1. *T*ri**azo**lam 2. *M*id**azo**lam * intermediate acting: 1. *L*or**aze**pam 2. *O*x**aze**pam 3. *C*lon**aze**pam 4. *A*lpr**azo**lam 5. *T*em**aze**pam * long acting: 1. *D*i**aze**pam 2. *C*hlorodi**aze**poroxide 3. *F*lur**aze**pam
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symptoms of benzodiazepine withdrawal
* disturbed sleep * rebound anxiety * tremor/convulsions
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which specific drug should be used for Peripheral Artery Disease (PAD)
**pentoxifylline** * MOA: 1. **platelet aggregation** AND reduce **blood viscocity** AND improve **deformability of RBCs** 2. non-selective **PDE** inhibitor and **adenosine 2** receptor antagonist → reduce **platelet adhesion and aggregation** AND prevent **vasoconstriction** + promote **vasodilation** ## Footnote ALL IN ALL they help to **improve blood flow**
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revise pharmacological management of DVT
ANTICOAGULANTS 1st — monotherapy using Direct Oral Anticoagulants (DOACs): * rivaro**xa**ban or api**xa**ban * Factor **Xa** inhibition → ↓ thrombin generation ⇒ prevents clot growth 2nd — when DOACs are not suitable: * **LMWH + warfain** OR **LMWH + dabigatran/edoxaban** ## Footnote * LMWH: activator of antithrombin III → inhibits Factor **Xa** * warfarin: **Vit K** antagonist → reduces Factors **II, VII, IX, X** * dabigatran: also a DOAC but works by directly inhibiting **thrombin (Factor IIa)**
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which CNs provide visceral motor innervation to * carotid body and sinus * aortic body and sinus respectively?
* **carotid** body and sinus = CN **IX** * **aortic** body and sinus = CN **X**
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what nerve is the latissimus dorsi innervated by
**thoraco***dorsal* nerve "cos lats are at the *back* and are located more inferiorly, at the **thorax** rather than scapula"
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what nerve are the rhomboids (major, minor) innervated by
*dorsal* **scapular** nerve "cos rhomboids are at the *back* and are located **bet the scapula**"
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risk factors of Systemic Lupus Erythematosus (SLE)
* **UV** exposure * **SMOKING**
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features of SLE
"RASH OR PAIN" * Rash: butterfly (erythematous patches over cheeks and nose), **spares nasolabial folds** * Arthritis * Serositis: pericaritis, pleuritis * Haematological involvement: **anaemia**, cytopenia * Oral or nasal ulcers * Renal involvement: lupus **nephritis** * **Photosensitive** * Autoantibodies seen in investigations * Immune disorder * Neurological involvement: stroke, seizure | serositis = inflammation of serous membranes ## Footnote other conditions: ILD, oesophagitis
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investigations for SLE: * inflammation markers? * autoantibodies?
* **ESR** if wanna check for inflammation * sensitive: **ANA** specific: anti-**Smith**, anti-**dsDNA**
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treatment for SLE
* conservative: **sun protection** * topical (for treatment of cutaneous only): corticosteroids, calcineurin inhibitors, retinoids * oral/systemic: **hydroxychloroquine**
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histological features of SLE
deficiency of classical **complement** proteins (C1Q, C2, C4) -> loss of tolerance -> **autoantibody** production => antibody-antifen **immune complex** formation and **deposition** in microvasculature * deposition at **dermoepidermal junction**, resulting in **positive LUPUS band test** immune complex also results in complement activation => **inflammation** and tissue **injury** (including damage to vessel walls by neutrophils) * cutaneous small vessel vasculitis * leukocytoclastic vasculitis (due to said neutrophils then undergoing fragmentation) ## Footnote leukocytoclastic vasculitis: * suspect when there is **palpable purpura** * evaluare with **skin punch biopsy** and **immunofluorescence**
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3. A patient with **systemic lupus erythematosus** (SLE) develops **nephritis**. Which of the following is the most likely immunofluorescence finding in his kidney biopsy? A) IgG and C3 deposits with a "lumpy-bumpy" appearance B) "Full house" immunofluorescence with IgG, IgA, IgM, C3, and C1q C) Linear IgG deposits along the basement membrane D) Apple-green birefringence under polarized light with Congo red staining
B) **"Full house" immunofluorescence** with IgG, IgA, IgM, C3, and C1q nephritic syndrome associated w/ SLE = **lupus nephritis**
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types of stroke * ischaemic: (3) * haemorrhagic: (2)
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# resulting in haemorrhagic stroke causes of intracerebral/intraparenchymal bleed
* **structural** vascular abnormalities (e.g. **arteriovenous** malformations) * **HTN** → charcot bouchard MICROaneurysms ⇒ *single large* haematoma * various causes (e.g. **fat embolism**, malaria, vasculitis, acute hypertensive encephalopathy) → **petechial** haemorrhage ⇒ *multiple small "dot-like"* haemorrhages * cerebral **amyloid** angiopathy → amyloid proteins deposited on **walls** of blood vessels ⇒ predispose to bleeding
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characteristics of epidural haemorrhage: * cause * shape on imaging * presenting feature
* tear in **MMA** ← trauma to pterion * **lens**-shaped / **biconvex** * lucid interval before deterioration
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characteristics of subdural haemorrhage: * causes (chronic vs acute) * imaging features (shape, acute vs chronic)
* tear in **bridging** veins ← **chronic**: **falls** in elderly **acute**: MAJOR **trauma** (e.g. acceleration-deceleration injuries) * **crescent**-shaped * **hyper**dense for acute, **hypo**dense for chronic
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characteristics of subarachnoid haemorrhage: * cause * symptoms * imaging features (location of blood) * investigation * associated w/ what condition
* **berry** aneurysm: majority is **anterior communicating artery**, but sometimes MCA * symptoms of **meningism** <- blood can irritate the meninges <- blood is in subarachnoid space and in contact w/ **pia mater**, which is packed w/ **sensory nerve endings** * **hyper**dense blood in **sulci** and **basal cisterns** * check for **xanthochromia** in **LP** **8h** after onset (or headache if have) * associated with **ADPKD** ## Footnote * don't check for RBCs ← presence cld be from trauma when performing LP * only after around 8h ← enough time for RBCs to lyse and release bilirubin and thus result in yellow discolouration of CSF (= xanthochromia)
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what are the symptoms of meningism
* headache * **neck stiffness** * **photophobia** * (+) **Kernig** sign = pain when stretching meninges via straigtening leg from hip and knee flexion position * (+) **Brudzinski** sign = involuntary flexion of hips and knees upon passive neck flexion of a supine patient
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features of ischaemic stroke on non-contrast CT
ischaemia → decrease perfusion → cytotoxic **oedema** ⇒ brain tissue becomes **HYPOdense** and loses contrast bet structures * loss of grey-white differentiation * sulcal effacement * possible midline shift
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unique features of **MCA** ischaemic stroke on non-contrast CT
* dense MCA sign: **HYPERdense** *thrombus* * loss of **insular** ribbon
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features of haemorrhagic stroke on non-contrast CT
* **HYPERdense** bright *ACUTE blood* * surrounding **HYPOdense** *oedema*
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features of ischaemic stroke on MRI (DWI/ADC)
"*D*on't *W*orry, *I*t's just **A** **D**ark **C**loud" * *DWI*: bright * **ADC**: dark
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types of clot: * location * pathophysiology * treatment
"WHITE thrombi" * **rapid** turbulent flow in **ARTERIES** -> atherosclerotic **plaque ruptures** -> endothelial **damage** => **PLATELETS** recruited for rapid repair * treatment: antiplatelets (e.g. aspirin, clopidogrel, ticagrelor) "RED thrombi" * **slow** flow in **VEINS** (emboli commonly are too) -> stasis -> **clotting factors** accumulated -> **fibrin** formation => **RBCS** trapped by fibrin mesh * treatment: anticoagulants (e.g. DOAC, warfarin, LMWH)
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stroke involving INFERIOR div of MCA: * lobes of cortex supplied * regions affected => consequences
affects INFERIOR part of **parietal** lobe AND whole **temporal** lobe * IF lesion occurs at **non-dominant** side => **hemineglect** = **ignoring** CONTRALATERAL side of body and space * Wernicke's **receptive aphasia** * **Meyer's** loop (= **inf** optic radiations) => CONTRALATERAL **superior quandrantopia** ## Footnote receptive aphasia presents w/ * poor comprehension * **fluent BUT nonsensical** speech * also poor repetition
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stroke involving SUPERIOR part of MCA: * lobes of cortex supplied * regions affected => consequences
affects **lateral** part of **frontal** lobe * Broca's **expressive aphasia** * **motor** cortex (specifically **face and arms** area) => face and arm **weakness** * **frontal eye field** => **gaze** preference **toward lesion** ## Footnote expressive aphasia presents w/ * good comprehension * **non-fluent, effortful** speech * poor repetition
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stroke affecting ACA: * lobes of cortex supplied * regions affected => consequences
affects **medial** part of **frontal** lobe AND **medial** part of **parietal** lobe * **motor** cortex (specifically lower limbs area) => leg > arm **weakness** AND urinary incontinence
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how to identify which artery is affected in brainstem stroke
1. determine if medial or lateral 2. determine which part of brainstem via CN affected 3. match to the artery
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general principles of neurolocalisation in stroke: 1. differentiate cerebellum vs cerebral hemspheres and brainstem 2. differentiate cerebral hemispheres vs brainstem 3. differentiate within cerebral hemispheres: cortical vs subcortical
1. cerebral hemispheres, brainstem: **UMN** signs cerebellum: NO UMN signs, ONLY cerebellar signs (**DDASHING**) 2. cerebral hemispheres: **visual field defects** and *contralateral hemiparesis and/or sensory loss* brainstem: **ipsilateral CN deficits** (including **eye movement abnormalities**), **cerebellar** signs (vertigo and ataxia), **Horner** syndrome, impairment of loss of **consciousness** and *contralateral hemiparesis and/or sensory loss* 3. cortical (= involving grey matter): **higher cortical dysfunction** (e.g. affecting languge, awareness) ## Footnote * visual field defects = problem with **visual pathway** (usually optic radiation or occipital cortex) => patient sees **missing part of the world** * eye movement abnormalities = problem with nuclei **CNs III, IV, VI**, medial longitudinal fasciculus or gaze centers -> eyes **cannot align** tgt => **diplopia**
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gross (48h, 2-10d, 2-3 weeks) vs microscopic (12h, <48h, 2d, 1-3 weeks) appearance of ischaemic cerebrovascular disease ## Footnote * correspond microscopic -> gross * microscopic always occur first, followed by results seen in gross
microscopic: * 12h: ischaemic neuronal change (**red neurons**, oedema) * <48h: **neutrophils** * 2d: **foamy** macrophages (microglia) * 1-3 weeks: even more macrophages + reactive **gliosis** (astrocytes) gross: * 48h: soft, **pale**, swollen * 2-10d: **gelatinous**, **friable** * 2-3 weeks: **liquid** filled **cavity** ## Footnote reactive gliosis is how the brain "heals": astrocytes around edge of hole starts to enlarge and proligerate => astrocytic scar
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monoamine theory ## Footnote principle behind antidepressants
depression is associated w/ **deficiency or dysregulation** of monoamine neurotransmitters — **norepinephrine/noradrenaline**, **serotonin** (5-HT) and **dopamine** — in the CNS
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MOA of monoamine oxidase inhibitors (MAOIs)
* MAO breaks down **NOREPINEPHRINE, SEROTONIN and DOPAMINE** in **presynaptic** neuron "mouse eating NORTH COMPASS and SMILEY FACE cheese" "mouse biting through DOPAMINE rope" * MAOI is a **NON-SELECTIVE** and **IRREVERSIBLE** inhibitor of MAO "mouse trap KILLS ALL the mouses" -> increased conc of neurotransmitters in presynaptic neuron -> more neurotransmitters released into synaptic cleft => increased signaling
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example of MAOIs
phenelzine
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A/Es of MAOIs
* postural hypotension * restlesness and insomnia
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serotonin syndrome * caused by which classes of drugs * clinical features (triad)
* MAOIs, SSRIs, SNRIs * neuromuscular **excitation**: tremors, clonus, hyperreflexia, myoclonus, rigidity * **autonomic** dysfunction: hyperthermia, tachycardia, diaphoresis, HTN * altered **mental** state: agitation, confuision, delirium ## Footnote think of an angry boss: he's agitated, red from anger and trembling and tapping his feet angrily
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MOA of tricyclic antidepressants (TCAs)
inhibit **PRESYNAPTIC** UPTAKE of **NOREPINEPHRINE** and **SEROTONIN** -> increased conc of neurotransmitters in synaptic cleft => increased signaling "Boy on tricycle hit by ball, and thus prevented from PICKING UP NORTH COMPASS and SMILEY FACE balls"
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A/Es of TCAs
* sedation <- H1 **histamine** receptor **antagonism** "bee swatter" * *postural hypotension* <- **ALPHA-adrenoceptor** sympathetic **block** "ball hits girl holding a cake with an **ALPHA** flame, causing her to *fall down*" * *anticholinergic* side effects (e.g. dry mouth, blurred vision, constipation) <- **muscarinic** receptor **antagonism** "ball also hits and thus disrupts the *"Alice in wonderland"* party"
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examples of TCAs
"amy has an im**print** on her face from the ball hitting her, which also caused her to *trip* over her tricycle" * imi**pr**am**ine**, desi**pra**m**ine** * ami*trip*tyline, nor*trip*tyline ## Footnote some are **selective for norepinephrine** transporter => **fewer** side effects * nortriptyline, desipramine while others are non-selective * AMI*trip*tyline, IMI**pr**am**ine** "AMY has an IM**print** on her face from the ball hitting her, which also caused her to *trip* over her tricycle"
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MOA of Selective Serotonin Reuptake Inhibitors (SSRIs) and **Serotonin** and Noradrenaline Reuptake Inhibitors (SNRIs)
inhibit **presynaptic** UPTAKE of **norepinephrine** and/or **serotonin** -> increased conc of neurotransmitters in synaptic cleft => increased signaling
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advantages of SSRIs over TCAs
* much greater 5-HT reuptake **selectivity** -> lack of **effect** at **histamine** receptors, low **affinity** for **a-adrenoceptors** and low **affinity** for **muscarinic** receptors => fewer of those **A/Es** ## Footnote **citalopram** still has some degree of **histamine** receptor antagonim => causes **sedation**
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A/Es of SSRIs
* **SEXUAL DYSFUNCTION**: delayed ejaculation, anorgasmia * *nausea* * *insomnia* "girl REJECTS EX, while one friend *watches on excitedly* and another *almost vomits* out of disgust"
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examples of SSRIs
"travel agency has posters, including one with the words "*Fly Out"* and another with the words "the **City**"" * *fluo*xetine * **cita**lopram
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A/Es of SNRIs
* (same as SSRIs) sexual dysfunction, insomnia and nausea * **withdrawal** effects: dizziness, nausea, headache, anxiety, etc
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examples of SNRIs
"the office has a *fax* machine and a **dual** copier/scanner machine" * venla*fax*ine * desvenla*fax*ine * **dulo**xetine
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NorAdrenaline Reuptake Inhibitors (NARIs): * example * A/Es
* e.g. **reboxetine** * all A/Es are due to increased NA resulting in increased sympathetic activity: tachycardia, insomnia, anticholinergic effects (e.g. dry mouth, constipation)
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MOA of antipsychotics
**D**2 **antagonism** <- dopamine is increased in acute schizophrenia
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examples of TYPICAL antipsychotics
"VAN GOGH's painting about star g**azing**, which has a moon *halo* in it" * chlorprom**azine** * fluphen**azine** * trifluoper**azine** * *halo*peridol
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examples of ATYPICAL antipsychotics
"MODERN art gallery with a sign stating "quiet please, *only* **whispering** is appropriate"" * *olan*zapine * **risperi**done "MODERN art gallery also has a *closet* as an artpiece" * *cloza*pine just remember lol * amisulpride
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advantage of using ATYPICAL antipsychotics over typical ones
LESS **extra**pyramidal symptoms (EPS) due to * lower D2 receptor **occupancy** in striatum at therapeutic doses * concurrent **antagonism** of **serotonin** 5-HT2A receptors -> **modulate *dopamine* release** in striatum "MODERN art gallery has *smiley face* cheese being cut up and served to guests" ## Footnote *nigo***striatal** pathway: * DOPAMINE pathway involved in MOVEMENT CONTROL * involves both *substantia nigra* and **striatum** * has serotonin acting as an inhibitor of dopamine release in striatum
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what does EPS consist of: * reversible (1) * irreversible (2)
* reversible: acute **dystonia** = **parkinsonism**-like symptoms (cogwheel rigidity, resting tremor) * irreversible: 1. tardive **dyskinesia** = repetitive and stereotyped **involuntary** movements of **face, tongue** and limbs 2. **akathisia** = **involuntary** movements and **compulsion** to act associated w/ **restlessness, anxiety and agitation**
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A/Es mainly associated with atypical antipsychotics
* sedation (esp in C & O), postural hypotension and reflex tachycardia (esp in R) and anticholinergic side effects (e.g. dry mouth) (esp in C & O) <= **HAM** antagonism * *hyperglycaemia*, *diabetes* and **weight gain** (C, O & R) "painting of a **fat** face and *all the candies he's eating*" * clozapine only: **AGRANULOCYTOSIS** "FALLING GRANULES within hourglass in painting in closet" * **amisulpride** only: (females) breast swelling, lactation, pain (males) **gynaecomastia** <= increase in **prolactin**
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causes of increased ICP
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some other antidepressants: MOA of * mirtazapine * bupropion * agomelatine AND A/Es of * vortioxetine
* *mars*-tazapine: *NASA* (NorAdrenaline and **Serotonin** antidepressant) * buproprion: noradrenaline and **dopamine** reuptake inhibitor * agomelatine: **agonist** of **melatonin** MT1 and MT2 receptors * vortioxetine: pro-cognitive effects but also **increased risk of suicidal thoughts or actions**
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there are 2 types of hydrocephalus, communicating and non-communicating. what's the difference?
* communicating = no obstruction in flow of CSF => should be due to disturbance to** formation** or **absorption** of CSF (e.g. meningitis causing **scarring** and thus ventricular outflow obstruction, SAH **blocking arachnoid villi**) * non-communicating = obstruction in **flow** of CSF **WITHIN ventricles** (e.g. congenital malformations like Arnold Chiari malformation)
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clinical signs and symptoms of increased CSF
* nausea and vomiting * headache which is **worse**: 1. when **waking up** in the morning 2. on **lying down** 3. on **bending over** 4. on **coughing/sneezing/straining**/valsalva * **papilloedema** on **fundoscopy** ## Footnote papilloedema is NOT associated w/ increased cup disc ratio (trick qn!)
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complications of increased ICP: * cranial nerve palsies: CN (...) is MOST vulnerable * Cushing's triad: (...), (...) and (...) * LOC * WORST! => (...)
* cranial nerve palsies: CN **VI** is MOST vulnerable * Cushing's triad: abnormal **B**P (widened pulse pressure), **B**radycardia and abnormal **B**reathing (irregular respiration) * LOC * WORST! => cerebral **herniation** ## Footnote cerebral herniation results in **haemorrhage** and **necrosis** of affected area, compression and infarction of **artery** there, compression of **cranial nerves** there and **DEATH**
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what is the most dangerous cerebral herniation
**tonsillar** herniation <- compression of **cardiorespiratory** vital centres in brainstem
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imaging seen in meningitis * general * unique to TB and bacterial causes
* leptomeningeal ENHANCEMENT due to infection -> inflammation -> **exudate** => **thickening** and enhancement of meninges * EFFACEMENT (= narrowing) of sulci and basal cisterns * (TB and bacterial) ventricular enlargement (mild) due to **thick inflammator exudate** -> block CSF flow => obstructive **hydrocephalus**
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investigations for stroke
* 1st line: NON-CONTRAST **CT** => to check for **haemorrhage** * if haemorrhage is ruled out: **CT** angiogram (w/ CONTRAST) => identify location of clot * later: **MRI** (DWI/ADC) => gold-standard for accuracy and detail ## Footnote * don't use contrast initially as BOTH fresh blood and contrast looks bright white on imaging -> unable to differentiate
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diff bet empyema and cerebral abscess
both are **localised** collections of **pus** * empyema: **"outside"** brain parenchyma, **pressing in** * cerebral abscess: **within** brain parenchyma
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types of empyema and their respective: 1) causes 2) complications
* (majority!) **subdural**: 1) due to **infection** of paranasal **sinus** 2) could result in **thrombophlebitis** of **bridging** veins => **infarction** of **brain** * **epidural**: 1) associated w/ **osteomyelitis** where **local infection** (e.g. sinusitis) -> osteomyelitis of bone -> pus breaks through bone => epidural abscess 2) can result in **spinal cord** epidrual infection => cord **compression** ## Footnote * thrombophlebitis = inflammation of vein which then leads to a clot -> venous congestion -> increased pressure in veins and thus in capillaries => blood cannot enter brain tissue cos of high pressure
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cerebral abscess: * most commonly caused by (bacteria/fungi/virus), esp (...) and (...) * imaging
* most commonly caused by **bacteria**, esp **Streptococcus** and **Staphylococcus aureus** * imaging: **capsule** seen in later stage of development ## Footnote Strep does NOT refer to strep pneumoniae or meningitides, but rather strep **viridans**, strep anginosus or strep intermedius
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investigations for CNS infections (e.g. meningitis, encephalitis, cerebral abscess)
* **imaging**: 1) **CT** (**non-contrast** first) 2) MRI * obtain **CSF** via **lumbar puncture** and carry out a CSF **examination**: 1) appearance: **cloudy** = **meningitis** 2) cytology: increased **polymorphs** = bacterial increased **lymphocytes** = viral 3) biochemistry: **low glucose** = **bacterial** or **fungal** normal = viral 4) microbiology: send for PCR and culture * if LP cannot be done, do **blood culture** ## Footnote * **imaging** must be done FIRST -> checks for pathologies which can cause **raised ICP** (e.g. haemorrhages, ischaemia) => if raised ICP, then **cannot do LP**
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give 1 impt cause of neural tube defects
**folate** deficiency bcos neural tube closure requires rapid DNA synthesis ← rapid purine and pyrimidine synthesis ⇐ requires a lot of folate
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which virus can result in forebrain abnormalities (e.g. lissencephaly = severe reduction in neurons polymicrogyria = too many small, abnormal gyri)
CMV
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which **chromosomes** are associated with Alzheimer's Disease
**"10 + 9 = ?"** * chromosome **19** * chromosome **21**
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histological features and gross appearance of Alzheimer's Disease
* histo: abnormal **protein deposition** in brain, including 1) **amyloid** plaques OUTSIDE neurons 2) **neurofibrillary tangles** = hyperphosphorylated **tau** protein WITHIN neurons * gross: 1) diffuse **cortical ATROPHY** , esp at **temporal** lobe 2) shrunken gyri and prominent sulci ## Footnote note: since BOTH AD and HSV1 encephalitis affect **temporal** lobe (which is where limbic structures like **hippocampus** and amygdala sit), they both present w/ **anterograde amnesia** (= inability to form new memories), just that AD is more progressive while HSV1 **encephalitis** is **acute and severe**
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clinical presentation of vit B1 (= thiamine) deficiency * acute * chronic
* acute: **Wernicke** encephalopathy where vit B1 is **co-factor** for several **enzymes in glucose metabolism**, -> **unable to use glucose** despite sufficient glucose -> acute neuronal energy failure => LESIONS in areas w/ **high metabolic requirements** presents w/ triad: **opthalmoplegia**, **ataxia**, confusion * chronic: **Korsakoff's** syndrome: chronic NECROSIS and GLIOSIS of areas crucial for **memory formation**, presents with **anterograde** AND **retrograde amnesia**, **confabulation**
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histological features and gross appearance of Parkinson's disease
* histo: mutation of **a-synuclein** protein, resulting in 1) **Lewy bodies** (= accumulation of a-synuclein) IN neurons 2) **pallor** in **SUBSTANTIA NIGRA**
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anterior cord syndrome * cause * clinical symptoms (*think abt tracts affected*, *then think abt sensory and motor*)
* **infarct** in **ANTERIOR spinal** artery * affects **spinothalamic** tracts (ventral and lateral) => loss of **pain + temp** below lesion * also affects **corticosoinal** tracts (ventral and lateral) => bilateral **motor weakness**
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posterior cord syndrome: * causes * clinical symptoms (*think abt tracts affected*, *then think abt sensory and motor*)
* vit **B12** deficiency -> failure of **myelin synthesis** => demyelination of nerve fibres (esp longer ones), tabes dorsalis (**neurosyphilis**) => **damage** to nerve fibres, either directly or through inflammatory response * affects **DCML** => loss of **vibration + proprioception** below lesion ## Footnote loss of proprioception => **sensory** ataxia * presents w/ **instability** that worsens when eyes are closed — (+) **Romberg** test * diff from cerebellar ataxia, which presents w/ **incoordination**
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clinical symptoms of Cauda Equina syndrome | first think abt whether it's considered UMN or LMN lesion
* **L**MN signs <- collection of **nerve roots** that extend below the spinal cord * **asymmetric** leg weakness * **saddle** *anaesthesia*: S3-S5, *loss of sensation* in **buttocks, perineum and inner thighs** * **urinary retention** and/or overflow incontinence AND poor **anal (sphincter) tone**: S2-S4