12.3 Flashcards

1
Q

Name the common flexor origin (forearm muscles)

A

Medial epicondyle

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2
Q

Name the common extensor origin (forearm muscles)

A

Lateral epicondyle

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3
Q

The flexor forearm compartment (anterior compartment generally) is composed of 8 muscles. List them all.

A

2 pronators of forearm (pronator teres + quadrates)

2 long flexors of fingers (flexor digitorum superficialis + flexor digitorum profundus)

1 long flexor of thumb (flexor pollicis longus)

2 flexors of wrist (flexor carpi radialis + flexor carpi ulnaris)

1 long muscle of palm (palmaris longus - vestigial in humans + absent in 10-15% of population)

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4
Q

Most flexor muscles of forearm are innervated by median nerve.

Which are innervated by ulnar nerve?

A

Flexor carpi ulnaris

Medial part of flexor digitorum profundus

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5
Q

Which is deeper - pronator quadratus or pronator teres?

A

Pronator quadratus

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6
Q

Which type of forearm muscles are anterior and medial?

A

Flexor muscles

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7
Q

Which type of forearm muscles are posterior and lateral?

A

Extensor muscles

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8
Q

How many extensor muscles of the foerarm are there?

A

12 - all supplied by radial nerve

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9
Q

Which forearm muscle is responsible for supination?

A

Supinator;

The biceps is also a supinator..

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10
Q

Why is the brachioradialis muscle unusual?

A

Lies in posterior compartment of forearm but is a weak flexor at elbow but still supplied by radial nerveIt lies on thumb side.

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11
Q

How many tendons pass through the carpal tunnel?

A

9 flexor tendons

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12
Q

Which nerve passess between the tendons of flexor digitorum profundus and superficialis?

A

Median nerve

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13
Q

List the main contents of the anatomical snuffbox?

A

Radial artery

Radial nerve branch

Cephalic vein

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14
Q

What is carpal tunnel syndrome?

A

o Conditions that cause swelling (e.g. arthritis, pregnancy, oedema) can lead to median nerve compression as it passes through the carpal tunnel

o This leads to loss of sensation in the hand in region supplied by median nerve + reduced movement of the thumb as the median nerve supplies the muscles of the thumb

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15
Q

Name 2 tests for carpal tunnel syndrome.

A

 Tinel’s sign – tapping the nerve in carpal tunnel to elicit pain in median nerve distribution

 Phalen’s manoeuvre – holding the wrist in flexion for 60 seconds to elicit numbness/pain in median nerve distribution

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16
Q

What is finger abduction?

A

When fingers move away from middle finger

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17
Q

Name all the carpal bones in the proximal row from lateral to medial from anterior view.

A
  • Scaphoid – has tubercle on lateral, palmar surface
  • Lunate – dislocates uncommonly but have severe morbidity associated with them if the diagnosis is delayed
  • Triquetrum
  • Pisiform – can be felt
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18
Q

List all the carpal bones in the distal row from lateral to medial from anterior view.

A
  • Trapezium – has tubercle on palmar surface
  • Trapezoid
  • Capitate – largest carpal bone
  • Hamate – has hook on palmar surface
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19
Q

A single synovial sheath surrounds 8 of the 9 flexor tendons. Which tendon is surrounded by its own synovial sheath?

A

Flexor pollicis longus (flexor digitorum profundus and superficialis have 4 tendons each and around surrounded by the single synovial sheath)

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20
Q

Bennett’s fracture

A
  • Fracture of the 1st metacarpal base
  • Extending into the carpometacarpal joint
  • Caused by hyperabduction of the thumb
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21
Q

Boxer’s fracture

A
  • Fracture of 5th metacarpal neck
  • Usually caused by a clenched fist striking a hard object
  • Distal part of fracture is displaced posteriorly, producing shortening of affected finger
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22
Q

Metacarpal I is related to the thumb. What is the 3rd metacarpal related to?

A

Middle finger

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23
Q

Dorsal venous network of hand is a network of veins in superficial fascia on dorsum of hand formed by dorsal metacarpal veins.

Where are they found and what do they give rise to?

A

Found on back of the hand and give rise to cephalic and basilic veins

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24
Q

Which digits are affected by an ulnar nerve lesion at the wrist at rest?

A

Digits 4 and 5

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25
Q

Which digits are affected by a median nerve lesion at wrist or elbow when attempting to make a fist?

A

Digits 2 and 3.

Only digits 4 and 5 flex

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26
Q

List 4 common fracture sites.

A

 Distal radius

 Vertebra

 Proximal femur

 Proximal humerus

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27
Q

Function of deep fascia

A

o Covers muscles + helps divide the muscular sections into compartments – which work in functional units

o Fascia prevent the contracting muscles from causing friction in the subcutaneous fat/dermis above as it’s a smooth barrier

o Deep fascia does not stretch –> when muscles work (especially in distal LL) the pressure they cause to increase in size within the compartment helps w/ venous return – muscular venous pump

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28
Q

Which property of deep fascia is what leads to compartment syndrome?

A

Deep fascia does not stretch –> when muscles work (especially in distal LL) the pressure they cause to increase in size within the compartment helps w/ venous return – muscular venous pump

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29
Q

Muscles that make up quadratus femoris

A

o Rectus femoris
o Vastus lateralis
o Vastus intermedius
o Vastus medialis

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30
Q

Which compartment are the following muscles a part of?

  • Sartorius
  • Pectineus
  • Iliopsoas
  • Quadratus femoris
A

Anterior thigh compartment

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31
Q

Which compartment do the following muscles belong to?

  • Adductor brevis
  • Adductor longus
  • Adductor magnus*
  • Gracilis
  • Obturator externus
A

Medial thigh compartment

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32
Q

Which compartment do the following relate to?

  • Obturator nerve (L2-L4 ant)
  • Obturator artery
  • Adduction of hip
A

Medial thigh compartment

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33
Q

Which compartment do the following relate to?

  • Femoral nerve (L2-L4 post)
  • Femoral artery
  • Extension of knee + Flexion of hip
A

Anterior thigh compartment

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34
Q

Which compartment do the following relate to?

  • Sciatic nerve (L4-S3)
  • Profunda femoris + perforating arteries
  • Extension of hip + Flexion of knee
A

Posterior thigh compartment

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35
Q

Which compartment do the following muscles belong to?

  • Biceps femoris
  • Semitendinosus
  • Semimembranosus
A

Posterior thigh compartment

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36
Q

Which compartment do the following muscles belong to?

  • Tibial anterior
  • Extensor digitorum longus
  • Extensor hallucis longus
  • Fibularis tertinus
A

Anterior leg compartment

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37
Q

Which compartment do the following relate to?

  • Deep fibular nerve
  • Anterior tibial artery
  • Dorsiflex ankle (L4, L5)
  • Bound by extensor retinacula
A

Anterior leg compartment

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38
Q

Which compartment do the following relate to?

  • Superficial fibular nerve
  • Fibular artery*
  • Evert ankle (L5, S1)
A

Lateral leg compartment

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39
Q

Which compartment do the following muscles belong to?

  • Fibularis longus
  • Fibularis brevis
A

Lateral leg compartment

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40
Q
Which compartment do the following muscles belong to?
Superficial group:
o	Gastrocnemius
o	Plantaris
o	Soleus
Deep group:
o	Popliteus
o	Tibialis posterior
o	Flexor digitorum longus
o	Flexor hallucis longus
A

Posterior leg compartment

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41
Q

Which compartment do the following relate to?

  • Tibial nerve
  • Posterior tibial artery
  • Plantar flexors (S1, S2)
A

Posterior leg compartment

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42
Q

The lumbar plexus is formed by the anterior primary rami of which spinal roots?

A

L1-4

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43
Q

Where does the trunks of the lumbar plexus lie within?

A

Substance of psoas major

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44
Q

Name the 6 major peripheral nerves which branch from the lumbar plexus.

A
o	Iliohypogastric
 o	Ilioinguinal
o	Genitofemoral 
o	Lateral cutaneous of thigh 
o	Obturator 
o	Femoral
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45
Q

I, I Get Love On Fridays

What is this a mnemonic for?

A

Lumbar plexus branches

o	Iliohypogastric 
o	Ilioinguinal
o	Genitofemoral
o	Lateral cutaneous of thigh
o	Obturator
o	Femoral

*H comes before I so ilioHypogastric is before ilioInguinal

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46
Q

Which plexus is formed by the anterior primary rami of S1-4 (with contributions from L4 + 5)?

A

Sacral plexus

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47
Q

List the 5 major branches of sacral plexus.

A
o	Superior gluteal nerve
o	Inferior gluteal nerve
o	Sciatic nerve
o	Posterior femoral cutaneous
o	Pudendal nerve
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48
Q

When injecting into the gluteal region, which quadrant should you go for?

A

Upper lateral quadrant

Medial upper and lower quadrants is bad because of the superior gluteal nerve

Lateral inferior quadrant - there’s a greater chance of hitting sciatic nerve

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49
Q

Name the line on the posterior surface of the femoral shaft

A

Linea aspera

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50
Q

Where is the pectineal line?

A

Proximally, on the medial border of linea aspera becomes pectineal line

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51
Q

What can a neck of the femur fracture cause?

A

 Shortened limb
 Externally rotated limb (iliopsoas axis of action)
 Torn retinacular arteries –> risk of avascular necrosis

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52
Q

Are intra- or extra- capsular fractures more common in elderly people?

A

Intra

 They are result of minor trip or stumble

 Facture occurs within capsule of hip joint

 Can damage medical femoral artery which causes avascular necrosis of femoral head

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53
Q

Neck of fracture causes external or internal rotation?

A

External

And leg is shortened

With a dislocation leg is shorted and medially rotated

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54
Q

Where are osteogenic cells located?What do they develop into?

A

In inner layer of periosteum and endosteum

Develops into an osteoblast

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55
Q

What are bisphosphonates?

A

o Inhibit mineralisation or bone resorption by inhibiting osteoclasts

o Bisphosphonates are enzyme-resistant analogues of pyrphosphoric acid, which norammly inhibits mineralisation in the bone

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56
Q

MoA of bisphosphonates used in the inhibition of bone resorption.

A

 BPs attach to hydroxyapatite binding sites in bone

 They are a prodrug

• Action of osteoclast forming sealing zone releases bisphosphonate, this is taken up by osteoclasts

 When osteoclasts resorb bone impregnated w/ BP, BP released during resorption impairs ability of osteoclasts to:
• Form the ruffled border
• Adhere to the bony surface
• Produce the protons for bone resorption

 BPs decrease osteoclast activity by decreasing osteoclast progenitor development + recruitment + increasing osteoclast apoptosis

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57
Q

SE of bisphosphonates.

A

 Osteonecrosis of the jaw bone is the widest adverse effect of BP therapy

 There is an increased risk of osteonecrosis of jaw bone due to:
• Poor oral hygiene
• Invasive dental procedures
• Prolonged exposure to high doses of IV bisphosphonates

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58
Q

Calcitonin moa

A

o Another pharmacological approach is trying to modulate the calcitonin/PTH levels to control calcium

o Calcitonin is secreted by thyroid gland when blood calcium level increases:

 Decreases blood calcium levels
 Stimulates calcium deposition in bones
 Reduces calcium uptake in kidneys

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59
Q

PTH is secreted by parathyroid gland when blood calcium level decreases. What does it do?

A

 Increases blood calcium levels

 Stimulates calcium release from bones

 Increases calcium uptake in kidneys

 Increases calcium uptake in intestines

 Must be careful about dosage of PTH:
• Low dose – increases osteoblast activity – desired result
• High dose – increases bone reabsorption + thins bone

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60
Q

Why does steroids need to be withdrawn slowly?

A

• Adrenal gland starts to shrink + reduces steroid production significantly when steroids used long term.

o So steroids need to be withdrawn slowly, so steroid production increases overtime

o If steroid treatment abruptly stopped –> atorpy

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61
Q

What are DMARDs?

A

Drugs used for other conditions but at low doses help w/ RA.

Disease-modifying antirheumatic drugs

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62
Q

Effects of DMARDs?

A
  • Slow down disease progression
  • Reduce damage to the joints
  • Usually taken for rest of life
  • They suppress body’s overactive immune systems
  • Need to have regular blood tests, to see if DMARDs are having any side effects
  • But serious side-effects affecting the blood, liver, or kidneys (rare)
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63
Q

What is synovial membrane?

A

Specialised connective tissue that lines inner surface of capsules of synovial joints + tendon sheath

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64
Q

Function of synovial membrane?

A

 It makes direct contact w/ synovial fluid lubricant

 It is primarily responsible for maintaining synovial fluid lubricant

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65
Q

At tissue surface, there are many rounded macrophage-like synovial cells (type A) + fibroblast-like (type B) synovial cells. What are the functions of A and B type cells?

A

 Type A cells – maintain synovial fluid by removing wear-and-tear debris by phagocytosis

 Type B cells – secrete hyaluronic acid + protein complex (mucin) of synovial fluid

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66
Q

What is cartilage?

A

A smooth elastic tissue that covers + protects the ends of long bones at the jointsIt’s a structural component of the rib cage, ear, nose, bronchial tubules, intervertebral discs, other body component

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67
Q

Name 3 types of cartilage.

A

 Elastic – provides strength, elasticity, maintains shape

 Hyaline – weakest cartilage found on many joint surfaces, precursor of bone
 Fibrous – strongest cartilage, alternating layers of hyaline + collagen

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68
Q

Pick the most appropriate synovial joint.Permits movement in several axis; a rounded head fits into a concavity (glenohumeral joint)

	Hinge 
	Saddle 
	Plane 
	Pivot 
	Condyloid 
	Ball and socket
A

Ball and socket

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69
Q

Pick the most appropriate synovial joint.Permits flexion and extension (elbow joint)

	Hinge 
	Saddle 
	Plane 
	Pivot 
	Condyloid 
	Ball and socket
A

Hinge

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70
Q

Pick the most appropriate synovial joint.Concave and convex joint surfaces unite at this joints (metatarsophalangeal joint)

	Hinge 
	Saddle 
	Plane 
	Pivot 
	Condyloid 
	Ball and socket
A

Saddle

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71
Q

Pick the most appropriate synovial joint.Permit gliding/sliding movements (acromioclavicular joint)

	Hinge 
	Saddle 
	Plane 
	Pivot 
	Condyloid 
	Ball and socket
A

Plane

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72
Q

Pick the most appropriate synovial joint.Allows rotation; a round bony process fits into a bony ligamentous socket (atlantoaxial, proximal radio-ulnar)

	Hinge 
	Saddle 
	Plane 
	Pivot 
	Condyloid 
	Ball and socket
A

Pivot

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73
Q

Pick the most appropriate synovial joint.Permits flexion, extension, adduction, abduction, circumduction (metacarpophalangeal joint)

	Hinge 
	Saddle 
	Plane 
	Pivot 
	Condyloid 
	Ball and socket
A

Condyloid

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74
Q

Other than synovial joints, name 3 types of joints.

A

Fibrous

Primary cartilaginous (synchondrosis)

Secondary cartilaginous (symphyses)

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75
Q

Define rheumatoid arthritis

A

Long lasting autoimmune disorder that primarily affects joints

RA = chronic, symmetrical, inflammatory, deforming, polyarthritis

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76
Q

Signs and symptoms of RA

A

o Insidious onset (gradual)o Joint swelling – inflammatory arthritis

o MCPs, MTPs, wrists commonly affected

o Classically symmetrical in terms of affected joints

o Early morning stiffness – joints stiffen when not used

o Responds well to NSAID

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77
Q

List the 3 stages of progression of RA

A

 Initiation phase – non-specific inflammation

 Amplification phase – T-cell activation

 Chronic inflammatory phase – tissue injury due to cytokines IL-1, TNF-alpha, IL-6

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78
Q

What can trigger RA?

A

An external trigger (e.g. infection, trauma, smoking) sets of an autoimmune reaction (perhaps in genetically susceptible individuals)

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79
Q

What does T cell stimulation in RA activate and result in?

A
  • Activates macrophages, fibroblasts, B cells

* Result of this activation = production of whole range of cytokines

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80
Q

What is detected in blood tests for RA?

A

B cells produce RF and anti-CCP antibody which is detected in blood test

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81
Q

List the 3 main cytokines involved in RA

A
  • TNF-alpha – main cytokine involved
  • IL-1
  • IL-6
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82
Q

How can inflammation cause joint damage in RA?

A

o The inflammation happens within the synovial layer

o This gets organised together + starts to invade the adjacent cartilage (this is termed invading mass pannus)

 Invading mass pannus – organised synovial cells which are invading + attacking the cartilage + bone

o The cartilage + bone start to break down – this can be seen on an x-ray as joint space narrowing (cartilage degradation)o Bone erosion can be seen as punched out areas on x-ray

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83
Q

List 5 consequences of chronic systemic inflammation in RA

A

o Early ischaemic heart disease (leading cause of mortality in RA)

o Sarcopenia (damage to muscles w/ inflammation) - muscles become damaged + atrophied (thus not as strong)

o Pain sensation can increase - unusual effects on pain sensitizer + nerve endings –> more susceptible for chronic pain

o Osteoporosis - in patients w/ lots of inflammation

o Insulin resistance + metabolic syndrome

o Dementia

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84
Q

Inflammatory markers are used to predict the prognosis of RA.List some erosion (bone) prognostic factors

A

Common prognostic factors: smoke status, RF, anti-CCP, ESR, CRP

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85
Q

Inflammatory markers are used to predict the prognosis of RA.List some disability prognostic factors

A

Specific HLA antigen implicated, RF, anti-CCP

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86
Q

Inflammatory markers are used to predict the prognosis of RA.List some mortality prognostic factors

A

Specific HLA antigen implicated, RF, anti-CCP

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87
Q

RA summary

A

 Synovial inflammation

 Genetic + environmental factors

 Articular + extra-articular complications

 Morbidity + mortality associated with the disease

 Early assessment + diagnosis is essential

 Treat inflammation early + aggressively

 Established severe RA is bad

 MDT approach needed

 RA = chronic, symmetrical, inflammatory, deforming, polyarthritis

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88
Q

Action of TNF-alpha

A

T lymphocyte + macrophage
o Increases pro-inflammatory cytokines + chemokines (IL-1, IL-6, IL-8) -> increased inflammation
o Increased adhesion molecules –> increased cell infiltration (affects vascular lining)

Endothelium
o Increased vascular endothelial growth factor
 increased angiogenesis

Hepatocyte
o Increased acute phase response
 increased CRP in serum (used in RA blood tests)Epidermis
o Increased keratinocyte hyperproliferation
 skin plaques

Synoviocytes
o Increased metalloproteinase syntheses
 causes articular cartilage degradation

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89
Q

What is the most common joint disorder/disease that results from breakdown of joint cartilage + underlying bone?

A

OA (osteoarthritis)

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90
Q

Which joints does OA affect?

A

 Distal interphalangeal joints (DIP)

 Proximal interphalangeal joints (PIP)

 Carpometacarpal joints

 Metatarsophalangeal joints

 Axial skeleton

 Large weight bearing joints

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91
Q

Symptoms of OA

A

 Tend to come with activity + get better w/ rest

 Little inflammation present – repair causes inflammation (wear, tear, repair)

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92
Q

What is anti-CCP?

A

Anti-cyclic citrullinated peptide (anti-CCP) is an antibody present in most rheumatoid arthritis patients. Levels of anti-CCP can be detected in a patient through a blood test.

A positive anti-CCP test result can be used in conjunction with other blood tests, imaging tests, and physical examinations to reach a rheumatoid arthritis diagnosis.

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93
Q

Bouchard’s nodes

A

PIP joints – bony outgrowths or gelatinous cysts form

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94
Q

Heberden’s nodes

A

DIP joints – bony swellings form

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95
Q

List all the causes of pain in OA

A

o Prostaglandins

o Cytokineso Synovitis

o Subchondral fractures

o Periosteal elevation

o Muscle spasm

o Venous congestion

o Biomechanical effects

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96
Q

Does RA or OA have an earlier onset?

A

RA (20-40) whereas OA is >50

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97
Q

What is gout?

A

A form of inflammatory arthritis characterised by recurrent attacks of red, tender, hot, swollen joints

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98
Q

What is the most common type of inflammatory arthritis in young men?

A

o Gout is the most common type of inflammatory arthritis in young men

o It affects 1-2% of adult population

o Prevalence increases w/ age

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99
Q

Co-morbidities in gout

A

o Renal impairment typically (cannot excrete uric acid)

o Coronary heart disease

o Metabolic syndrome – obesity, dyslipidaemia, hypertension, type II diabetes

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100
Q

Modifiable risk factors of gout

A

 Hyperuricemia

 Diet – seafood, purines (metabolised to uric acid), red meat, beer

 Alcohol consumption

 Obesity

 Certain drugs – low dose aspirin, thiazide diuretics, furosemide, cyclosporine, levodopa, nictonic acid

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101
Q

Which foods/drinks should be avoided in gout?

A

Products with high purine

Seafood, beer, red meat

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102
Q

Not everyone w/ high levels of uric acid get gout, usually there is a trigger event –> mobilise uric acid in blood. List some triggers.

A
  • Direct trauma
  • Intercurrent illness/surgery the triggers an acute phase response
  • Dehydration/acidosis – including alcoholic binge
  • Rapid weight loss
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103
Q

Summaries gout

A

o Common metabolic disorder, increasing in incidenceo Associated w/ high-purine diet + high alcohol intake

o Hyperuricemia is the cause of gout

o Attacks caused by deposition of urate crystals in joints, resulting in inflammation

o Gout is a recurrent + progressive condition. Eventually leading to advanced tophaceous gout

o Identification of crystals in joint or tophus aspirate, allows a definitive diagnosis

o Primary care, clinical diagnosis is reasonable accurate for typical presentations (wo/ aspirate)

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104
Q

What is septic arthritis?

A

Acute swollen joint presentation, think infective arthritis

o Especially if it’s a single joint or there’s a risk factor e.g. IV drug users

o They may be presenting w/ sepsis

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105
Q

How to confirm septic arthritis?

A
  • Aspirate + confirm
  • Choose appropriate antibiotic based on gram status + species if it’s septic arthritis
  • Septic arthritis can mimic other things like acute gout, treat sepsis w/ broad spec antibiotics if suspicious, wait for results (?gout)
  • Duration of antibiotics in confirmed case can be difficult
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106
Q

What is bursitis?

A

o Inflammation of one or more bursae (small sacs) of synovial fluid in the body

o They are lined w/ synovial membrane that secretes a lubricating synovial fluid

o When bursitis occurs, movement relying on the inflamed bursa becomes difficult + painful

o Moreover, movement of tendons = muscles over the inflamed bursa aggravates its inflammation

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107
Q

What is tenosynovitis?

A

o Inflammation of the synovium that surrounds a tendon

o Symptoms include pain, swelling + difficulty moving the particular joint where the inflammation occurs

o Tenosynovitis most commonly results from the introduction of bacteria into a sheath through a small penetrating wound such as that made by the point of a needle or thorn

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108
Q

List the 5 big complementary therapies.

A

Acupuncture:
 Fine needles are inserted at certain sites in the body for therapeutic or preventative purposes

Osteopathy:
 Moving, stretching and massaging a person’s muscles + joints

Chiropractic:
 Spinal manipulation which aims to treat ‘vertebral subluxations’ which are claimed to put pressure on nervesHerbal medicine
 Medicines with active ingredients made from plant partsHomeopathy
 Based on use of highly diluted substances (H2O) which practitioners claim can cause body to heal itself

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109
Q

List assessment tools for pain.

A

o Visual analogue score

o Verbal rating score
o Brief pain inventory

o HAD score – Hospital anxiety + depression scale

o McGill pain score – Self-report questionnaire that allows individuals to describe quality + intensity of their pain to S-LANSS score – Aims to identify pain of neuropathic origin, as distinct from nociceptive pain, wo/ clinical examination

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110
Q

List factors that lower pain threshold

A
  • Discomfort
  • Insomnia
  • Fatigue
  • Anxiety
  • Fear
  • Sadness
  • Depression
  • Boredom
  • Introversion
  • Mental isolation
  • Social abandonment
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111
Q

List factors that raise pain threshold

A
  • Relief of symptoms
  • Sleep
  • Rest
  • Empathy
  • Companionship
  • Diversional activity
  • Reduction in anxiety
  • Elevation of mood
  • Analgesics
  • Anxiolytics
  • Antidepressants
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112
Q

Neurovasculature of knee joint

A

o Vasculature: genicular anastomoss (supplied by genicular branches of femoral + popliteal arteries)

o Innervation: femoral, tibial, common fibular nerves

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113
Q

Where do collateral ligaments of the knee attach?

A

Medial and lateral epicondyles

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114
Q

What is the intercondylar fossa?

A

Depression found on posterior surface of femurLies between 2 condyles and contains 2 facets for attachment of internal knee ligaments (cruciate)

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115
Q

What is the tibial plateau (proximal) formed by?

A

Formed by the lateral + medial condyles

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116
Q

What does the knee capsule contain?

A

Patella, ligaments, menisci, bursa

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117
Q

What is menisci?

A

The medial + lateral menisci are fibrocartilage structures in the knee that serve 2 functions:

o Deepen the articular surface of the tibia, thus increasing stability of joint

o Act as shock absorbers

Hence increase stability + weight distribution
They are avascular

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118
Q

What shape is the medial meniscus?

A

C (crescent shaped)

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119
Q

What shape is the lateral meniscus?

A

O (oval shaped)

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120
Q

Which meniscus is attached to MCL?

A

Medial

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121
Q

Which meniscus is attached to popliteus tendon?

A

Lateral

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122
Q

Is the medial and lateral menisci fixed of mobile?

A

Medial = fixed

Lateral = free from LCL hence mobile

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123
Q

What is the function of bursae?

A
  • Synovial filled sac found between moving structures in a joint
  • Function = reduce wear + tear on structures
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124
Q

Name the 4 bursa found in knee joint.

A

o Suprapatellar bursa,
o Prepatellar bursa,
o Infrapatellar bursa,
o Semimembranosus bursa

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125
Q

Ligaments of knee joint

A

o Tibial collateral ligament resists medial displacement
 Assisted by the sartorius, semitendinosus, gracilis
 Aided by the quadriceps femoris

o The fibular collateral ligament resists lateral displacement
 Assisted by the iliotibial tract
 Aided by the quadriceps femoris

o The cruciate ligaments prevent hyperextension by becoming taut

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126
Q

Function of quadratus femoris in knee stabilisation.

A

The quadriceps femoris prevents anterior dislocation when the knee is flexed

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127
Q

Axial rotation of leg is limited due to what?

A

o The intercondylar eminence of the tibia lodging in the intercondylar notch of the femur forming the pivot

o The cruciate and collateral ligaments

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128
Q

Which nerve innervates quadriceps muscles?

A

Femoral nerve (L2-L4)

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129
Q

Function of iliotibial band

A

Pulls knee into hyperextension

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130
Q

What is the iliotibial band?

A

o It is a thickening of fascia lata + provides lateral knee support.

Acted on by:

  • Tensor fascia latae
  • Gluteus maximus
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131
Q

Innervation of hamstrings

A

Scaiatic nerve

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132
Q

List hamstrings muscles

A

o Semitendinosus

o Semimembranosus

o Biceps femoris

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133
Q

What is pes anserinus made up of?

A

3 conjoined tendons of muscles.

One from each thigh compartment.

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134
Q

Name the muscle tendons that conjoin to form pes anserinus

A

 Sartorius – from anterior thigh compartment

 Gracilis – from medial thigh compartment

 Semitendinosus – from posterior thigh compartment

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135
Q

Contents of popliteal fossa

A

 Popliteal artery

 Popliteal vein

 Tibial nerve

 Common fibular nerve

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136
Q

How to test for posterior cruciate ligament damage?

A

o Flex knee to 90 degrees

o Look from the side of the knee checking for a poster sag or setback of the tibia

o This would suggest posterior cruciate ligament damage

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137
Q

Describe the anterior draw test (for anterior cruciate ligament)

A

o Place both hands around upper tibial tuberosity + index finger tucked under the hamstrings to make sure these are relaxed

o Stabilise the lower tibia with your forearm + gently pull the upper tibia forward

o In a relaxed, normal patient there is normally a small degree of movement

o More significant movements suggest anterior cruciate ligament damage

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138
Q

How to test medial + lateral collateral ligament?

A

o Flex knee to 15 degrees

o Alternatively stress the joint line on each side

o Place hand on opposite side of the joint line of that which you are testing + apply force to lower tibia

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139
Q

What is knock knees aka?

A

Genus valgus

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140
Q

What is bol-legs aka?

A

Genu varus

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141
Q

The chief cause of genu varus

A

Rickets

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142
Q

When does ACL rupture occur?

A

o Occurs when the biomechanical limits of the ligament are exceeded (over-stretched)

o Frequently occurs in athletes

o Consequence depends on how much knee stability affected + the extent to which other structures have been involved

o If instability is evident then the menisci may get injured, this may lead to progressive, degenerative, arthritis of the knee

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143
Q

PCL rupture

A

o <20% of knee ligament injuries
o Usually caused by blow to knee whilst flexed

 E.g. falling on bent knee, impact from dashboard

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144
Q

What is the terrible triad?

A

Torn:
 Medial (tibial) collateral ligament
 Medial meniscus
 Anterior cruciate ligament

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145
Q

How to know which collateral ligament is damaged?

A

 Pain on medial rotation indicates damage to the medial ligament.

 Pain on lateral rotation indicates damage to the lateral ligament

o If tibial (medial) collateral ligament is damaged, it is likely that medial meniscus is torn, due to their attachment

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146
Q

From proximal to distal, name the 7 tarsals

A

Talus.

Calcaneus.

Navicular.

Cuboid.

Cuneiforms (there are 3 of these)

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147
Q

Which tarsal bone articulates with ankle joint?

A

Talus

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148
Q

Name the largest tarsal

A

Calcaneus.

Achilles tendon attaches to it.

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149
Q

Which compartment does the dorsiflexors lie in?

A

Anterior leg

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150
Q

Which compartment do ankle evertors belong to?

A

Lateral leg

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151
Q

Which compartment do plantar flexors belong to?

A

Posterior leg

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152
Q

Which compartment does the deep fibular nerve supply?

A

Anterior leg compartment

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153
Q

Which compartment does the superficial fibular nerve supply?

A

Lateral leg compartment

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154
Q

Which compartment does the tibial nerve supply?

A

Posterior leg

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155
Q

Which compartment does the anterior tibial artery supply?It continues as dorsalis pedis

A

Anterior leg

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156
Q

Which compartment does the posterior tibial artery supply? It is a continuation of the popliteal arterty

A

Posterior leg compartment

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157
Q

Which compartment does the fibular artery supply?

A

Lateral leg compartment

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158
Q

Name the 3 dorsal foot muscles

A

 Extensor digitorum brevis
 Extensor hallucis brevis
 Dorsal interossei

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159
Q

Name the 3 superficial plantar foot muscles

A
  • Abductor hallucis
  • Flexor digitorum brevis
  • Abductor digiti minimi
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160
Q

Name 2 intermediate plantar foot muscles

A
  • Quadratus plantae

* Lumbricals

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161
Q

Name 4 deep plantar foot msucles

A
  • Flexor hallucis brevis
  • Adductor hallucis
  • Flexor digiti minimi brevis
  • Plantar interossei
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162
Q

Short saphenous vein

A

 Found on the lateral side

 Runs up the posterior leg + becomes the popliteal vein

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163
Q

Great saphenous vein

A

 Anterior to medial malleolus = where the origin of the great saphenous vein is found.

 This is the longest vein in the body.

 Runs up until the inguinal ligament where it becomes the femoral vein.

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164
Q

The tarsal tunnel runs from the medial malleolus to the calcaneal tuberosity.

Tendon order only applies here, proximally the tibial artery + flexor digitorum longus swap.

Using the mnemonic - ‘Tom, Dick, ANd Harry’ list tendons, arteryand nerve

A

T - Tibialis posterior tendon

D - flexor Digitorum

A - posterior tibial Artery

N - tibial Nerve

H - flexor Hallucis longus tendon

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165
Q

What type of joint is the ankle joint (talocrural joint)?

A

Hinge joint - movements possible in 1 plane (plantarflexion + dorsiflexion)

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166
Q

What is the subtalar joint?

A

An articulation between 2 of the tarsal bones in the foot (talus + calcaneus)

Ball-and-socket

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167
Q

Which movements occur at the subtalar joint?

A

It is the chief site within the foot for generation of eversion + inversion movements

  • Eversion movement is produced by muscles of the lateral leg compartment
  • Inversion movement – tibialis anterior muscles
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168
Q

Which muscles produce plantar flexion and dorsiflexion at the talocrural joint?

A
  • Plantarflexion – produced by muscles in posterior compartment of leg.
  • Dorsiflexion – produced by muscles in anterior compartment of leg.
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169
Q

When is the ankle joint most stable?

A

Dorsiflexion - anterior talus held tightly in mortise.

High heels force plantarflexion which increases injury risk as the joint is least stable in this position.

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170
Q

How many arches does the foot have?

A

3

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171
Q

Name the arches of the foot.

A

 2 longitudinal (medial + lateral) – formed between the tarsal bones + proximal end of metatarsals

  • Medial longitudinal arch - formed by the calcaneus, talus, navicular, 3 cuneiforms, first 3 metatarsal bones
  • Lateral longitudinal arch - formed by the calcaneus, cuboid, 4th + 5th metatarsal bones

 1 anterior transverse
• Formed by the metatarsal bases, the cuboid + the 3 cuneiform bones

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172
Q

What does pes cavus mean?

A

High arches

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173
Q

What does pes planus mean?

A

Low arches (flat footed)

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174
Q

What is hallux vagus?

A

Hallux is deviated medially, towards the body

Uncommon

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175
Q

What is hallux valgus?

A

aka bunion.

Hallux deviated laterally.

1st metatarsal bone deviates medially.

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176
Q

What does the following describe?

 Foot condition in which the longitudinal arches have been lost

 Arches do not develop until about 2-3 years of age so flat feet during infancy is normal causes few, if any, symptoms – may result in ache after prolonged activity

A

Pes planus

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177
Q

Posture

A. Area demarcated by body’s point of contact with ground (+ any additional walking aids)

B. Theoretical balancing point.

C. A genetic term used to describe the dynamics of body posture to prevent falling.

D. Point location of the body ground reaction foot vector (vGRF) on the floor.

E. The orientation of any body-segment relative to the gravitational vector.

F. Vertical projection of the COM onto the ground

A

E. The orientation of any body-segment relative to the gravitational vectorIt is an angular measure from the vertical

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178
Q

Centre of mass

A. Area demarcated by body’s point of contact with ground (+ any additional walking aids)

B. Theoretical balancing point.

C. A genetic term used to describe the dynamics of body posture to prevent falling.

D. Point location of the body ground reaction foot vector (vGRF) on the floor.

E. The orientation of any body-segment relative to the gravitational vector.

F. Vertical projection of the COM onto the ground

A

B. Theoretical balancing point

o Weighted average of the COM of each body segment combined in 3D space

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179
Q

Balance

A. Area demarcated by body’s point of contact with ground (+ any additional walking aids)

B. Theoretical balancing point.

C. A genetic term used to describe the dynamics of body posture to prevent falling.

D. Point location of the body ground reaction foot vector (vGRF) on the floor.

E. The orientation of any body-segment relative to the gravitational vector.

F. Vertical projection of the COM onto the ground

A

C. A genetic term used to describe the dynamics of body posture to prevent falling

o It is related to the inertial forces acting on the body + the inertial characteristics of body segments

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180
Q

Centre of gravity

A. Area demarcated by body’s point of contact with ground (+ any additional walking aids)

B. Theoretical balancing point.

C. A genetic term used to describe the dynamics of body posture to prevent falling.

D. Point location of the body ground reaction foot vector (vGRF) on the floor.

E. The orientation of any body-segment relative to the gravitational vector.

F. Vertical projection of the COM onto the ground

A

F. Vertical projection of the COM onto the ground

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181
Q

Centre of pressure

A. Area demarcated by body’s point of contact with ground (+ any additional walking aids)

B. Theoretical balancing point.

C. A genetic term used to describe the dynamics of body posture to prevent falling.

D. Point location of the body ground reaction foot vector (vGRF) on the floor.

E. The orientation of any body-segment relative to the gravitational vector.

F. Vertical projection of the COM onto the ground

A

D. Point location of the body ground reaction foot vector (vGRF) on the floor

o When standing this is between the 2 feet

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182
Q

Base of support.

A. Area demarcated by body’s point of contact with ground (+ any additional walking aids)

B. Theoretical balancing point.

C. A genetic term used to describe the dynamics of body posture to prevent falling.

D. Point location of the body ground reaction foot vector (vGRF) on the floor.

E. The orientation of any body-segment relative to the gravitational vector.

F. Vertical projection of the COM onto the ground

A

A. Area demarcated by body’s point of contact with ground (+ any additional walking aids)

o When feet are separate apart, it is easier to maintain balance

o A walking stick + frame will increase base of support –> more like to keep COG within that area –> maintain balance

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183
Q

What does postural control consist of?

A
  • Postural control consists of keeping body’s COG over/within base of support (BOS) during stance + active movements, respectively
  • 2/3rd of our body mass is located 2/3rd of body height above the ground
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184
Q

Breakdown the sensory component of balance

A

Somatosensory – skin receptors:
 Motion of the body with respect to support surface.

Proprioceptive – muscle spindles + golgi tendon organs:
 Motion of body segments relative to each otherSomatosensory + proprioceptive = 60-70% Visual – eyes (10-20%)
 Motion of the body w/ resect to extra-personal space

Vestibular – inner ear (10-20%):
 Detects accelerations of the head

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185
Q

What is the postural ankle strategy?

A

o In response to smaller, slower perturbations

o Shifts COG about the ankle joint w/ minimal contribution from knee or hip

o Distal to proximal muscle activation

o Used on surfaces w/ low resistance to shear forces

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186
Q

What is the postural hip strategy?

A

o In response to larger, faster perturbations

o Shifts COG about hip joint by flexion/extension

o Ability to generate larger torque, more rapid response

o Produces mostly shear forces

o Transmits horizontal shear force to surface, therefore not suitable for slippery surfaces

o Suitable on surface that have low resistance to torque (narrow bean)

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187
Q

What is the stepping strategy?

A

o In response to largest, fastest perturbation (or the inability to generate an ankle/hip strategy)

o Shifts COG about hip joint by flexion/extension

o Realigns BOS under the new position of the COG w/ rapid steps, hops or stumbles

o Used when ankle + hip strategies are inadequate

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188
Q

Describe balance in the elderly

A

o Progressive age-related changes in healthy elderly subjects

o The old were more dependent on proprioceptive input

o They were unable to visually compensate for the disruption if proprioceptive input

o Disruption of proprioceptive input is the most important determinant of quantitative balance performance in >80 years

o The old did not adapt as well to repeated platform perturbations compared with younger elderly

o Deficit in central integration of sensory input or in motor output response

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189
Q

Describe balance in fallers

A

o No significant difference in functional reach between non-fallers and fallers

o No significant differences were found between non-fallers and fallers for the anterior LOS test

o Significant difference found between non-fallers and fallers for the mean sensory organisation test

o Significant positive correlation for anterior displacement on LOS test and SOT composite score for fallers but not for non-fallers

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190
Q

Main function of fibrous layer of eyeball

A

To provide shape to eye + support deeper structures

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191
Q

How many layers is the eyeball divided into?

A

3 main layers:

  • FIbrous
  • Vascular
  • Neural
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192
Q

Name the innermost layer of the eyeball.

A

Neural layer

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193
Q

Name the 2 main structures in the fibrous layer (they are continuous with each other).

A

Cornea (anteriorly)

Sclera (posteriorly) - makes up 85% of fibrous layer

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194
Q

Vascular layer consists of 3 main structures which are continuous with one another (anterior to posterior) name them.

A

Iris

Ciliary body

Choroid

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195
Q

What is the coloured bit of the eye that changes pupil size called?

A

Iris

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196
Q

Which structure makes up the majority of the fibrous layer?

A

Sclera

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197
Q

Which structure in the eyeball provides attachment to the extraocular muscles responsible for movement of eye?

A

Sclera (white part of eye)

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198
Q

Which structure provides 2/3rds of the focusing power of the eye?

A

Cornea (light entering eye is refracted by cornea)

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199
Q

Which 2 muscles alter pupil size?

A

Dilatory muscles sympathetic stimulation)

Anterior sphincter muscles

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200
Q

When to dilator muscles relax?

A

In bright light, pupils smaller

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201
Q

What action do miotics and mydriatics have on iris (hence pupil size)?

A
  • Mydriatics dilate iris

* Miotics – constrict iris

202
Q

When do anterior sphincter muscles contract and relax?

A
  • Contract in response to parasympathetic stimulation

* Relax in dim light so pupil larger

203
Q

Where is the iris situated between?

A

Lens and cornea

204
Q

What is the ciliary body?

A

Muscular layer that controls shape of lens and contributes to formation of aqueous humour

205
Q

How does the ciliary body focus on more distant and less distant objects?

A

 More focusing power (closer up objects) – lens get rounder

 More distant objects – lens get flatter

206
Q

What is the ciliary body composed of?

A

CIliary muscles (smooth muscle fibres) and ciliary processes (attach to lens)

207
Q

What is the choroid?

A

o Connective tissue + dense vascular network that provides nutrients to outer surface retina

o Choroid receives its blood supply from central retinal artery (that emerges from back of eye)

o Retinal arteries + veins supply the inner surface of retina is (come in through optic nerve vasiculus)

o Choroid provides all eye layers w/ 90% of their blood supply

208
Q

What is the light detecting part of the eye?

A

Retina

209
Q

The neural layer of the retina is split into 3 layers of nerve cells and 2 synapses. List them from deep to superficial.

A
  • Photo receptor cells (outermost layer) – rods + cones
  • Bipolar cells – transmit signals from photoreceptors to ganglion cells
  • Ganglion cells (innermost layer) – final output neurons in the retina
210
Q

What are the rod and cone cells sensitive to?

A

o Rod cells – sensitive to dim light, provide black + white vision

o Cone cells – sensitive to bright light, support perception of colour

211
Q

Name the other 2 types of cells in the middle layer along with bipolar cells.

A

Amacrine cells

Horizontal cells

212
Q

Function of amacrine cells in neural layer.

A

Inhibitory neurons that interact with retinal ganglion cells and/por bipolar cells

213
Q

Function of horizontal cells found in middle layer of neural layer of eyeball

A

Integrate info horizontally allowing communication between adjacent cells

214
Q

The retina is composed of neural layer and pigmented layer. What is the function of pigmented layer?

A

 Acts to support neural layer + continues around whole inner eye surface

 Anteriorly, the pigmented layer (non-visual retina) continues but the neural layer does not

 Posteriorly + laterally, both layers of retina are present (optic part of retina)

215
Q

Where is the lens?

A

• Located between the vitreous humour + pupil

216
Q

What happens when the shape of the lens changes?

A
  • The shape of the lens is altered by the ciliary body, changing its refractive power.
  • In old age, the lends can become opaque (cataract).
217
Q

Where is the anterior and posterior chambers located?

A

Anterior chamber - Located between cornea + iris.

Posterior chamber - Located between iris + ciliary processes.

218
Q

What are both chambers of the eyeball filled with?

A
  • Both chambers are filled w/ aqueous humour – clear plasma-like fluid that nourishes/protects eye
  • Aqueous humour is produced constantly + drains via the trabecular meshwork
  • Trabecular meshwork: an area of tissue at the base of the cornea, near the anterior chamber
  • If drainage of aqueous humour is obstructed, glaucoma can result
219
Q

The eyeball receives arterial blood primarily via which artery?

A

Ophthalmic artery

220
Q

What is the opthalmic artery a branch of?

A

Internal carotid

221
Q

The opthalmic artery gives rise to many branches which supply different components of the eye. Name the most important branch.

A

Central artery of the retina - supplies internal surface of retina.

Occlusion of it will quickly result in blindness.

222
Q

Venous drainage of the eyeball is carried out by which veins?Where do they drain?

A

Superior and inferior ophthalmic veins

They drain into cavernous sinus (a dorsal venous sinus in close proximity to the eye.

223
Q

Name 2 types of eye movements

A

o Gaze stabilisation (automatic)

o Gaze shifting (voluntary)

224
Q

We have voluntary control over gaze shifting eye movements. Name the movements and describe them.

A

Saccade:
• Directs eyes towards visual target (v. quickly)
• We have most voluntary control over theseSmooth pursuit
• Follows moving visual target e.g. tracking bird flying in sky

Vergence:
• Adjusts eyes for different viewing distance (depth)

225
Q

Name the 2 almost automatic gae stabilisation eye movements.

A

Vestibulo-Ocular

Optokinetic

226
Q

LR6 SO4 R3 meaning?

A

Lateral rectus muscle innervated by CN 6

Superior oblique by CN 4

Remaining 4 muscles by CN3

227
Q

Main movement of superior rectus muscle?

A

Elevation

228
Q

Main movement of inferior rectus muscle

A

Depression

229
Q

Main movement of medial rectus

A

Adduction

230
Q

Main movement of lateral rectus

A

Abduction

231
Q

Main movement of superior oblique?

A

Intorsion

232
Q

Main movement of inferior oblique?

A

Extorsion

233
Q

Secondary movement of Inferior and superior oblique muscles have a tertiary movement of what?

A

Abduction

234
Q

Name the only muscle that is capable of elevating the eye when it is in a fully adducted position

A

Inferior oblique

235
Q

When is supplementary eye field used?

A

When planning eye movements

236
Q

When is the frontal eye field?

A

Part of primary motor cortex that controls eye movements

237
Q

When is posteiror parietal cortex used in eye movement control?

A

Visual attention

238
Q

When is superior colliculus used?

A

In orientation to an object in visual field that catches attention

239
Q

Miosis

A

o Pupil constriction

o Iris sphincter active

o Iris dilator relaxed

o Response to light increase

o Parasympathetic control

o Relaxed state

o Also helps focus (accommodation)

240
Q

Mydrasis

A

o Pupil dilationo Iris sphincter relaxed

o Iris dilator active

o Response to light decreases

o Sympathetic control

o Elevated emotional/aroused state

o Let’s in more light

241
Q

Purpose of the accommodation reflex?

A

To focus on objects

242
Q

The accommodation reflex is under sympathetic or parasympathetic control?

A

Parasympathetic

243
Q

When does lens become rounder (thick)?

A

To focus on near object

244
Q

When does lens become thin?

A

To focus on distant object

245
Q

What is convergence?

A
  • When looking at distant image, pupils diverge

* When looking at near image, pupils converge

246
Q

What type of humour is produced by ciliary body constantly and circulates through anterior chamber?

A

Aqueous

247
Q

Where does aqueous humour exit?

A

Thorough trabecular meshwork between iris + lens

248
Q

Function of aqueous humour

A

 Maintains intraocular pressure + inflates the globe of the eye

 Provides nutrition for avascular ocular tissues

 Presence of immunoglobulins indicated a role in immune response

 Provides inflation for expansion of cornea

 For refractive index

249
Q

In which chamber is aqueous humour produced?

A

Posterior chamber and then flows through narrow cleft between front of lens and back of iris to escape through the pupil into the anterior chamber

250
Q

Production to drainage route of aqueous humour

A
  • Through posterior chamber (secreted by ciliary body)
  • Narrow space between posterior iris + anterior lens
  • Through pupil to enter anterior chamber
  • Trabecular meshwork
  • Schlemm’s canal
251
Q

Where is vitreous humour found?

A

 In area between lens + retina (posterior cavity/vitreous chamber)

 Vitreous humour is fluid-like near the centre, and gel-like near the edges

 It makes up 4/5th of the volume of the eyeball

252
Q

Function of vitreous humour

A

 It’s composed mostly of phagocytes, which remove unwanted cellular debris in the visual field

 Unlike the fluid aqueous humour which is continuously replenished, the gel in the vitreous chamber is stagnant

 Therefore, if blood, cells, or inflammation by-products get into vitreous, they remain there unless surgically removed• These are known as floaters

253
Q

What is opacification (clouding) of the lens caused by compaction + protein deposition, commonly known as?

A

Cataracts

254
Q

Most common type og glaucoma?

A

Primary open-angle glaucome

255
Q

Glaucoma treatment

A

Beta- blockers, alpha-2-adrenoceptor agonist, carbonic anhydrase, prostaglandin analogues, miotics (muscarinic agonist

256
Q

What is papilloedema?

A

o Swelling of optic disc, visible during ophthalmoscopy

o The optic disc is the area of the retina where the optic nerve enters

o Swelling occurs secondary to raised intracranial pressure

o High pressure within cranium resists venous return from the eye

o This causes fluid to collect in the retina -> swollen optic disc

257
Q

Describe horner’s syndrome.

A

Triad of symptoms produced by damage to the sympathetic trunk in the neck:

 Partial ptosis (drooping of upper eyelid)

 Miosis (pupillary constriction)

 Facial anhydrosis (absence of sweating)

258
Q

Extraocular muscles are innervated by 3 cranial nerves. Damage to CN III causes what?

A

CN III – eye adopts a position known as ‘down + out’

259
Q

Damage to CN IV causes?

A

No obvious effect of the resting orientation of eyeball

260
Q

Damage to CN VI cause?

A

Affected eye is adducted by resting tone of medial rectus

261
Q

Protanopes lack which type of cone?

A

Lack ‘L’ red conesLong wavelengh

262
Q

Tritanopes lack which type of cone?

A

S (blue) conesNot x-linked (chromosome 7)Short wavelength

263
Q

Deuteranopes lack which type of cone?

A

M (middle wavelength) green cone

264
Q

What are anomalous trichromats?

A

People with 3 cone types, but one is ‘weak’, this is more common than dischromacy:

265
Q

What is protanomalous trichromat?

A

Weak red cones

They shift their sensitivity to higher wavelength (more sensitive to green) making it difficult to distinguish between red + green

266
Q

What is deuteranomalous trichromat?

A

Weak green cones

They shift their sensitivity to lower wavelength (more sensitive to red) making it difficult to distinguish between red + green

267
Q

What is. tritanomalous trichromat?

A

Weak blue cones

268
Q

Where do about 90% of the axons in the optic nerve fo to?

A

The lateral geniculate nucleus in the thalamus

269
Q

What happens at the optic chiasm?

A

o The optic nerves from both eyes meet and cross at the optic chiasm, at the base of the hypothalamus of the brain

o Info coming from both eyes is combined and then splits according to the visual field

o The corresponding halves of the field of view (R + L) are sent to the L + R halves of the brain, respectively, to be processed

 R side of the primary visual cortex deals with the L half of the field of view from both eyes, + similarly for left brain

270
Q

What are optic tracts?

A

o Info right visual field (now on the left side of the brain) travels in the left optic tract

o Info from the left visual field travels in the right optic tract

o Each optic tract terminates in the lateral geniculate nucleus in the thalamus

271
Q

From eye to brain.

Order the following: optic chiasm, optic nerve, optic tract, visual cortex, optic radiation, extrastriate visual areas, lateral geniculate nucleus

A

Optic nerve

Optic chiasm

Optic tract

Lateral geniculate nucleus

Optic radiation

Visual cortex

Extrastriate visual areas

272
Q

Name the sensory relay nuclei in the thalamus of brain for visual info.

A

Lateral geniculate nucleus

273
Q

Name the primary visual cortex

A

Straite cortex

274
Q

Where does the primary visual cortex receive info from?

A

Directly from LGN

275
Q

Feature of the frontal lobe

A

Intellectual function

Praxia - giving/carrying out tasks in ordered sequenceInhibition

Bladder continence

Saccadic eye movement - voluntary horizontal eye movements (eyes deviate towards side of destruction and away from side of irritation)

Motor function

Expression of language in dominant lobe (usually L)

276
Q

Features of tempral lobe

A
  • Memory
  • Smell
  • Hearing
  • Vestibular function
  • Emotion (limbic system)
277
Q

Features of parietal lobe

A

Sensory integration
o Info on sight/smell etc. comes from the other lobes
o The parietal lobe interprets this info + integrates it together

Receptive language
o Making sense of language

278
Q

Occipital lobe

A

Vision - lesions may cause hemianopia

279
Q

Arterial supply to cerebrum

A

Anterior Cerebral Arteries - Branches of internal carotid arteries, supplying the anteromedial aspect of the cerebrum.

Middle Cerebral Arteries - Continuation of internal carotid arteries, supplying most of the lateral portions of cerebrum.

Posterior Cerebral Arteries - Branches of basilar arteries, supplying the medial + lateral sides of cerebrum posteriorly.

280
Q

Cranial nerve summary

A

• Cerebrum – cranial nerve I, II

• Midbrain – cranial nerve III, IV
o CN III emerges from pontine-medulla junction
o CN IV comes from posterior side of midbrain + has longest intracranial length of all cranial nerves

  • Pons – cranial nerve V, VI, VII, VIII
  • Medulla – cranial nerve IX, X, XI, XII
281
Q

List features of cerebellar dysfunction (VANISH’D).

A
  • Vertigo
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Slurred, staccato, scanning speech
  • Hypotonia
  • Dysmtria
282
Q

Summary of brainstem

A

 Made up of: midbrain, pons, medulla

 As a role, motor cranial nerve nuclei are situated more medially + purely sensory nuclei more laterally

 Nerves with an intermediate function are in-between

 Substantia nigra – dopamine production

 Red nucleus – important for coordination

 Respiratory centre

 Cardiac centre

 Reticular activating system

 Conduit for white matter tracts

  • Eye movements
  • Motor – e.g. corticopontine, corticobulbar, corticospinal
  • Sensory – e.g. spinothalamic
  • Coordination – e.g. spinocerebellar
283
Q

Cerebellum summary (functional/anatomical sections)

A
  • Vermis (vestibulocerebellum) – balance + equilibrium.
  • Paravermis (spinocerebellum) – postural tone.
  • Cerebellar hemispheres (pontocerebellum/cerebrocerebellum) – fine coordination
284
Q

What is this a definition of an abrupt loss of focal brain function lasting more than 24 hours due to either spontaneous haemorrhage into brain substance or inadequate blood supply to part of the brain i.e. ischaemia (thrombosis, embolism)?

A

Stroke

285
Q

What is Wernicke-Korsakoff syndrome?

A

o Associated w/ heavy drinking + malnutrition (B1 deficiency)

o Combination of Wernicke’s encephalopathy + Korsakoff’s syndrome

o Atrophy in mammillary bodies, thalamus, periaqueductal grey, wall of 3rd ventricle, cerebellum + frontal lobe

 Amnesia – due to atrophy of the structures in the diencephalon

 Confabulation – hold memories they think is true; anterograde + variable retrograde amnesia

286
Q

S+S of frontal lobe dementia?

A

o Disinhibited behaviour

o Change in appetite – they develop a sweet tooth

o Reduced sense of smell

o Bladder dysfunction

o Gait apraxia

o Progressive motor (expressive) dysphasia

287
Q

S+S of temporal lobe epilepsy?

A

Memory :
 Déjà vu – Somewhere familiar seems unfamiliar
 Amnestic seizures – Don’t remember activities during seizure

Smell:
 Olfactory hallucinations

Hearing:
 Auditory hallucinations (noises/random words)Vestibular function
 VertigoEmotion (limbic system)
 Sudden anger/fear

288
Q

A lesion on R cranial nerve nuclei in the brainstem will cause what?

A

R sided (ipsilateral) LMN weakness

289
Q

A lesion to the R side of the spinal cord will cause what?

A

R sided (ipsilateral) UMN weakness below the level of the lesion

290
Q

A lesion in R motor cortex or in the R internal capsule will cause weakness where?

A

L sided (contralateral) UMN weakness

291
Q

Functionally, the ascending tracts can be divided by the type of info they transmit:

  • Conscious tracts
  • Unconscious tracts

What are conscious tracts comprised of?

A

Dorsal column-medial lemniscal pathway (DCML) -  Fine touch, vibrations, proprioception

Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure.

Lateral spinothalamic tract – carries the sensory modalities of pain and temperature)

292
Q

Functionally, the ascending tracts can be divided by the type of info they transmit:

  • Conscious tracts
  • Unconscious tracts

What are unconscious tracts comprised of?

A

Spinocerebellar tracts - unconcious proprioception:

Posterior spinocerebellar tract – Carries proprioceptive information from the lower limbs to the ipsilateral cerebellum.

Cuneocerebellar tract – Carries proprioceptive information from the upper limbs to the ipsilateral cerebellum.

Anterior spinocerebellar tract – Carries proprioceptive information from the lower limbs.

The fibres decussate twice – and so terminate in the ipsilateral cerebellum.

Rostral spinocerebellar tract – Carries proprioceptive information from the upper limbs to the ipsilateral cerebellum.

293
Q

Which modalities does the anterior spinothalamic tract carry?

A

Crude touch and pressure

294
Q

Which modalities does the lateral spinothalamic tract carry?

A

Pain and temp

295
Q

Which modalities does the DCML carry?

A

Fine touch, vibration, proropception

296
Q

Which modalities does the spinocerebellar tracts carry?

A

Unconscious poproioception

297
Q

Where do DCML tracts decussate?

A

Contralateral – decussate in medulla

298
Q

Where do spinothalamic tracts decussate?

A

Contralateral – decussate in spinal cord (2-3 levels above entry)

299
Q

Where do spinocerebellar tracts decussate?

A

They don’t.

They are ipsilateral

300
Q

Motor (descending) tracts can be divided into pyramidal and extrapyramidal groups.Name the pyramidal tracts.

A

Corticospinal

Corticobulbar

301
Q

Motor (descending) tracts can be divided into pyramidal and extrapyramidal groups.Name the extrapyramidal tracts.

A

Vestibulospinal
Tectospinal
Reticulospinal
Rubrospinal

302
Q

Where do pyramidal tracts originate and what are they responsible for?

A

 Originate in cerebral cortex and go to spinal cord + brainstem

 Responsible for voluntary control of musculature of body + face

303
Q

Where do extrapyramidal tracts originate and what are they responsible for?

A

 Originate in the brain stem and go to spinal cord

 Responsible for muscle tone, balance, posture + locomotion

304
Q

What do lateral corticospinal tracts control?

A

Distal muscles

305
Q

What do anterior corticospinal tracts control?

A

Proximal movements

306
Q

Are corticospinal (pyramidal) tracts contralateral or ipsilateral?

Where do they decussate if they do?

A

Contralateral - 90% decussate in medulla (lateral corticospinal)

Ipsilateral - 10% decussate in spinal cord (anterior corticospinal

307
Q

What do corticobulbar tracts supply?

A

Muscles of face and neck

308
Q

What muscles do vestibulospinal tracts innervate?

A

Balance and posture

309
Q

Are vestibulospinal, tectospinal, reticulospinal, rubrospinal, corticobulbar, corticospinal tracts contralateral or ipsilateral?

A

Vestibulospinal - ipsilateral

Tectospinal - contralateral

Reticulospinal - ipsilateral

Rubrospinal - contralateral

Corticobulbar - mixed

Corticospinal - contralateral

310
Q

Desrribe a CN XII palsy

A

 Tongue deviates towards the side of the weakness, not the side of the lesion
 Ipsilateral in LMN lesion
 Contralateral in UMN lesion

311
Q

CN XII lesion

A

 Wastage of muscle + probably fasciculations
 Weakness of tongue
 Dysarthria

312
Q

What does the hypoglossal nerve CN XII supply?

A

Motor function of tongue

313
Q

What does CN XI control?

A

 Turning of head – sternocleidomastoid muscle

 Shrugging of shoulders – trapezius muscle

314
Q

CN XI palsy can be caused during neck injury. What does it look like?

A

Sternocleidomastoid and trapezius muscles do not contract when patient shrugs or turns head on one side

315
Q

What’s Bell’s palsy?

A

LMN lesion of facial nerve (CN VII)

316
Q

Facial nerve lesion of UMN and LMN

A

 UMN lesion – Gives rise to contralateral weakness of bottom half of the face

 LMN lesion – Gives rise to weakness of the whole side of the ipsilateral face (Bell’s palsy)Muscles of the forehead are represented bilaterally in the cortex and so an UMN lesion of one side can be overcome by the opposing side

317
Q

How is muscle bulk, tone, power affected by UMNLs and LMNLs?

A

UMNL

  • Bulk decreases
  • Tone increases
  • Power increases

LMNL:

  • Bulk decreases more than UMNL
  • Tone decreases
  • Power decreases
318
Q

How are reflexes affected in an UMN and LMN lesions?

A

UMNL - increases

LMNL - decreases

319
Q

CN III lesion (oculomotor nerve)

A

o Eye is situated ‘down + out’

o Pupil dilated – oculomotor n. supplies parasympathetic fibres responsible for pupillary constriction

o Partial ptosis – from paresis of levator palpebrae superioris

320
Q

Describe decerebrate posturing (damage to upper brainstem)

A

o Arms adducted

o Legs extended

o Feet plantar flexed

o Wrists pronated

o Fingers flexed

321
Q

Describe decorticate posturing (damage to corticospinal tracts)

A

o Arms adducted + flexed

o Wrists + fingers flexed on chest .

o Legs extended + internally rotated

o Feet plantar flexed

322
Q

Arefasciculations present in an UMN or LMN lesion?

A

LMN

323
Q

Gait summary

A

 Spastic – scissoring if bilateral

 Cerebellar – broad based + unsteady (they walk like drunk)

 Frontal (marche a petit pas) – small steps (looks similar to parkinsonian)

 Parkinsonian – slow + shuffled becoming festinant in later stages

 Waddling – proximal leg muscle weakness

 Antalgic – if sensory dysaesthesia in feet

 High steppage (equine – lift feet high like horse) – if sensory loss in feet

 Dropped foot gait – if weakness of ankle dorsiflexion

 Atasia-abasia – psychological; malingering

324
Q

What is anterior spinal artery syndrome

A

o Anterior spinal artery (primary blood supply to the anterior portion of the spinal cord) is interrupted

o Causing ischaemia or infarction of spinal cord in anterior 2/3 of the spinal cord + medulla oblongata

325
Q

What is. anterior spinal artery syndrome characterised by?

A

 Loss of motor function below the level of injury

 Loss of temperature and pain sensation (spinothalamic)

 Preservation of sensations carried by the posterior columns – Fine touch, vibration, proprioception

326
Q

Central cord lesion is characterised by?

A

o Characterised by loss of motion + sensation in arms + hands

o Usually results from trauma –> causes damage to neck –> major injury to central grey matter of spinal cord

o Sensation above + below level of damage is normal, but as level of damage there’s compromised sensation

 Hung sensory loss

 Disassociative sensory loss

 UMN signs below level if pressure on corticospinal tracts

327
Q

4 types of stroke

A

Haemorrhagic
Thromboembolic
Embolic
Lacunar

328
Q

What is haemorrhagic stroke?

A

Blood vessels in brain rupture –> spilling blood into surrounding tissues

329
Q

What is thromboembolic stroke?

A

Blood clot develops in blood vessels inside brain

330
Q

What is embolic stroke.

List causes of it

A

Blood clot develops elsewhere in body + breaks loose –> carried in blood to plug vessel in brain

Causes:
o	MI w/ dyskinesia cardiac chamber 
o	Atrial fibrillation
o	Valvular heart disease 
o	Endocarditis
331
Q

What is lacunar stroke?

A

Occlusion of small penetrating arteries that provide blood to brain’s deep structures

332
Q

Sites of brain haemorrhage?

A

o Intracerebral (stroke)
o Subarachnoid
o Subdural
o Extradural

333
Q

o Occurs when blood accumulates between skull + dura mater
o Typically follows head injury
o High pressure bleeding is a prominent symptom

A. Intracerebral (stroke)
B. Subarachnoid
C. Subdural
D. Extradural

A

D. Extradural

334
Q

o Occurs when there is bleeding between the dura + arachnoid mater
o Typically, is result of head moving rapidly forwards + stopping (such as in car accident)
o This type of haemorrhage is more common than other ICHs in older people + alcoholics

A. Intracerebral (stroke)
B. Subarachnoid
C. Subdural
D. Extradural

A

C. Subdural

335
Q

o Bleeding between arachnoid + pia mater

o A sudden, sharp headache usually precedes a subarachnoid haemorrhage

o This type of ICH can be due to alcohol or drug abuse + tends to run in families

A. Intracerebral (stroke)
B. Subarachnoid
C. Subdural
D. Extradural

A

B. Subarachnoid

336
Q

o Bleeding in brain caused by the rupture of blood vessels within the head

o This is not usually result of injury .

o A prominent warning sign = sudden onset of neurological deficit.

Causes:
	Rupture of aneurysm
	Arteriovenous malformation 
	Carmona 
	Bleed into infract 
	Bleed into tumour 
	Trauma

A. Intracerebral (stroke)
B. Subarachnoid
C. Subdural
D. Extradural

A

A. Intracerebral (stroke)

337
Q

Different elements of postural control

A

Brainstem:
 Most important
 Controls automatic functions

Cerebral cortex:
 Controls voluntary control of posture

338
Q

How are LMNs organised in spinal cord?

A

 Posture – Motor neurons innervating axial or proximal musculature – located medially (ventromedial)

 Voluntary – Motor neurons innervating distal musculature – located laterally (dorsolateral)

339
Q

Name the 4 descending tracts originating in the brainstem and terminating in the spinal cord, involved in controlling posture.

A

 Vestibulospinal tract – info from vestibular nuclei about sense of balance relative to gravity

 Tectospinal tract – info from visual system (superior colliculus) used for orientating to visual stimuli

 Pontine reticulospinal tract – brings info from pons for large movement of trunk + limbs

 Medullary reticulospinal tract – brings info from medulla

340
Q

Function of vestibulospinal and tectospinal tracts?

A

 Function – keep head balanced on shoulders as body moves (controls posture of head + neck)

341
Q

Name the tract that carrying sensory input from vestibular labyrinth in inner ear

A

Vestibulospinal tract

342
Q

Which tract carries input from retina to superior colliculus (optic tectum)?

A

Tectospinal tract

343
Q

What is decerebrate rigidity?

A

Massive increase in tone of extensor muscles caused by disinhibition of brainstem nuclei.

Normally the tonic activity of the lateral vestibular + reticular nuclei in brainstem (causing muscle extension) are under tonic inhibitory control by cerebral + cerebellar inputs.

344
Q

What is the decerebrate response?

A

With extensive cortical damage, there is increase extensor tone due to brainstem action wo/ cerebral inhibition

345
Q

Where is the vestibular system located?

A

Located in the inner ear, just above cochlea

346
Q

All info from vestibular system is carried by which nerve?

A

Vestibular nerve (vestibular branch of vestibulocochlear nerve, CN VIII)

347
Q

Function of vestibular system

A

o Provides sense of balance

o Motion detectors

o Provides info about head orientation, displacement, and movement in 3D space

348
Q

Otolith organs + semicircular canals contain hair cells which do what?

A

Convert motions in the head to neural signals

349
Q

Name the 2 otolith organs

A

Utricle + saccule.

They sense motion in 2 different directions

350
Q

Does the utricle or saccule sense motion in vertical direction?

A

Saccule

351
Q

Does the utricle or saccule sense motion in horizontal direction?

A

Utricle

352
Q

Both the utricle and saccule (otolith organs) work inthe same way.

They are made up of hair cells and gelatinous cap.

How does the. utricle maculae encode horizontal linear motion and acceleration?

A

 Moving head side to side which changes utricle

 Macula is horizontal

 Kinocilia towards striola (midline along centre of macula)

 Mainly encodes horizontal linear motion + acceleration

353
Q

Moving head up and down causes in changes saccule. What does this encode?

A

Verticle linear motion and acceleration

354
Q

Difference between kinocilia and sterocilia (hair cells that generate APs at a steady baseline rate, hey can be inhibited or excited)

A
  • Kinocilia – longer ones
  • Sterocilia – the rest The cilia may be:
  • Excited (depolarised) – when cilia are pushed in direction of kinocilium
  • Inhibited (hyperpolarised) when cilia are pushed in direction of stereocilium
355
Q

What is otoliths?

A

Calcium carbonate crystals that encrust the surface of the gelatinous cap

They act like weights - tilting head down causes gravity pulls crystals down which causes drags gelatinous cap down which causes gelatinous cap displaces hair cells

356
Q

Function of sermicricular canals?

A

Sensitive to head rotation; rotational motion + angular acceleration

357
Q

How is 3D space represented by the anterior, posterior, horizontal (lateral) semicircular canals?

A
  • The canals on both sides of head (in each ear) work together.
  • They are filled w/ a fluid called endolymph.
  • Main sensory structure of each canal located in the ampulla (base on canals).
358
Q

Seicircular canals summary

A
  • Semicircular canals have an otolith like structure called ‘cupula’ in the ampulla.
  • The cupula is a gelatinous structure.
  • Inside there are hair cells embedded.
  • Moving the head one way will cause endolymph to move in the same direction.

• This displaces the cupula + pushes it in opposite direction
.
• This triggers hair cells to depolarise (opposite side will hyperpolarize).

359
Q

The sensory nerve fibres (CN VIII) project info from semi-circular canal and otolith organs to vestibular nuclei in brainstem.

They send projections via medial longitudinal fasciculus to?

A

 Cerebellum – important for coordination of movement in response to head/body position changes

 Limb motor neurons – to control axial muscles + proximal limb muscles

 Extra-ocular motor neurones (CN III, IV, VI) – to control extraocular eye muscles .

 Neck motor neurones – to control head position

360
Q

Vestibulo-ocular reflex?

A

The compensatory movement of the eyes in the opposite direction of head rotation

o Input from vestibular system (semicircular canals or otolith organs) directly to the extra-ocular muscles

o Causes compensatory movement of eyes in the opposite direction of head movement so one can keep the visual world stable on retina during movement

361
Q

Function of vestibulo-ocular reflex?

A

Maintain stable vision during head movements

o Person turns head to the left.

o Left horizontal canal excited (right inhibited).

o Signal sent to vestibular nuclei, then to oculomotor nuclei.

o Right abducens (CN VI) flexes right lateral rectus.

o Left oculomotor nerve (CN III) flexes left medial rectus.

o Eyes turn to the right.

362
Q

VOR and posture

A

o Allows image to remain steady on retina despite head movements.

o If it is not working, then corrective eye movements are not made.

o Disconcerting feeling that world is moving when head moves, makes standing, walking, maintaining posture very difficult.

o Because it is vestibular system-based, it still works in the dark or when you have your eyes closed.

363
Q

Caloric testing?

A

 Irrigate ear with cold or warm water.

 Temp gradient will set up convection currents in endolymph, distorting the cupula to increase firing of afferents.

 Induces the VOR.

Results:
 Brainstem intact – both eyes move towards the side with the water in ear.
 Medial longitudinal fasciculus lesion – only eye. closest to water moves towards water, the other stays still.
 Low brainstem lesion – no VOR at all, eyes stay still.

364
Q

What is Meniere’s syndrome?

A

o Endolymphatic hydrops

o Idiopathic increase in volume of endolymph distrust function of membranous labyrinth of inner ear

365
Q

Symptoms of Meniere’s syndrome

A

Symptoms: attacks of vertigo, deafness, tinnitus (because endolymph also in cochlea)

366
Q

Meniere’s syndrome treatment

A

Treatment: no cure, but can treat vertigo, nausea + vomiting with: prochlorperazine + antihistamines

367
Q

Cause of Benign paroxysmal positional vertigo?

A

Caused by calcium carbonate crystals dislodged from otolith organs, disrupting flow of endolymph in semicircular canals

368
Q

BPPV symptoms

A

Suddenly feeling dizzy on moving head in a certain direction; rolling over in bed (room spinning); nausea/vomiting

369
Q

BPPV treatment

A

Epley or Semont manoeuvre reposition CaCO3 crystals

370
Q

To maintain posture we need what type of tone?

A

Significant extensor tone

371
Q

Sound in the cochlea

A

o Sound wave travels through external ear, causes vibration of ear drum + ossicles

o Footplate of stapes vibrates in oval window

o Causes wave to travel along scala vestibuli in perilymph and back along scala tympani to round window (loose membrane where sound is absorbed)

o Also causes displacement of basilar membrane and vibration of organ of Corti

372
Q

Basilar membrane

A

o Most stiff nearest to base of cochlea and least stiff at helicotrema

 Thus, only high-frequency sound can displace basilar membrane at the base

 Lower frequencies will travel further along the cochlea (before crossing membrane)

o High-pitched sounds sensed at the base of cochlea, low pitches at apex – this is known as tonotopy

373
Q

Organ of Corti

A

o Located in cochlear duct

o Transduces pressure waves into action potentials

o Contains 15,000-20,000 auditory receptors, each with its own hair cell

o Displacement of basilar membrane –> shear of hair cells –> opening non-selective transduction ion channels –> depolarisation

374
Q

Cochlear hair cells

A

o Outer hair cells – Amplify mechanical input to inner hair cells

o Inner hair cells – Send information to brain via spiral Cochlear hair cells are identical to sensory hair cells found in vestibular part of labyrinth

375
Q

Function of auricle (aka pinna)

A
  • Capture + transmit sound to external acoustic meatus
  • Funnels sound into ear canal
  • Aids in the vertical localisation of sounds
  • Filters sound (human auricle preferentially selects sounds in frequency range of human speech)
  • In other mammals, pinna may have other roles – signalling mood; assisting thermoregulation
376
Q

Innervation and vasculature of auricle

A

Innervation:
• Greater auricular n.
• Lesser occipital n.
• Branches of the facial + vagus nerves

Vasculature (arteries + veins):
• Posterior auricular
• Superficial temporal
• Occipital

377
Q

Structure of external acoustic meatus

A
  • Sigmoid shaped tube; 7mm in diameter + ~25mm long
  • Extends from concha of auricle to tympanic membrane
  • Has double layered structure covered w/ skin on outside + mucus membrane on inside
  • Contains hair, sebaceous + ceruminous (ear wax) glands
  • Walls are given their structure by: cartilage from auricle + bony support from temporal bone
  • It is connected to surrounding temporal bony by a fibrocartilaginous ring
378
Q

Function of external acoustic meatus

A
  • Focuses sound energy on ear drum

* Amplifies by 10-15dB, sound corresponding to frequencies of human speech

379
Q

Function of middle ear

A

o Transmit vibrations from tympanic membrane to inner ear via the 3 bones (ossicles)

o Ossicles amplify the sound waves by 20x

380
Q

Structure of middle ear

A

o It is the air-filled chamber between ear drum + inner ear

o Middle ear lies within the temporal bone

o Middle ear can be split into 2 sections:tympanic cavity and epithympanic recess

381
Q

List bones of the middle ear from outer to inner

A

Malleus (hammer).

Incus (anvil).

Stapes (stirrup).

382
Q

Name the 2. muscles of the middle ear

A

Tensor tympaniStapedius

383
Q

Tensor tympani

A

o Attached to the handle of malleus

o Innervated by the mandibular part of trigeminal nerve (CN V)

o Activated during chewing

384
Q

Stapepdius

A

o Attached to the stapes

o Innervated by facial nerve (CN VII)

o Activated during speaking

385
Q

Auditory tube (eustachian tube)

A

 This tube is normally closed – opens when there are pressure changes between outer + middle ear.

 It is a cartilaginous + bony tube that connects the middle ear to the nasopharynx.

 Acts to equalise pressure of middle ear to that of the extender auditory meatus.

 In joining 2 structures, it’s a pathway by which an upper respiratory infection can spread into middle ear.

 This tube is normally closed – opens when there are pressure changes between outer + middle ear.

 It is a cartilaginous + bony tube that connects the middle ear to the nasopharynx.

 Acts to equalise pressure of middle ear to that of the extender auditory meatus.

 In joining 2 structures, it’s a pathway by which an upper respiratory infection can spread into middle ear.

386
Q

Main functions of inner ear?

A

Cochlea uses movement of fluid to sense external pressure changes (sounds)
- Conversion of mechanical (kinetic) signals from middle ear (ossicles)

 hydraulic energy of fluid in inner ear

 electrical signals in vestibulocochlear nerve (CN VIII)
- Which can transfer info to auditory pathway in the brain Vestibular part of labyrinth uses movement of fluid to sense rotational + translational accelerations to maintain balance

387
Q

Where is the. inner ear located?

A

WIthin the petrous part of the. temporal bone

388
Q

Name the 2 components of. the inner ear

A

Bony labyrinth and Membranous labyrinth

389
Q

What is the bony labyrinth composed of?

A

Cochlea, vestibule, 3 semicircular canals

390
Q

Semi-circular canals

A

 There are 3: anterior, lateral, posterior canals

 Contain semi-circular ducts, which are responsible for balance (along w/ utricle + saccule)

 The canals are situated superioposterior to vestibule

 They have a swelling at one end, the ampulla

391
Q

Hearing

A
  • Sound waves travel through external ear, cause vibration of ear drum = ossicles
  • Foot plate of stapes vibrates in oval window
  • Wave travels along scala vestibuli in perilymph + back along scala tympani to round window
  • Also causes displacement of basilar membrane + vibration of Organ of Corti
392
Q

Cochlea has 3 sections (chamber)

A
  • Scala vestibuli – filled w/ perilymph
  • Scala media (or cochlear duct) – filled w/ endolymph
  • Scala tympani – filled w/ perilymph
393
Q

Vestibule

A

 Central part of body labyrinth

 Separated from middle ear by oval window

 Communicates anteriorly w/ cochlea + posteriorly w/ the semi-circular canal

 2 parts of membranous labyrinth: saccule + utricle – are located within vestibule

394
Q

Cochlea

A

 Houses cochlea duct of membranous labyrinth – auditory part of inner ear

 It twists upon itself around a central portion of bone called the modiolus

 Branches from the cochlear portion of CN VIII are found at base of modiolus

395
Q

Membranous labyrinth

A
  • System of tubes + chambers within bony labyrinth, filled w/ endolymph (fluid w/ high K+ conc)
  • Bony + membranous labyrinth separated by layer of perilymph (fluid w/ high Na+ conc)
  • Membranous labyrinth conforms to shape of bony part except in vestibule region
  • Consists of the cochlear duct, semi-circular ducts, utricle + saccule
396
Q

Cochlear duct

A

 Situated within cochlea + filled w/ endolymph

 Organ of hearing – houses epithelial cells of hearing + organ of corti

397
Q

Saccule and utricle

A

 2 membranous sacs located in the vestibule

 Endolymph drains from saccule + utricle into endolymphatic duct

 Duct travels through vestibular aqueduct to post. aspect of petrous part of temporal bone

 Here the duct expends to a sac where endolymph can be secreted + absorbed

398
Q

Semicircular ducts

A

 Located within semicircular canals (share their orientation)

 Upon movement of head, flow of endolymph within ducts changes speed and/or direction

 Sensory receptors in the ampullae of semi-circular canals detect this change + send signals to brain, allowing for processing of balance

399
Q

The inner ear has 2 openings into the idle ear, both covered by membranes. Oval and round window. Where does the oval window lie?

A

Oval window – lies between middle ear + vestibule

400
Q

Where does the round window lie?

A

Round window – separates middle ear from scala tympani (part of cochlear duct)

401
Q

The body labyrinth and membranous labyrinth have different arterial supplies.

The bony labyrinth receives 3 arteries, which also supply the surrounding temporal bone.

Name them

A
  • Anterior tympanic branch (from maxillary artery)
  • Petrosal branch (from middle meningeal artery)
  • Stylomastoid branch (from posterior auricular artery)
402
Q

The membranous labyrinth is supplied by labyrinthine artery, a branch of inferior cerebellar artery (or, occasionally, the basilar artery).

It divides into 3 branches - name them.

A
  • Cochlear branch – supplies the cochlear duct

* Vestibular branches (x2) – supply the vestibular apparatus

403
Q

Sound wave is transmitted through 4 separate mediums. Name them.

A

Outer ear - air

Middle ear - mechanical

Inner ear - liquid

Brain - neural

404
Q

From vestibulocochlear nerve (CN VIII), sound impulse travels through auditory pathway to the auditory cortex.

Using the mnemonic SLIM list where the impulses travel.

A

 Superior olivary complex

 Lateral lemniscus

 Inferior colliculus

 Medial geniculate nucleus

405
Q

Where does decussation occur in the auditory pathway?

A

Decussation occurs between the cochlear nuclei and superior olivary complex, and at inferior colliculi

406
Q

Where is the auditory cortex located?

A

Temporal lobe at margin with frontal lobe.

Brodmann areas 41 and 42

407
Q

Auditory cortex

A

o Axons leaving the medial geniculate nucleus project to the auditory cortex via the internal capsule in an array.

o The auditory cortex is tonotopic, like the basilar membrane.

 I.e. high frequencies processed at the posterior part and low frequencies at the anterior part

408
Q

Sound localisation

A

Decussation enables inputs from left + right ears to be compared in superior olivary nuclei (SON) + localise sound

 Medial SON – Detects differences in the time that sounds reach each ear

• Localisation of low-frequency sound (<800Hz) occurs by detection of time differences in sound reaching each ear

 Lateral SON – Detects differences in sound intensity reaching each ear

• Localisation of high-frequency sound (>1600Hz) occurs by detection of differences in sound intensity at each ear.

A mixture of both methods is used for sounds between 800 + 1600Hz

409
Q

Common causes of conductive hearing loss

A

 Infection – otitis externa + otitis media

 Build-up of earwax

 Perforated eardrum

 Fluid in the middle ear

 Membrane tension

 Damage to the small bones within the middle ear

410
Q

Conductive hearing loss

A

Sounds become quieter, although not usually distortedDepending on its cause, a conductive hearing loss can either be temporary or permanent

411
Q

Common causes of sensorineural hearing loss

A

 Presbycusis – naturally occurs damage to cochlea when ageing

 Noise-induced – regular + prolonged exposure to loud sounds

 Ototoxic drugs

 Inflammatory disease e.g. measles, mumps, meningitis, syphilis

 Complications at birth

 Congenital

 Physical trauma

 Benign tumours on the auditory nerve

 Meniere’s disease

412
Q

Sensorineural hearing loss

A

o Problem in cochlea (organ of corti), vestibulocochlear nerve, auditory cortext of brain

o This type of hearing loss is sometimes referred to as sensory, cochlear, neural, or inner ear hearing loss

o A permanent sensorineural hearing loss is the result of damage to hair cells within the cochlea or hearing nerve (or both)

o Sensorineural hearing loss changes our ability to hear quiet sounds, + reduces the quality of the sounds heard, meaning that individuals with this type of hearing loss will often struggle to understand speech

o Once the cochlea hair cells become damaged, they will remain damaged for the rest of a person’s life, therefore sensorineural hearing loss is irreversible + cannot be cured

413
Q
  • Rinne and Weber tests are exams that test for hearing loss
  • They help determine whether the individual may have conductive or sensorineural hearing loss

What is the Rinne test?

A

Rinne test evaluated hearing loss by comparing air conduction to bone conduction

 Air conduction hearing occurs through air near the ear, and it involves the ear canal and eardrum

 Bone conduction hearing occurs through vibrations picked up by the ear’s specialised nervous system

414
Q

Results of Rinne test?

A

 Normal hearing will show an air conduction time that is twice as long as the bone conduction time – AC > BC

 Conductive hearing loss – Bone conduction (BC) is heard longer – BC > AC

 Sensorineural hearing loss – Air conduction (AC) is heard longer but may not be twice as long – AC > BC

415
Q

What test is this?

 Strikes a tuning fork and places it on the middle of patient’s head

 Note where the sound is best heard – the left ear, the right ear, or both equally

A

Weber test

416
Q

Results of Weber test

A

 Normal hearing will produce equal sounds in both ears

 Conductive hearing loss – Sound to be heard best in abnormal ear

 Sensorineural hearing loss – Sound to be heard best in normal ear

417
Q

Are most strokes ischaemic or haemorrhagic?

A

Ischaemic (85%)

418
Q

Types of ischaemic strokes.

A

 Thrombosis – Obstruction of a blood vessel by a blood clot forming locally

 Embolism – Obstruction due to an embolus from elsewhere in the body

 Systemic hypoperfusion – General decrease in blood supply (e.g. in shock)

 Cerebral venous sinus thrombosis – Obstruction in the dural venous sinuses

419
Q

Types of haemorrhagic stroke

A

 Cerebral haemorrhage (intracerebral haemorrhage) – bleeding within the brain itself

 Subarachnoid haemorrhage – Bleeding that occurs outside the brain tissue but still within the skull (between the arachnoid mater and pia mater)

420
Q

Causes of infarct in young people?

A

 Dissection – commonest cause in young people
 Cardio-embolism – due to: patent foramen ovale (PFO), endocarditis
 Vasculitis (uncommon)
 Genetic – very rare, e.g. CADASIL, Fabrys, MELAS
 Illicit drug use – amphetamines, cocaine

421
Q

Intracranial haemorrhage causes in young people?

A

 Arteriovenous malformation (AVM) – abnormal blood vessel connections, fragile vessels burst

 Aneurysm – may be familial

422
Q
Are these medications taken by ischaemic or haemorrhagic stroke?
	Clopidogrel
	Statin
	Anti-hypertensive
	Anticoagulant if AF
A

Ischaemic stroke

423
Q

What do people end up taking after haemorrhagic stroke?

A

Anti-hypertensives

424
Q

Non modifiable risk factors for stroke?

A

o Age

o Gender

o Race – south Asian’s w/ western lifestyle

o Family history – rarely congenital

425
Q

Modifiable risk factors for stroke?

A

Hypertension - most important for cerebral haemorrhage

Diabetes

Atrial fibrillation

Smoking

Hyperlipidaemia

Obesity

426
Q

Parietal lobe

A

o Post central gyrus – Sensory cortex

o Wernicke’s area – Receptive area for language comprehension
 Damage causes receptive dysphasia (can hear words but cannot understand them)

o Dominant – Handling numbers, calculations

o Non-dominant – Concepts of body image + awareness of external environment

o Visual pathways – Optic path runs through here

427
Q

Temporal lobe

A

o Auditory cortex

o Learning + memory

o Olfactory sensation

o Emotional behaviour

o Visual pathways

428
Q

Frontal lobe (including primary motor cortex)

A

o Contralateral movements – Arms, leg, face, trunk

o Broca’s area (dominant hemisphere) – Expressive centre for speech, damage causes expressive dysphasia

o Prefrontal areas – Personality, initiative

o Cortical inhibition of bladder + bowels – People with frontal lobe lesion may urinate/defecate in strange places

429
Q

Branches of external carotid

A
o	Some – Superior thyroid 
o	Ancient – Ascending pharyngeal
o	Lovers – Lingual 
o	Find – Facial 
o	Old – Occipital 
o	Positions – Posterior auricular 
o	More – Maxillary
o	Stimulating – Superficial temporal
430
Q

Internal carotid

A

Passes through carotid syphon into brain, where it forms circle of Willis) arterial loop anastomosis)

Branches:
 Ophthalmic artery - Supplies structures of orbit
 Posterior communicating artery - Acts as an anastomotic vessel Circle of Willis
 Anterior cerebral artery Internal carotids then continue as middle cerebral arteries

431
Q

Name the arteries that supply the brain?

A

2 large carotid arteries (anterior)

2 smaller vertebral arteries (posterior)

432
Q

Branches of vertebral artery

A
  • Meningeal branch – supplies the falx cerebelli, a sheet of dura mater
  • Anterior + posterior spinal arteries – supplies the spinal cord, spanning its entire length
  • Posterior inferior cerebellar artery – supplies the cerebellum
433
Q

Anterior cerebral artery syndrome

A

o Hemiparesis or hemiplegia contralaterally, involving primarily LLs + pelvic floor musculature

o Sensory deficits contralaterally, involving leg + perineum

o Apraxia (due to branches to supplementary motor area + corpus callosum)

o Disconnection syndrome (due to callosal branches)

o Anosmia (due to branches of the olfactory bulb + olfactory tract)

434
Q

Middle cerebral artery syndrome

A

o Hemiparesis or hemiplegia of lower half of contralateral face

o Hemiplegia of contralateral upper + lower extremities

o Sensory loss of contralateral face, arm, lego Ataxia of contralateral extremities

o Aphasia: Broca’s area, Wernicke’s, Global aphasia - Result of a dominant hemisphere lesion (usually L brain)

o Perceptual deficits: hemispatial neglect, anosognosia, apraxia, spatial disorganisation - As result of a non-dominant hemisphere lesion (usually the right brain)

o Visual disorders: Contralateral homonymous hemianopia + Conjugate eye deviation – gaze preference towards side of the lesion

435
Q

Posterior cerebral artery syndrome

A

o Visual deficits: agnosia, prosopagnosia (face blindness), cortical blindness (w/ bilateral infarcts)

o Contralateral homonymous hemianopia – examine via visual field testo Dyslexia

o Involuntary movements: chorea, intention tremor

o Contralateral hemiplegia (paralysis)

o Weber’s syndrome: oculomotor nerve palsy

o Bálint’s syndrome: loss of voluntary eye movements optic ataxia, asimultagnosia

436
Q

How common are subarachnoid hemorrhages?

A

5% of all strokes

437
Q

How common are parenchymal (intracranial) haemorrhage strokes?

A

15% of all strokes

438
Q

How common are atherothromboemobilsms causing stroke?

A

50% of all strokes

439
Q

How common are intracranial small vessel disease and cardiac sources of embolism leading to stroke?

A

 Intracranial small vessel disease 25%

 Cardiac sources of embolism 20%

440
Q

Symptoms of carotid artery occlusion

A

 Contralateral hemiplegia, hemisensory disturbance (blurring vision in ipsilateral eye)

 Homonymous hemianopia (half vision lost, same side in both eyes)

 Deterioration in consciousness level – because of increased intracranial pressure from large area of damage

 Gaze palsy (eyes deviated to side of lesion)

 Dominant hemisphere global aphasia

 Expressive dysphasia (Broca’s) – difficult putting words together in meaningful way

 Receptive dysphasia (Wernicke’s) – difficulty comprehension

441
Q

Symptoms of middle cerebral artery occlusion

A

 Contralateral hemiplegia, hemianaesthesia, hemianopia

 Dominant hemisphere – aphasia, acalculia, agraphia, alexia

 Non-dominant hemisphere – sensory neglect, dressing apraxia, failure to recognise faces

442
Q

Symptoms of lacunar stroke?

A

 Pure motor stroke – contralateral loss of power

 Pure sensory stroke – contralateral loss of light touch + proprioception

 Dysarthria – slurred speech

 Ataxic hemiparesis

 Sensorimotor stroke

443
Q

Symptoms of posterior circulation occlusion.

Occlusion in vertebral, basilar, posterior cerebral arteries (supply brainstem, cerebellum, posterior occipital lobe)

A

 Vertigo – damaged to CN VIII –> N+V

 Ataxia – balance problems

 Paresis – motor tracts

 Paraesthesia – sensory tracts

 Isolated hemianopia

 Branch occlusion

444
Q

Dural reflections

A
  • In some areas within skull, meningeal layer of dura mater folds inwards as dural reflections
  • They partition brain + divide cranial cavity into several compartments; example: Tentorium cerebelli - tough connective tissue
445
Q

Brain injury can be specific to one area (focal) or affect large area of brain (diffuse).

What is focal primary brain injury?

A

o Contusion (bruised brain) – coup + contrecoup

o Haemorrhage

o Skull fractures

o Penetrating head injury

446
Q

What is diffuse brain injury?

A

o Diffuse axonal injury – damage to the white matter of brain

o Hypoxic brain injury - brain can be diffusely injured secondary to hypoxia

o Diffuse brain swelling

o Concussion

447
Q

What is secondary brain injury?

A

 Occurs immediately after trauma + produces effects that may continue for a long time

 This can be prevented, unlike primary injury

448
Q

Examples of secondary brain injury

A
  • Raised ICP – worsens the primary damage
  • Hypoxic brain injury
  • Ischaemic brain injury
  • Seizures
  • Infection
  • Brain herniation
  • Cerebral oedema
  • Hydrocephalies
  • Chronic traumatic encephalopathy
449
Q

What is progressive brain damage?

A

 This may develop after initial injury

 They are a chain of events that occur in primary brain injury + are worsened by increased ICP + reduced perfusion

450
Q

What is a normal ICP?

A

7-15mmHg for a supine adult

o 10mmHg – normal
o >20mmHg – abnormal
o >40mmhg – severe

451
Q

Extradural haematoma (lemon)

A

 White lens shape - Blood outside of dura (middle meningeal artery which sits around the temporal side of head)
 Trauma to temporal part of head may cause middle meningeal artery to rupture
 Falx cerebri has been pushed over to side
 Severe mass effect from this extra-dural haematoma

452
Q

Subdural haematoma (banana)

A

 Slower bleed
 Bi-convex shape
 Bleed below dural layer (usually venous)
 More likely to happen in older people (brain shrinkage to age and dehydration)
 Mass effect - Midline shift and effacement of lateral ventricle (pushed onto other side, brain squashed)

453
Q

Emergency response of head injured patients

A

Airway (with cervical spine control):
 Can be blocked with food, etc.
 Unconscious person - Jaw may drop back and block airway
 Injured brain sensitive to hypoxia so airway must be managed (must be put on a ventilator if GCS score 8 or below)

Breathing:
 Keep oxygenation
 Collapsed lungs, etc.

Circulation:
 Make sure bleeding is stopped and blood replaced
 Healthy people - aggressive resuscitation is very important
 Elderly people - Not always carried out because other factors involved
 Cerebral blood flow (CBF) = Mean arterial pressure (MAP) - Intracranial pressure (ICP)

Management:
 ABC
 Treat threats to life
 Normalise oxygenation, ventilation and circulatory status

454
Q

PET

A
o	Lengthy process
o	Preparation time needed
o	Invasive - Uses radioactive tracer
o	Very expensive
o	Poor spatial resolution
o	Very high sensitivity
o	Established clinical tool
o	Typically used for oncology
o	Only one research scan per lifetime for volunteers
455
Q

EEG

A
o	Lengthy process
o	Lots of preparation time needed
o	Electrical activity on scalp generated from neural activity
o	Very cheap 
o	Portable
o	Good time resolution
o	Poor spatial resolution
o	Clinically established
o	Data is very noisy
456
Q

MEG

A
o	Much quicker than EEG
o	Little preparation time needed
o	Magnetic fields on scalp generated from neural activity
o	Entirely passive
o	Expensive
o	Good time resolution
o	Good spatial resolution
o	New clinical tool
o	Data interpretation is complicated
457
Q

MRI

A

o Relatively quick

o Little preparation time needed

o Moderately expensive

o Poor time resolution

o Good spatial resolution

o Variety of contrast regimes

o Established clinical tool

o Sensitivity is poor

o Many different applications

458
Q

CT and XR

A

o Very quick processes

o Little preparation time is neededo Relatively cheap

o Good for hard tissue (bone)

o Poor for soft tissue (brain)

o Use ionising radiation

o Clinically established

459
Q

Symptoms of Alzheimer’s disease

A

 Insidious onset, gradual progression
 Memory loss – Initially short-term memory, later global
 Language impairment, loss of coherent speech and eventually mutism
 Decline in motor skills + ADL (dressing, mobility)
 Loss of recognition skills - Objects, people, themselves
 Disorientation – Can get lost in familiar places and get disorientated about time
 Altered personality e.g. apathy, irritability, etc.

460
Q

On scan what is visible in Alzheimer’s

A

 Diffuse cerebral atrophy
• Especially medial temporal + parieto-temporal lobes
 Ventricular dilatation, widening sulci, narrowed gyri
 Temporal lobes are affected first, especially hippocampus

461
Q

What is visible by microscopy of brain in Alzheimer’s?

A

Amyloid plaques + neurofibrillary tangles

462
Q

What are amyloid plaques?

A
  • Abnormal processing of amyloid precursor protein leads to excess beta amyloid
  • Deposition of beta amyloid in/around nerve cells (senile/neurotic plaques) and cerebral arterioles (amyloid angiopathy)
  • Associated inflammatory response
463
Q

What are neurofibrillary tangles?

A
  • Formed from abnormally phosphorylated tau proteins

* Which disrupt cerebral architecture + functioning

464
Q

Treatments of Alzheimers?

A

Acetylcholinesterase inhibitors (AChEI).

N-methyl D-aspartate (NMDA) receptor antagonists.

465
Q

Acetylcholinesterase inhibitors (AChEI)

Alzheimer’s disease treatment

A
  • E.g. donepezil, galantamine, rivastigmine
  • Reduce breakdown ACh
  • Used in mild-moderate AD
  • 2/3 response with stabilisation or slight improvement over 6-12 months
  • Slow deterioration + institutionalisation
466
Q

N-methyl D-aspartate (NMDA) receptor antagonists

Alzheimer’s disease treatment

A
  • E.g. memantine
  • Reduce glutamate
  • Moderate-severe AD
  • May reduce behavioural symptoms/ delay institutionalisation
  • Benefit in other dementias unknown
467
Q

What is vascular dementia (20-30% of all dementia) caused by?

A

Caused by disease/injury affecting vasculature of brain, typically involving a series of minor strokes

468
Q

Symptoms of vascular dementia?

A

 Small vessel disease (SVD) causes a type of vascular dementia with ischaemic changes

  • Insidious onset, gradual progression – slow than AD
  • Apathy/slowness of thought
  • Problems w/ executive functioning
  • Reduced attention
  • Relative preservation of higher cortical functions (gnosis, praxis, visuospatial)
469
Q

Treatment of vascular dementia

A

 Lifestyle changes – smoking, diet, alcohol, exercise

 Control of blood pressure, cholesterol, diabetes

 Aspiring, clopidogrel, warfarin

470
Q

Lewy body dementia

A

o Abnormal collection of Lewy body proteins in the wrong places

o Primary symptoms: fluctuations in cognition/performance, visual hallucinations, parkinsonism

471
Q

Pathophysiology of lewy body dementia (10-15%)?

A

 Abnormal alpha-synuclein protein collection within the cytoplasm of neurons– Lewy bodies

 Loss of dopamine-producing neurons in the substantia nigra, similar to Parkinson’s disease

 Atrophy especially present in midbrain, temporal lobe, parietal lobe, cingulate gyrus

472
Q

Frontotemporal dementia 2-5%

A

o Mainly early onset <65 years old
o 10% familial – mutation in tau gene (in microtubules)

3 common syndromes:
 Dementia of frontal type – w/ emotional + behavioural changes due to frontal lobe atrophy.
 Progressive non-fluent aphasia – progressive difficulty in language.
 Semantic dementia – loss of knowledge of meaning of worlds/fluent aphasia.

Pathology:
 Unspecific
 Pick type
 Motor neuron disease

473
Q

Type of dementia

A
o	Alzheimer's disease 
o	Vascular dementia 
o	Lewy body dementia 
o	Frontotemporal dementia 
o	Parkinson’s disease 
o	Huntington’s disease 
o	Creutzfeldt-Jakob disease o	MS
474
Q

Medical management of dementia

A

o Review of physical health + medication
o Exclude alcohol, pain, co-morbid depression/anxiety, etc.
o ABC/Behavioural Approach

Drug management:
 Symptomatic treatments e.g. antidepressants, anti-psychotics, etc.
 Disease modifying treatments e.g. AChEI

475
Q

Risks of general anaesthetic

A
  • Airway problems (lose reflexes)
  • Aspiration
  • CNS, CVS, RS – depression
  • Awareness (if not enough anaesthesia)
  • Post-operative nausea + vomiting
  • Death – extremely rare
476
Q

What are these?

Tubocurarine.
Atracurium.

A

Neuromuscular blocking agents - antagonists

o Non-depolarising + competitive

o Block stimulation of muscles by competitively blocking the binding of ACh to its receptors

o Reversed by acetylcholinesterase inhibitors

477
Q

What is suxamethonium?

Suxamethonium:
 The only depolarising neuromuscular blocking agent used clinically
 Has rapid onset (30 seconds) but v. shot duration of action (5-10 mins) due to hydrolysis by various cholinesterases

A

Neuromuscular blocking agents - agonists

o Depolarising + non-competitive agent

o Depolarise muscles to a point where they can no longer be stimulated

o Have prolonged effects under the influence of acetylcholinesterase inhibitors

478
Q

Epilepsy

A

 60% of individual w/ epilepsy have partial seizures

 60-70% of partial seizures originate in temporal lobe

 60-70% of patients become seizure free after treatment w/ anticonvulsant

479
Q

Stroke classification

A

TACI (Total Anterior Circulation Infarct)
o Hemi motor + sensory deficit
o Hemianopia
o Cortical dysfunction

PACI (Partial Anterior Circulation Infarct)
o Any 2 of the above or isolated cortical dysfunction

LACI (Lacunar Circulation Infarct)
o Pure motor hemiplegia
o Pure sensory loss
o Motor + sensory loss

POCI (Posterior Circulation Infarct)
o Vision related because occipital infarct
o Vertigo, diplopia, ataxia

480
Q

2 types of nociceptive pain

A

Somatic - localised + easy to describe

Visceral - poorly localised, associated with autonomic changes

481
Q

2 cells in synovium

A

Type a - macrophage derived

Type b - fibroblast-derived

482
Q

Pseudogout

A

Calcium pyrophosphate deposition (CPPD) disease.

A type of arthritis that causes spontaneous, painful swelling in joints.

483
Q

4 most common fracture sites from a fall

A

Distal radius
Vertebra
Proximal femur
Proximal humerus

484
Q

Classic clinical feature of hip fracture?

A

Shortened and externally rotated leg

485
Q

Ways to classify hip fractures on xray?

A

Intra-capsular.
Intra-trochanteric.
Extra-capsular.

Intracapsular much more likely cause of avascular necrosis than extracapsular.

486
Q

What is spina bifida?

A

Posterior spine elements (lamina, facets + spinous processes) fail to develop, allowing the contents of the spinal cord to prolapse through the defect

487
Q

What is the medullary cavity found in long bones composed of?

A

Yellow fatty marrow or red haematopoietic marrow (children)

488
Q

Describe the inner surface of the endosteum (of bones)

A

Inner surface is lined by a layer of flattened cells

489
Q

Which word describes this: thin vascular membrane of connective tissue that lines the inner surface of the bony tissue that forms the medullary cavity of long bones

A

Ednosteum

490
Q

Where does the cortical/compact bone layer lie relative to the trabecular/cancellous bone layer?

A

Compact bone is the outer layer

Trabecular bone is the inner layer

491
Q

What is the periosteum?

A

A connective tissue membrane surrounding the bone

492
Q

What is endochondral ossification?

A

The cartilage is removed and replaced with bone.

It occurs in the skeleton from the second month of intrauterine life

493
Q

Where does long bone growth occur?

A

From the physis.

It occurs by endochondral ossification of the cartilage continually produced by the cells of the physis

494
Q

What happens when long bone growth ceases?

A

Epiphyseal bones + metaphyseal bone fuse

495
Q

What is the blood supply of bone?

A

Partly from a nutrient artery which penetrates though a nutrient foraemen via a vascular network in the periosteum.

There is also an intramedullary component

496
Q

What word describes the following - lateral deviation of spine in the coronal plane associated with rotation?

A

Scoliosis

497
Q

What word describes the following - increased posterior convexity of spine in the sagittal plane?

A

Kyphosis

498
Q

What word describes the following - increased anterior convexity of spine in the sagital plane?

A

Lordosis

499
Q

How many vertebrae are there?

A

Cervical 7

Thoracic 12

Lumbar 5

Sacrum 5 - fused

Coccygeal 3-5 fused

500
Q

Which nerve may be damaged by a fracture of the medial epicondyle

A

Ulnar nerve - it passes the medial epicondyle posteriorly