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Block 4- Kim > Muscles > Flashcards

Muscles Flashcards

1
Q

What muscles make up the anterior forearm 1st layer?

Where is there common attachement point?

A

Medial epicondyle

FCR

FCU

Palmaris Longus

Pronator Teres (inserts into midradial shaft)

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2
Q

What muscles make up the anterior forearm 2nd layer?

Where is it’s origin?

A

Medial epicondyle

FDS (to PIP)

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3
Q

What makes up the anterior forearm 3rd layer (deepest)

A

FDP (to DIP)

Pronator Quadratus

FPL

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4
Q

What makes up the posterior forarm superficial layer

(6 + 1)

What is the common attachment point of some of the muscles? Indicate this with a *

A

Brachioradialis (this is a flexor though)

*EDM

*ED

ECRL

*ECRB

*ECU

Anconeus

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5
Q

What makes up the posterior arm deep layer?

A

EPL (DIP)

EPB (MCP)

AbPL

EI (PIP)

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6
Q

Name the tendons found in the extensor compartments

with lateral being compartment one

A

1: AbPL & EPB
2: ECRL & ECRB
3: EPL
4: ED & EI
5: EDM
6: ECU

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7
Q

What compartment is De Quervians Tenosynovitis associated with?

A

Compartment 1- EPB, AbPL

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8
Q

What is the name of the tenosynovitius associated with compartment one?

A

De Quervians Tenosynovitis

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9
Q

What can happen to compartment 3?

A

EPL can wear on the Dorsal Radial Tubercle

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10
Q

What can happen to extensor compartment 6?

A

ECU can wear on the Ulnar styloid process

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11
Q

Where does the brachial artery bifurcate?

A

Cubital fossa

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12
Q

What makes up the cubital fossa?

What runs down the middle- why is this useful?

What is the contents?

A

Intercondylar line

Laterally: Brachioradialis

Medially: Pronator teres

2) Biceps tendon. Medial is median nerve and brachial artery
3) Really need, Beer to, Be at, My nicest

Radial artery

Biceps tendon

Brachial artery

Median nerve

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13
Q

Where does the Radial nerve run?

A

Off brachial plexus posteriorly

Through Triangular interval w/ Profunda Brachii

Down Spiral groove

Anterior to elbow

1cm lateral to biceps tendon

Then deep- Posterior Interosseous runs near radial neck

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14
Q

Where does the median nerve run?

A

Off brachial plexus laterally to axillary artery

Passes anterior to elbow

Medial to biceps tendon

Under plamaris longus

Through carpal tunnel

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15
Q

Describe the route of the ulnar artery

A

Comes of brachial plexus medially to axillary artery

Passes through cubital tunnel (near elbow)

Passes behind medial epicondyle

Runs under cover FCU

Lateral to pisiform

(NOT THOUGH CARPAL TUNNEL- through Guyons canal)

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16
Q

What runs medial to the biceps tendon?

A

Median nerve & Brachial artery

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17
Q

How would you expect a posterior hip dislocation to present?

A

Shortened, flexed and internally rotated

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18
Q

How would you expect an anterior hip dislocation to present?

A

ABducted & externally rotated

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19
Q

How would you expect a NOF to present?

A

LL shortened and externally rotated

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20
Q

What are the nerves off the lumbar plexus

A

Indecent Ian Gets Laid on Fridays Luckily

Iliohypogastric L1

Ilioinguinal L1

Genitofemoral L1&2

Lateral Cutaneus nerve of Thigh L2,3,4

Obturator L2-4

Femoral L2-4

Lumbosacral trunk L4-5

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21
Q

For pronation/ supination in relation to ulnar and radius, what bone moves?

A

Radius moves around the ulnar

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22
Q

What can an extracapsular # of the femur also be called?

A

Intertrochanteric

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23
Q

Describe how blood reaches the femoral head

A
  • External Iliac
  • Femoral (under inguinal ligament)
  • Profunda Femoris
    • Lateral/ Medial Circumflex
      • Circumflex femoral/ Retinacular arteries
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24
Q

What is the Fascia Lata?

What does it form?

A

Fasica surrounding the compartments of the thigh

Forms the Ilio tibial tract (lateral thickening of facia lata)

  • Muscle attachemnt Glut max
  • Assist knee extension/ stability
  • Saphenous vein runs superficial to fascia
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25
Q

What are the ligaments that divide up the sciatic foramen?

A
  • Sacrotuberos
  • Sacrospinous
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26
Q

What makes up the joint capsule of the hip?

A

Synovial membrane

Fibrous membrane:

  • Iliofemoral
  • Pubofemoral
  • Ischiofemoral
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27
Q

Where can a psoas abscess infection track to? What can it mimic?

A

Fibrous sheath over psoas which infection can track down into femoral triangle mimicking a femoral hernia

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28
Q

In a neural mass:

What would you expect the movemnts to be?

What symptoms may be elicited when pressing on it?

A

Medial to lateral movement

Pain, Tingling, Sensory loss

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29
Q

How could you determine if something is more likely to be a hernia? (Palpable masses lecture)

A

If you cannot get your hands above the swelling more likely to be a hernia

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30
Q

What are the boarders of the femoral traingle

What are the contents of the femoral traingle

A

a)

  • SAIL
  • Sartorius
  • Adductor Longus
  • Inguinal Ligament (PT to ASIS)

b) NAVEL

  • Femoral nerve
  • Femoral Artery
  • Femoral Vein
  • Lymphatics

Femoral Art, vein and lymphatics in femoral sheath

Femoral art and vein outer wall are bound by the femoral sheath

Lymphatics in femoral canal but fascia does not bind to them

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31
Q

Where may a femoral hernia present?

Where do they appear?

A

Swelling in the femoral triangle in the region of the lymphatics

Appear via the saphenous opening

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32
Q

What are the boarder of the femoral canal? What is this known as?

A

Femoral ring

  • Inguinal ligament
  • Lacunar ligament
  • Pectineal ligament

Rigid boarder so high chance of hernial sac strangulation

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33
Q

Where can the femoral artery be felt?

What does this also mark?

A

Midinguinal point +/- 1cm

Marks the deep inguinal ring

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34
Q

What is dilation at the saphenofemoral junction called?

What can it be mistaken for?

A

Saphena Varix

Femoral hernia

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35
Q

Where do the superficial inguinal lymph nodes recieve from?

A
  • Proximal: Penis, Scrotum, Perineal skin, Buttock, Abdo wall below umbilicus
  • Distal: Superficial lymph vessels of lower limb
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36
Q

Where do the deep inguinal lymph nodes recieve lymph from?

A
  • Deep lympahtics from lower limb
  • Glans of penis and spongy urethra

Cloquet’s node sits in femoral canal

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37
Q

How do the femoral vessels and saphenous nerve enter the politeal fossa?

A

Through adductor canal (deep to sartorius down the middle 1/3 of the medial thigh)

Passes deep and posterior to Adductor hiatus (In adductor magnus) to enter popliteal fossa

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38
Q

Give some differential diagnosois for a groin swelling in females

A
  • Femoral hernia
  • Canal of Nuck
  • Batholin gland cyst
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39
Q

A lump appears in the umbilical region: where may the cancer have tracked from?

A
  • Sister Mary Joseph Nodule (on umbilicus) associated with pelvic or abdo cancer
  • Urachus from bladder
  • Falciform ligament which includes the ligamentum teres is was the umbilical vein
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40
Q

Where does lymph from the supraclavicular node left come from?

A
  • Breast tissue, Thoracic wall, Proximal foregut, Left upper lobe of lung
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41
Q

Describe the examination of a lump

A
  • Size, Shape, Surface
  • Position
  • Attachement
  • Consistency, Colour
  • Edge
  • Pulsation, Thrills, Fluctuance (fluid containing)
  • Inflammation
  • Transillumination
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42
Q

D: Osteoporosis

A

Complex skeletal disorder characteristed by low bone density & microarchitectural defects in bone tissue –> Increase bone fragility & susceptibility to fractures

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43
Q

Pathophysiology of Osteoporosis

A

Loss of balance between bone formation and resorption during remodelling

Reach peak bone mass: Nutrition, Genetic Factors, Physical activity

Menopause:

  • Decreased oestrogen
  • Increased IL/ TNF levels
  • Increased RANK and RANKL expression
  • Increased osteoclast activity

Ageing:

  • Decreased replicattive activity of osteoprogenitor cells
  • Decreases activity of osteoblasts
  • Decreased biological activity matrix bound GF
  • Reduced physical activity
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44
Q

DEXA scan scoring

A

T score- related to the mean bone density of a young adult

Normal T Score: >/= -1

  • Less than 1SD from the young adult mean

Osteopenia T score: <-1 to >-2.5

  • 1-2.5 SD below YA mean

Osteoporosis T score: <-2.5

  • >2.5SAD below YA mean
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45
Q

What is Rickets?

What do you observe?

Cause?

A

Inadequete mineralisation of bone

  • Occurs in children
  • Defective minerlisation @ growth plate –> widening of growth plate as chondrocytes hypertrophy (instead of die) –> Joint deformity
  • Growth retardation/ Bone deformities

Cause:

  • Lack Vitamin D –> Decrease Ca and Phosphate levels
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46
Q

What is Osteomalacia?

Symptoms?

Cause?

A

Inadequete mineralisation of bone

  • Adults and Children
  • Defective mineralisation of osteoid

Symptoms:

  • Asymptomatic
  • Muscle weakness
  • Bone pain
  • Bone Fracture

Cause:

  • Vitamin D deficiency –> Ca and Phospahte level decrease
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47
Q

What are the types of cancers that are benign in bone and cartilage?

A

Osteoma and Chondroma

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48
Q

What are the types of malignant cancers in bone?

A

Osteosarcoma and Chondrosarcoma

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49
Q

Cancer secondaries that tend to deposit in bone?

What are the characterisitc features?

A

Lungs and Breast:

  • Lytic lesions
  • Can lead to hypercalceamia

Prostate:

  • Sclerotic lesions- increased woven bone production
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50
Q

What is the pathophysiology of Paget’s Disease of bone?

What are the causes?

What type of lesions do you observe?

Symptoms?

A

Increase bone turnover, osteoclastic overactivity. Response by osteoblaststo lay down woven bone- weak

  • Lytic and Sclerotic lesions

Symptoms:

  • Bone overgrowth
  • Bone bowing
  • Pain
  • Fracture
  • Deformity
  • Can be focal or multifocal- may compress CN foramina

Cause:

  • Environemntal
  • Genetic
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51
Q

What Inx in Paget’s Disease of Bone

A
  • Bloods (High Alk P)
  • X Ray
  • Radionuclide bone scans- overactive OC
  • Bone Bx if suspected Ca
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52
Q

What bone disease may you need to consider cancer?

How do you know?

A

Paget’s disease of bone

High turnover of cells therefore more susceptible to mutation.

Suspicion if: Rapid bone growth and surrounding erythema

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53
Q

What pharmocological tx can be given for Paget’s Disease of Bone?

A

Bisphophonates- Alendronic Acid

  • Decrease OC recuitment
  • Increase OC apoptosis
  • Both the above decrease OB activity
  • Decrease depth of resorption site and maintain bone density

Other tx:

  • Walking aids
  • Analgesia
  • Supplements
  • Surgery
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54
Q

D: Osteogensis imperfecta

A

Genetic disorder characterised by defective production in Type I collagen

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55
Q

What are the types of Osteogenesis Imperfecta and what are the symptoms/ signs?

A

Type I:

Milder form. More fractures but not deformities

Type II:

  • Brittle bones
  • Bones may fracture in labour
  • Muscles for breathing can # bones
  • Kyphoscoliosis –> Respiratory compromise
  • Tend to die in first couple of weeks
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56
Q

What is the Tx of osteogenesis imperfecta?

A
  • Bracing
  • Orthotics
  • Ortho intervention
  • Bisphophonates
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57
Q

What blood tests would you use in osteomalacia and what would you expect to see?

A

Calcium: Low

Phosphate: (Normal/) Low

Vitamin D: Low

Alk P: High (OB secrete this)

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58
Q

What blood tests would you do in paget’s disease of bone- what would you expect to see?

A

Calcium: Normal/ High in fracture

Phosphate: Normal

PTH: Normal

Alk P: High (think you are laying down lots of new bone and OB secrete this)

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59
Q

What other symptoms (systemic) may a person with Osteogenesis Imperfect have?

A

Hearing loss

Sclera: Blue, Purple, Grey tint

Teeth problems- brownish

Growth retardation

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60
Q

Risk Factors for Osteoporosis

A
  • Female
  • Age
  • White Ethnicity
  • Post-menopausal
  • Low BMI
  • Family Hx
  • Smoking, Alcohol
  • Steroids
  • Vit D and Calcium deficiency
  • Immobility
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61
Q

Osteoporosis Tx

A
  • Supplements Vit D and calicum
  • Diet
  • Exercise
  • Pharmacological
  • Falls prevention
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62
Q

Tools that can be used in Osteoporosis

A
  • FRAX tool- past # and their risk factors
  • DEXA
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63
Q

What is the pathophysiology of Myasthenia Gravis

What is commonly affected? How can you test this?

Tx

A

Patho: Autoantibodies against nicotinic AchR on Post Synaptic membrane

Affects: Extra-occular muscles, Bulbar muscles speech/ swallowing, Facial Muscles. May become generalised. Fatiguability as cannot maintain muscle contraction

Test: Get patient to look at finger does it result in ptosis

Tx: Neostigmine (AchE Inhibitors)

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64
Q

What is Botulinum Toxin?

What does it cause?

A

Produced by Clostridium Botulinum.

Degrades SNARE protein (Helps dock Ach vesicle on pre-synaptic membrane) –> Blocks Ach release from pre-synaptic terminal –> Total blockage at NMJ

Result: Flaccid Paralysis/ Resp muscle paralysis

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65
Q

What is Duchenne Muscular Dystrophy?

What are the symptoms? When does it start?

What is the sign assoicated with it?

What are the Tx?

A

Absence of Dystrophin

Dystrophin links cytoskeleton with ECM (and thus stabalises the sarcolemma so when contraction occurs sarcolemma pulled with myofilament). Absence –> Cell membrane ripping and calcium flood ing –> necrosis & destruction of muscle fibres.

Replaced w/ Adipose or CT –> Psuedohypertrophy

Onset @ 3-4yrs with rapid progression

Sign: Gower’s sign (Use hands to push on thighs to stand)

Tx: Steroids reduce progression, PT and MDT

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66
Q

What is Beckers Muscular Dystrophy?

A

X linked genetic disorder

Reduction in amout of dystrophin

Presents in adolescence/ later childhood

Milder symptoms & slower progression

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67
Q

What is Poliomyositis?

What are the features?

Tx?

A

AI inflammatory disease affecting SK muscles. Infiltration of inflammatory cells –> Muscle fibre necrosis

Features: Proximal weakness- symmetrical & wasting (not normally painful/ tender)

Dysphagia (difficulty swallowing), Dysphonia (difficulty making the sound), Respiratory muscle weakness, Cardiac invovlement

General malasie- weight loss, fever (Acute phase)

Tx: Steroids and Immunosuppressants

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68
Q

What is Dermatomyositis?

What does it typically affect?

What are the skin changes seen?

A

Poliomyositis PLUS skin changes

Affects: Muscles, Skin (Joints, Oesophagus, Lungs, HEart)

May be part of paraneoplastic syndrome (conequence of cancer in body)

Skin changes: Heliotrope Rash: Purple around eyes and periorbital swelling

Grotton’s: Scaley, Erythematous rash on dorsum of hands

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69
Q

Define fall

A

Event causing person to unintentionally rest on ground or at a lower level

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70
Q

Give some intrinsic causes of falls

A
  • Syncope/ LOC
  • Seizure
  • Peripheral neuropathy
  • Stroke
  • Visual impairment
  • PD/ Cog impairment
  • Drugs, Alcohol
  • Age related frailty- Sarcopenia, OA, RA
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71
Q

Give some common causes of Falls

A

DAME

Drugs: Polypharmacy, Alcohol

Age Related Changes: Gait, Balance, Sarcopenia, Sensory Impairment

Medical: Syncope, PD, Stroke

Environement: Obstacles, Wires, light

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72
Q

Define Syncope

A

Sudden transient LOC due to decrease cerberal perfusion

State of unresposnivness, loss of postural control and spontaneous recovery

Causes:

  • Vasovagal
  • Situation Hypotension
  • Arrythimia, Outflow obstruction, PE
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73
Q

How should you conduct the Hx of Falls Ax?

A

SPLATTD

  • Symptoms
  • Previous falls
  • Location
  • Activity
  • Timing
  • Trauma
  • Drug hx
74
Q

In a falls assessment examination- what should you look for?

A
  • General Appearance
  • CVS:
    • Pulse
    • BP
    • Ascultation- Murmurs
  • CNS:
    • Neurological/ PD signs
    • Congnitive testing
    • Vision/ Hearing check
  • MSK:
    • Head and neck movements
    • Gait
75
Q

Define Orthostatic Hypotension

A

>20mmHg fall in systolic BP

OR

>10mmHg fall diastolic BP

within 3 mins of standing WITH SYMPTOMS

76
Q

Define Post-Parandial Hypotension

A

Fall >20mmHg systolic BP after Meal Ingestion

Effect is up to 90 mins

77
Q

What makes the posterior axillary fold?

A

Latissimus Dorsi & Teres Major

78
Q

Lateral Cutaenous nerve of the thigh

a) Where does it enter the thigh?
b) What can happen- what is the name of the condition?
c) What muscle does it emerge near? and how?

A

Enters Anterior thigh close to ASIS where it can get compressed

= Meralgia Paraesthetica

Emerges SUPERIOR to Sartorius

79
Q

What is the type of joint at the knee?

What are the movements?

A

Hinge joint

Flexion/ Extension

Rotation (medial & lateral)

Translocation

80
Q

What does the patella articulate with?

A

Femoral condyles

81
Q

What is the knee joint formed of?

A

Distal femur, Proximal Tibia and Patella

82
Q

Describe the location of the ACL attachment points

A

Intercondylar region of Tibia (blends with medial meniscus here)

to

Intercondylar fossa of Femur

Prevents anterior dislocation of the tibia on femur

83
Q

Describe Posterior cruciate ligament attachments

A

Posterior Intercondylar region of Tibia

(ascends anteriorly) to

anteromedial femoral condyle

84
Q

Describe the attachments of the lateral collateral ligament

A

Lateral Epicondyle of femur to depression on lateral surface of fibular hear

85
Q

Describe the medial collateral ligament attachments

A

Medial epicondyle of femur to the medial condyle of the tibia

86
Q

Where is the suprapatella bursa?

A

Between Quadraceps Femoris and Patella

Communicated w/ knee joint cavity

87
Q

Where is the Pre-patella bursa?

What is this called when it is inflammed?

A

Patella & Skin

HOUSEMAIDS KNEE

88
Q

Where is the Infrapatella Bursa?

What is this called when bursitis occurs?

A

Superficial: Skin & Patella Ligament

Deep: Patella Ligament & Tibia

CLERGYMEN’S KNEE

89
Q

What is meant by close packing of the knee?

What is the muscle that unlocks this?

A

Medial rotation of Femur on Tibia

Unlocked by Popliteal (lateral rotation). Found in posterior compartment- deep. Tibial nerve L5-S1

90
Q

Where is the Popliteal and Semimebranous bursa?

A

Posterior knee

Between Semimebranous and Gastrocnemius medial head

91
Q

Where is the Anserine Bursa?

A

Deep to the Pes anserine (Sarorius, Gracillis, Semitendinosus)

Medial Proximal tibia

92
Q

What muscles do foot inversion?

A

Tibialis Anterior (Ant compartment- Deep Fibular nerve L4 part)

Tibialis Posteior (Post compartment- Tibial nerve L4/5)

93
Q

What muscle does NOT do plantar flexion in the posterior compartment?

A

Tibialis Posterior (l4/5)

94
Q

What makes up the popliteal fossa?

A

Biceps femoris (Lat, superior)

Semimembranosus/ Semitendinosus (Med, Sup)

Gastrcnemius Medial and Lateral head

95
Q

In the popliteal fossa describe what is deepest to most superifical

A

Popliteal artery (deepest)

Vein

Nerve (superficial)

96
Q

What muscle can avulse the 5th metatarsal tuberosity?

A

Fibularis Brevis on excess inversion

97
Q

What does the lateral compartment of leg do?

A

Primary Evators, Weak Plantarflexors, Foot Eversion

98
Q

Where does the sciatic nerve divide?

A

Proximal to knee joint line

99
Q

What type of swellings can occur in the popliteal fossa?

If possible state where they can occur?

A

1) Neuroma
2) Popliteal artery aneyrysm
3) Popliteal cyst- from semimebranous bursa (semim and medial head of gastroc) APPEARS ABOVE KNEE JOINT LINE
4) Baker’s Cyst- Synovial cyst below joint line

100
Q

What is the nerve for the posterior thigh and nerve root values?

A

Tibial part of Sciatic

L5-S2

101
Q

What is the nerve for the posterior leg compartment?

Nerve route values

A

Tibial nerve S1-S2

102
Q

What is the nerve for the lateral leg? Nerve route values?

A

Superficial fibular nerve L5, S1

103
Q

What is the nerve for the anterior lef compartment with values?

A

Deep fibular nerve L4-S1

104
Q

What muscle in the posterior compartment of the THIGH is the exception for nerve innervation?

A

Biceps Femoris - Common Fibular nerve L5, S1

105
Q

What is the nerve innervation exception muscle for the anterior compartment THIGH muscles

A

Tensor Fascia Lata- Superior Gluteal nerve L4-S1

106
Q

When do you see trendelenburg gait?

A

Damaged Superior Gluteal Nerve (L4-S1)

Glut Medius and minimus ABduct the pelvis (& medially rotate LL).

They contract on the CONTRALATERAL side to foot off the ground

Pelvis drops towards the side of the raised limb.

(Eg: Left leg raised and drops towards that side the RIGHT abductor muscles are damaged)

107
Q

What is the innervation of the lateral rotators of the hip?

A

L4-S2

108
Q

What makes up the ankle joint?

What type of joint is this?

What movement does it permit?

A

Distal Fibular, Tibia and Talus

Synovial Hinge joint

Dorsiflexion and Plantarflexion of the Ankle

109
Q

What joints allow Inversion and Eversion at the ankle?

A
  • Subtalar (Talus and Calcaneus)
  • Talonavicular (Talus and navicular)
  • Talocalcanealnavicular
110
Q

What suppors the foot arches?

A
  • Long and Short Plantar ligaments
  • Plantarcalcaneonavicular ligament
  • Anterior leg compartment tendons
  • Posterior leg compartment tendons
  • Intrinsic foot muscles
111
Q

What is the sural nerve a branch of?

A

The common Fibular

(supplies the lateral dorsal and plantar foot)

112
Q

What does the superficial fibular nerve supply? Motor and Sensory?

A

Motor: Lateral leg compartment

Sensory: Majority of Dorsal foot

113
Q

What tendons are needed for the toe off phase in walking?

A

Flexor Digitorium Longus

Flexor Hallucis Longus

114
Q

Comparments of the plantar foot? What can happen with penetrating injury?

A
  • Deep tissue infection
  • Compartment syndrome
115
Q

What is the nerve route values for the medial and lateral plantar nerves? Where do they come from?

A

From tibial nerve

Medial and Lateral Plantar nerve = S1 & S2

116
Q

Describe the sensory innervation to the plantar foot

A
  • Sural from Common Fibular
  • Medial and Lateral Plantar (S1/2) from Tibial
  • Tibial nerve
  • Saphenous nerve (from femoral)
117
Q

Describe sensory to the dorsal foot

A
  • Superficial fibular
  • Saphenous (from femoral)
  • Deep fibular
  • Sural (common fibular)
118
Q

Role of the intrinsic foot muscles

A
  • Dynamic arch support
  • Support to digits during standing and gait (toe off phase)
119
Q

Name the muscles of the foot layers 1,3 & 4

Nerve supply

A

Layer 1- Most superficial:

  • Abductor Hallucis Brevis (Medial plantar)
  • Abductor Digiti Minimi Brevis (Lateral Plantar)
  • Flexor Digitorium Brevis (Lateral plantar- S1-2)

Layer 3:

  • Flexor Hallucis Brevis
  • Flexor Digiti Minimi

Layer 4:

  • Interossei (Lateral Plantar nerve)
120
Q

Ottawa ankle rules

A

X Ray series needed if:

1) Pain in medial malleolar zone AND:

  • Bone tenderness at posterior edge/ tip of lateral malleolus
  • Bone tenderness at posterior edge/ tip of medial mellolus
  • Unable to weight bear immediately & walk in ED for 4 steps

2) Pain in the midfoot area AND

  • Bone tenderness @ base of 5th metatarsal
  • Bone tenderness @ navicular
  • Inability to bear weight immediately & walk in ED for 4 steps
121
Q

Describe the foot arteries

A

Dorsal:

  • Anterior Tibilar becomes the Dorsalis Pedis (palpable lateral to EHL and medial to EDL)
  • Dorsalis pedis moves towards the 1st dorsal webspace to form an anastomoic supply with the lateral plantar artery

Plantar:

  • Posterior Tibial artery through tarsal tunnel –> Medial and Lateral Plantar arteries
  • Medial towards Hallus
  • Lateral gives rise to Plantar Arch supplying the digits along the sides (along with cutenous sensory digital nerves). Anastomoses with Dorsalis Pedis
122
Q

What happens in plantar fascitis?

A

Excess tension –> FIbres damaged/ pulled out of calcaneous

Pain exacerbated on dorsiflexion or pressure of medial calcaneal tubercle

Mostly occurs on medial aspect

123
Q

What is Morton’s Neuroma?

A

Site of painful growth passing between digital nerve 3 and 4

124
Q
A
125
Q

Pathophysiology of OA

A

Loss of articular cartilage +/- bone –> Synovitis

Stimulus –> Chondrocyte response –> Cytokine release –> Protease Enzymes and Macrophage release from cartilage –>

a) Degredation of cartilage –> Destruction of joint strutures –> stimulation of chondrocyte response
b) Loss of smooth articular surface/ Fibrilation –> surface crack development
bi) Fibrillation of cartilage –> Chronic Synovitis (triggered by cartilage fragements and synovial phagocytes release degradative enzymes)
bii) Destruction of sunchondral bone –> Osteocyte formation and Destruction of joint surfaces –> stimualtion of chondrocytes response

Result:

  • Change in cartilage composition (less proteoglycans and chondrocyte hypertrophy) –> reduced shock absorbing properties
  • Erosion –> Fibrillation/ Fissures
  • Ulceration exposes subchondral bone. Eburnation –> Microfractures & Subchondral cysts
  • Osteophytes/ Subchondral Sclerosis
  • Synovitis
  • Thickening of joint capsule (inflammed synovium and hyperplasia)

Radiography:

  • Loss of joint space
  • Osteophytes
  • Subscondral sclerosis
  • Subcondral cysts
126
Q

Define RA

A

Autoimmune condition which leads to inflammation of the synovial membrane & articular surfaces –> joint destruction

127
Q

Describe the pathophysiology of Gout

A

Inflammatory response to urate crystals depositive in & around joint and synovial fluid –> Synovitis, Cartilage destruction –> Joint degredation

128
Q

What is Chornic Gout associated with?

A

Renal impairment and long term diuretic use

  • Tophi- deposits of monosodium and urate crystasls in bursae, tendons, cartilage and periarticular cartilage. May ulcerate and discharge
129
Q

Radiographic changes with Gout

A
  • Narrowing of joint space
  • Opacities in soft tissue (Tophi)
  • Soft tissue swelling
  • Joint Effusion
  • Punch out bony erosions w/ sclerotic margins overhanging the edge
130
Q

Intramembranous Ossification

A
  • Mesenchyme –> Osteopregenitor cells –> Osteoblasts which secrete Osteoid (primary ossification centre)
  • Blood vessels invade. Sponge like trabeculae established. Vascular CT –> bone marrow
  • Mesenchyme on outside –> Fibrous periosteum. Bone cells form cellular layer of periosteum
  • Compact bone forms deep to cellular periosteum with trabecular bone inbetween
131
Q

Endochondral ossification

A
  • Mesenchyme –> Chondroblasts –> Cartilage model
  • Chondroblasts in Diaphysis hypertrophy, die and calcify –> Future marrow cavity
  • Osteoblasts secrete matrix and form subperiosteal bony colar
  • Vascularisation of perichondrium transforms it into periosteum
  • Blood vessels invade cartilage model w/ osteoprogenitor cells
  • Osteoprogenitor cells –> Osteoblasts secrete matrix on surface of calcified cartilage = Primary ossification centre

Similar process in Epiphysis- Secondary Ossification Centre

  • No bony collar
  • Except @ articular surfaces and epiphyseal plate
132
Q

Epiphyseal Growth Plate stages

A

1) Resting:
* Cartilage cells found here
2) Proliferation:
* Under insulin like growth hormone produced from hepatocytes
3) Hypertrophy
* Chondrocytes mature and hypertrophy
4) Calcification:
* Condrocytes die and cartilage matrix calcified. Osteoclasts remove the latter
5) Ossification:
* Osteoprogenitor cells invade. Osteoblasts lay down scaffold

133
Q

Stages of Fracture Healing

A

1) Haematoma:

  • Blood vessels rupture –> haematoma
  • Necrosis of bone fragments
  • Inflammatory response –> Phagocytes migrate to area to remove necrotic tissue

2) Granulation tissue:

  • Blood clot invaded by blood capillaries
  • Fibroblasts from surround CT –> Granulation tissue
  • Cytokines and Growth Factors –> Cellular Proliferation

3) Callus:

  • Fibrous tissue, Inflammatory cells and Cartilage form soft callus
  • Forms a bridge between bone ends

4) Woven:

  • Osteoprogenitor cells –> Osteoblasts –> Woven bone
  • Strenghtens callus and gives bone ridigity. When sufficiently firm and movement no long takes place the fracture sit is clincally united

5) Lamella bone
6) Remodelling

  • Osteoblasts and osteoclasts remodel lamellar bone in response to stresses
  • Excessiv callus resorbed and medullary cavity reestablised
134
Q

Cycle of Bone remodelling

A

Bone Quiescence:

  • Osteoclast recuitment, development & activity

Restoration:

  • OC: Apoptosis and Removal

Reversal:

  • Osteoblast recuitment, development & activity
  • Matrix synthesis

Formation:

  • Mineralisation
135
Q

Map out Degnerative and inflammatory disorders

A
136
Q

Theories of autoimmunity

A

1) Defects in regularatory T cells
2) Molecular mimicary
3) Polyclonal activation B cells –> recognition of self-antigen
4) Sequestered antigens

137
Q

Sarcoidosis

A

Sarcoidosis is a rare condition that causes small patches of red and swollen tissue, called granulomas, to develop in the organs of the body. It usually affects the lungs and skin.

138
Q

Genetic component associated with RA

A
  • HLA- DR4
139
Q

What is Rheumatoid Factor?

A

IgM directed against the FC fragement of IgG

140
Q

Clincal features of RA

A
  • Typical onset 20-50yrs
  • Female
  • Family history
  • Usually symmetrical- affects small joints (hands, wrists, feet, knees)
  • Generally/ systemically unwell
  • Smoking increases risk factor
  • Sudden onset within weeks/ months

Symmetrical

Hands & feet > 80% cases

Early morning stiffness

Symptoms:

  • Systemic: fatigue, anorexia, weight loss
  • Low grade fever, anaemia
  • Articular- joint aching and stiffness
141
Q

RA Hands

A
  • Ulnar deviation @ MCP
  • Boutonniere (Flexion @ MCP and hyperextension @ IP)
  • Swan neck (Hyperextension @ PIP and flexion @ DIP)
  • Fusiform swelling- Early MCP subluxation
142
Q

RA systemic disease

A
  • Atherosclerosis
  • Pericardidits, Valve problems, Vasculitis
  • Pulmonary fibrosis,
  • Anaemia, Splenomegalgy
  • Osteoporosis
  • Leg ulcers, Rheumatoid nodules, Vasculitis
  • C1/C2 subluxation, Nerve compression
  • Scleritis
143
Q

Pathogenesis of RA

A

Genetic predisposition (HLA DR4 or DR1) + Trigger –> Citrulination of own antigens

  • Citrulinated antigens picked up by APC and presented to T helper cells which help B cells differentiate into Plasma cells and produce antibodies which travel to joint.
  • These secrete cytokines which recuit macrophages which secrete cytokines and stimulate synoviocytes:
    • Proliferation and w/ immune cells –> Pannus (thick swollen synovial membrane w/ granulation/ scar tissue)
    • Synovitis
    • Protease secretion –> Cartilage breakdown
    • RANKL expression
  • ​​​RF enters joint space and Anti Cyclic Citrulinated Peptide (Anti- CCP) antibody binds to citrulianted protein activating complement system –> Infalmmation
  • Chronic inflammation –> Angiogensis and vascular permeability –> increased cells in joint
144
Q

Key macroscopic changes

A

Early

  • Synovium inflammation

Late:

  • Pannus
  • Pannus filled erosion
  • Angiogenesis
  • Cartilage breakdown
  • Bone degredation/ Subluxation
145
Q

X ray of RA

A
  • Soft tissue swelling
  • Juxta-articular osteopenia
  • Joint space narrowing
  • Erosions
  • Subluxation
  • Deformity
146
Q

Roles of calcium

A
  • Bone formation and teeth
  • Muscle contraction
  • Stabalisation of membrane potential
  • Enzyme co-factor
  • Nerve function
  • IC second messenger
147
Q

What type of hormone is PTH?

What does it bind to?

A

Peptide hormone

Binds to PTHR1

148
Q

What is the Extracellular Sensing Receptor?

Describe how it works

A

7 Transmembrane glycosylated protein

Interacts w/ G proteins

  • High Ca
    • activates inhibitory pathway of PLC –> IP3 –> Decreased PTH
    • decreases stimualtory pathway of AC- ATP –> cAMP which increases PTH
149
Q

Where does most Ca uptake occur in the gut?

How does Ca uptake occur in the Kidney

A

Gut: Duodenum and Upper jejunum

Kidney:

Passive- PCT (paracellularly)

Actively- DCT (active transport)

150
Q

Where is PTH synthesised?

Where is Calcitonin synthesised?

A

PTH: Chief Cells of Para Thyroid Gland

Calcitonin: Parafollicular C Cells of Thyroid gland

151
Q

Role of Phostphate

A
  • Phospholipid in membranese
  • Phosphorolyation
  • Intracellular metabolism
152
Q

Symptoms of Hypercalcaemia

A
  • Shortened QT interval
  • Abdo pain
  • Muscle weakness
  • Polydipsia/ Polyuria
  • Tiredness, COnfusion, Depression, Headaches
  • N & V, Constipation, Anorexia
  • Loss of bone, Kidney stone, Ectopic calcification
153
Q

Causes of Hypercalcaemia

A
  • Primary Hyperparathyroidism
  • Malignancy (breast or lung cancer)
154
Q

Hypocalcaemia symptoms

A
  • Caropedal spasm
  • Tetany
  • Paraesthesia
  • Seizure
  • Prolonged QT interval
  • Muscle cramps
155
Q

Causes of Hypocalcaemia

Consequences

A
  • Hypoparathyroidism
  • Calcium deficiency

Consequences:

  • Osteomalacia
  • Secondary hyperparathryoidism
156
Q

What causes secondary hyperparathyroidism?

What causes tertiary hyperparathyroidism?

A

Low Vit D –> Low Calcium absorption –> Hypocalcaemia –> Increased PTH secretion –> Hyperplasia of PTH Gland

(high PTH and low Ca and phospahte)

Secondary hyperparathyroidism for long time –> hyperplasia gland –> Increases PTH a lot so you get increase calcium and phosphate

157
Q

Explain how Calcium reabsorption occurs on a cellular level in the Gut and Kidney

A

Gut:

  • High serum calcium = Paracellularly
    • Ca-CaBP
  • Low serum calcium = Actively
    • TRPV6 on brush boarder
      • Endocytosis-Exocytosis: Ca-CaBP and Exocytosis
      • Active uptake & Extrusion: Ca, Ca-CaBP, CaATPase OR Ca/3Na Exchanger

Kidney: Only Extracellular, Bound, Anion Ca filtered

  • Passive reabsorption paracellularly in PCT mainly
  • Acitvely (PTH, Vit D) in DCT and CCT
    • TRPV5 on tubular lumen, bind to CaBP, Basolateral membrane: 3Na/Ca exchanger and CaATPase

Vitamin D and PTH upregulate: TRPV6, TRPV5 Ca-BP and Basolateral efflux transporters

158
Q

How does Phosphate reabsorption occur on a cellular level in the Gut and Kidney?

A

Gut:

  • Sodium dependant phosphate transporter 2b

Kidney:

  • Sodium dependant phosphate transporter 2a/c
159
Q

Role of connective tissue

A

–Structural support

–Metabolic support

–Cell adhesion

–Medium of exchange

–Defense, protection and repair

160
Q

Define wound

A

Injury/ trauma to tissues –> Disruption of the function and structure

161
Q

Define healing

A

Process of returning to health. Restoration of strucutre and function of injured/ diseased tissues

162
Q

Stages of wound healing

A

HIPR

Haemostasis <24hrs

  • Coagulation process
  • Platelet and Fibrin adhere to site
  • Thrombus formation

Inflammatory 0-4days

  • Platelets
  • Macrophages
  • Neutrophils

Proliferative 1-14days

  • Angiogenesis
  • Epithelialisation
  • Contraction
  • Fibrous tissue formation

Restoration 21days-years

  • Maturation
  • Collagen remodelled and realigned
  • Gets to 80% tensile strength
163
Q

Define regeneration

A

Healing in which growth completely restores portions of damaged tissues to their normal state

  • PDGF
  • VDGF
  • TGF (Transforming growth factors). Activated by macrophages. Converts fibroblasts –> Myofibroblasts which lay down collagen
  • ECM has major function
164
Q

Define Growth Factors

A

Proteins stimulating survival and proliferation of particular cells. Promote migration and differentiation

  • Produced transiently in response to external stimuli by macrophages and lympocytes at injury site or parenchymal cells or stromal cells in response to cell injury
  • Stimulate entry into cell cycle
  • Bind to cellular receptors

ECM Role:

  • Store and present GF
  • Scaffold that migrating cells adhere to
165
Q

Define Scar formation

A

Replacement of damaged parenchymal cells with CT. incomplete restoration of architecture and function

Occurs: Severe/ chronic injury or in permanent cells

Process: Normal –> tissue injury –> inflammation –> Granulation tissue –> Scar formation

166
Q

Describe First Intention wound healing

A

Uninfected surgical incisions approximated by surgical sutures

  • Focal distrption of epithelial B & death of relatively few epithelial and CT cells
  • Epithelial regneration = Principle mechanism
  • Small Scar formed but minimal wound contraction

MOA:

  • Incision filled with fibrin-clotted blood
  • W/in 24hrs neurophils seen at incision site migrating towards fibrin clot. GF & Fibroblasts activated
  • 24-48hrs: Epithelial cells from both edges migrate & proliferate along dermis
  • 3-7days: Neutrophils replaced by macrophages. Angiogenesis @ peak. Granulation tissue progressively invades incision space
  • Week 2: Continued collagen accumulation & fibroblast proliferation (scar maturation)
  • >Week 2: Scar remodel to increase tensile strength
167
Q

Elbow aspiration points

A
168
Q

What is remodelling

A

CT scar modified and remodelled to improve tensile strength

Balance between synthesis and degredation of ECM proteins acomplished by Matrix Metalloproteinases

Wound strength 70-80% of normal by 3 months (Does not substancially improve beyond this)

169
Q

What is second intention wound healing

A

Large wounds @ abscess formation sites, Ulceration and Infarction

  • Development of abundant granulation tissue with accumulation of ECM and formation of large scar
  • Wound contraction by myofibroblasts
170
Q

Differences betwee first and second intention healing

A
  • Larger clot
  • Inflammation more intense
  • Greater volume of granulation tissue
  • Wound contraction
171
Q

What is Fibrosis of internal organs?

A

Excessive deposition of collagen and other ECM components in tissue

  • Can lead to organ dysfunction- RA pannus & ankylosing. Pulmonary fibrosis
172
Q

Local factors that affect tissue remain

A
  • Infection
  • Mechanical factors
  • Foreign bodies
  • Size of wound
  • Location of wound
  • Type of wound
173
Q

Systemic factors that affect wound repair

A
  • Nutritional status
  • Metabolic status
  • Circularatory status
  • Age
  • Hormones
  • Collagen disorder
174
Q

How does infection affect tissue repair

A
  • Prolong inflammation
  • Potentially increase local tissue injury
  • Clinically most importnant
175
Q

What are the complications of tissue repair

A
  • Inadequete formation
  • Excess formation
  • Contracture formation
176
Q

Describe Inadequete formation

A
  • Dehiscence or Rupture- separation of layers of surgical wound
  • Exvisceration
  • Ulceration- Lesion through skin or mucus membranes resulting from tissue loss- usually inflammation
177
Q

Excessive Tissue Repair

A
  • Keloid formation- accumulation of excessive collagen –> raised prominent scars
  • Exuberent Granulation Tissue –> Protrude above level of surrounding skin hindering epithelialisatiokn
178
Q

Contracture Formation

A
  • Fibrosis of CT in skin, fascia muscle or joint capsule prevent normal mobility of related tissue
  • Myofibroblasts play a major role
179
Q

Sweat gland types

A
  • Appocrine- secrete oily fluid usually associated w/ hair follicle.
  • Eccrine- found all over body. Thermoregulation
  • Sebecaus- secrete sebum. Usually associated w/ hair follicle
180
Q

Types of skin cancer

A

BCC:

  • Superficial and nodular
  • Immunosupressed, UV expsoure, Genetic Predisposition
  • Slow growing, Do not metastasize, Rodent ulcer

SCC:

  • Range of presentations. Usually thick crust as still can produce ketatin
  • Immunosupression, UV exposure, Occupational hazard, Fair, Male

Melanoma:

  • Benign or Malignant- in situ (epidermis only) or invasive
181
Q

Lamellar bodies and Keratohyaline granules

A

Lamella bodies- Glycophospholipid, responsible for binding keratin flakes

Keratohyaline Granules- Responsilbe for keratin production in granular layers

182
Q

Langerhan cells

Merkel Cells

Melanocytes

Where are they found and functions?

A

Langerhan cells- APC. Not basal layer

Merkel Cell- Light touch. Basal layer

Melanocytes- Basal Layer

Block 4- Kim (13 decks)

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