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Medicine phase 2 limbs and back > week 2 - joints, connective tissue and the vascular tree > Flashcards

week 2 - joints, connective tissue and the vascular tree Flashcards

1
Q

health benefits of exercise

A

beneficial in prevention and treatment of disease
social and recreational benefits
feeling of healthy self awareness and reduction in smoking and alcohol

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2
Q

risks of physical activity

A

sudden death during exercise
risk of death due to nature of the sport
risk of injury

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3
Q

most common anatomical sites of injury from sport

A

lower leg - 32%
upper limp - 30%
head and neck - 17%
chest, upper leg and knee all less common

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4
Q

two types of sport injury

A

microtrauma (overuse) and macrotrauma

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5
Q

sports injuries to bone

A

acute - fracture and periosteal contusion

overuse - stress fracture, osteitis, periostitis

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6
Q

sports injuries to articular cartilage

A

acute - osteochondral fractures and minor osteochondral injury
overuse - chondropathy

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7
Q

sports injuries to joints

A

acute - dislocation and subluxation

overuse - synovitis and osteoarthritis

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8
Q

sports injuries to ligament

A

acute - sprain/tear

overuse - inflammation

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9
Q

sports injuries to muscle

A

acute - strain/tear, contusion, cramp, acute compartment syndrome
overuse - chronic compartment syndrome, delayed onset muscle soreness, focal tissue thickening/fibrosis

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10
Q

sports injuries to tendonn

A

acute - tear - complete or partial

overuse - tendinopathy including tendinosis and tendinitis

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11
Q

sports injuries to bursa

A

acute - traumatic bursitis

overuse - bursitis

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12
Q

sports injuries to nerve

A

acute - neuropraxia

overuse - entrapment, minor nerve injury, adverse neural tension

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13
Q

sports injuries to skin

A

acute - laceration, abrasion and puncture wound

overuse - blister, callus

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14
Q

traumatic sports injuries

A

fractures and dislocations
major muscle - ligament - tendon injuries
head and spinal injuries
chest and abdominal injuries

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15
Q

factors leading to overload - injury due to overuse

A

intrinsic factors - anatomical, muscle imbalance
increased participation in sport
increased intensity and duration of training
extrinsic factors - training errors, poor technique, incorrect equipment, poor conditions

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16
Q

clinical features of bone injury

A

pain, tenderness, localised bruising, swelling, deformity, restriction of movement

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17
Q

management of bone injury

A

anatomical and functional realignment
may need reduction
plaster cast or surgical stabilisation

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18
Q

classification of fractures

A

transverse
oblique
spiral
comminuted - harder to treat due to multiple fragments
avulsion - piece of bone attached to tendon or ligament is torn away

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19
Q

complications of bone injury

A

infection - most likely in open fractures
acute compartment syndrome
associated injury - nerve or blood vessel
DVT/pulmonary embolism
delayed union/non-union
malunion

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20
Q

acute compartment syndrome

A

secondary swelling in a muscle compartment with non-distensible fascial sheath
severe pain, pain on movement, numbness, absent pulses
treated by fasciotomy

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21
Q

problems with injury to bone

A

immobilisation - can result in muscle wasting and joint stiffness
growth plate fractures in children - danger of interruption of bony growth - distal radius at wrist, elbow, distal femur, tibia and fibula
soft tissue damage - commonly with fracture and can result in more severe problems than fracture
periosteal injury - uncommon but painful - nerve supply in periosteum

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22
Q

articular cartilage

A

lines the ends of long bones
absorbs shock and compressive forces and permits almost frictionless joint movement
does not show on x-ray

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23
Q

diagnosis and treatment of articular cartilage injury

A

diagnose on MRI
arthroscopy to confirm and remove loose fragments
may predispose to premature osteoarthritis
do not usually heal fully - treatment to improve healing: perforation, alteration of joint loading, cell transplantation

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24
Q

dislocation v subluxation

A

d - trauma produces complete dissociation of the articulating surfaces
s - some contact of articulating surfaces remains
all result in damage to surrounding joint capsule and ligaments

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25
Q

complications of dislocation and subluxation

A

associated nerve or blood vessel damage - axillary nerve in shoulder, brachial artery at elbow

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26
Q

treatment of dislocation and subluxation

A 
reduction 
muscle relaxants
protect to allow soft tissue to heal
early protected mobilisation 
rebuild muscle strength to prevent reoccurance
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27
Q

grades of ligament injury

A

1 - fibres stretched but normal range on stressing
2 - more fibres involved, laxity on stressing but definite end point
3 - complete tear, excessive laxity and no end point - may be pain free as nerve fibres torn

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28
Q

management of ligament injury

A

initial management is to minimise bleeding and swelling
grade 1 and 2 - promote tissue healing, prevent joint stiffness, protect against further damage, strengthen muscle to provide additional joint stability
grade 3 - surgical - direct repair or reconstruction

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29
Q

when do you get a strain/tear to muscle

A

when demands exceed muscles capacity
common - hamstring, quadriceps and gastrocnemius
common during sudden acceleration or deceleration

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30
Q

grades of muscle strain/tear

A

1 - few fibres, localised pain and no loss of strength
2 - significant no of fibres, swelling, pain on contraction, reduced strength and limitation of movement
3 - complete tear - most common at musculotendinous junctions

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31
Q

management of a muscle strain/tear

A 
first aid to minimise bleeding, swelling and inflammation 
electrotherapy eg ultrasound
soft tissue therapy 
stretching
strengthening
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32
Q

predisposing factors of muscle injury

A 
inadequate warm up
insufficient joint range of motion
excessive muscle tightness
fatigue/overuse/inadequate recovery
muscle imbalance
previous injury
poor technique
altered biomechanics
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33
Q

cause of quadriceps rupture

A

direct impact against contracted muscle or sudden vigorous contraction

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34
Q

myositis ossificans

A

occurs when haematoma calcifies

most resolve spontaneously

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35
Q

describe achilles tendonopathy

A 
chronic repetitive overload injury
pain especially uphill
local swelling and tenderness
crepitus on ankle movement
complications - rupture, chronic tendonitis, achilles bursitis
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36
Q

bursa

A

small fluid filled sacs usually situated between a tendon and bone
role is to reduce friction
hips, knees, feet, shoulders and elbow

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37
Q

neuropraxia

A

nerve injury

if severe may result in paralysis and weakness of muscles innervated with associated sensory loss

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38
Q

tendon structure

A

dense connective tissue
high proportion of collagen
closely packed parallel arrangement in direction of force
sparsely vascularised
fibroblasts/tenocytes
ECM - water 80% - 30% collage 1, ground substance, elastin and collagen 3

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39
Q

phases of tendon healing

A

inflammation - day 0-7
repair - day 3-60
organisation and remodelling - day 28-180

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40
Q

regulators of tendon healing

A

PDGF and TGF-beta

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41
Q

inflammation phase of tendon healing

A

inflammatory cells migrate from epitendinous tissues (sheath, periosteum, soft tissues) and epitendon and endotendon
defect is rapidly filled with granulation tissue, haematoma and tissue debris
matrix proteins laid down as scaffolding for collagen synthesis

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42
Q

repair stage of tendon healing

A

fibroblast/tenocyte migrate to zone of injury and begin to synthesise collagen by day 5
initially collagen type 3 produced which is laid down in a random orientation
4th week - intrinsic fibroblasts proliferate and these cells take over the healing process both synthesising and reabsorbing collagen
switch to production of type 1 collagen which is increasingly orientated along line of force
vascular ingrowth via collagen/fibronectin scaffolding

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43
Q

organisation stage of tendon healing

A

final stability acquired by the normal physiological use of tendon
accompanied by cross linking between fibrils further increasing tendon tensile strength
complete regeneration never achieved - defect remains hypercellular - thinner collagen fibres

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44
Q

patient rehab for tendon injuries

A

early controlled mobilisation can reduce scare adhesions and facilitate healing by stimulating remodelling
excessive loading will disrupt repair tissue
optimal healing requires - surgical apposition and mechanical stabilisation, minimal soft tissue damage, optimal mechanical environment for healing

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45
Q

causes of rotator cuff tears

A 
age - >65
multifactorial - smoking, diabetes, manual labour
tendinopathy leading to tear
bone spurs
acromion shape
trauma 
genetics
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46
Q

rotator cuff tear treatments

A

physio, injection for pain
operative - repair tendon to bone - arthroscopic/open surgery
platelet rich plasma injection

47
Q

4 compartments of tendinopathy

A

stromal
immune
neural
vascular

48
Q

stromal compartment of tendinopathy

A

includes tissue-resident tenocytes and matrix components

tendons acquire altered surface markers and pertubed intracellular signal pathways that have functional consequences

49
Q

immune compartment of tendinopathy

A

t cells, dendritic cells, mast cells and macrophages respond to initial tissue insult through damage associated molecular patterns or PAMPs

50
Q

neural compartment of tendinopathy

A

plays a role in propioception, interacts with mast cells to modulate adaptive responses in the normal tendon
in tendinopathy, excessive stimulation leads to tissue breakdown, degeneration and neoinnervation involving glatamatergic and autonomic systems
release of neuropeptides such as substance P stimulate mast cell degranulation, releasing a variety of agents which modulate a variety of cellular activities in the matrix

51
Q

vascular compartment of tendinopathy

A

most tendons are poorly vascularised but respond to hypoxia by secreting angiogenic factors that induce growth of neovessels, which compromise vascular compartment of tendinopathy pathogenesis
fibrin-rich exudates leak from neovasculature resulting in fibrinoid degeneration

52
Q

three layers of an artery or vein

A

tunica intima
tunica media
tunica externa

53
Q

tunica media structure and function

A

smooth muscle
activated by sympathetic NS
vasoconstriction and vasodilation
elastic fibres stretch and then passively recoil

54
Q

tunica intima structure and function

A

single layer of flat epithelial cells with a supporting layer of elastin rich collagen
provides a smooth, friction-reducing lining for the vessel

55
Q

tunica externa structure and function

A

outermost layer, made of fibrous connective tissue and vasa vasorum
protective and supporting layer

56
Q

anastomoses

A

arteries communicating with each other or veins communicating with each other form anastomoses
can be anatomical or functional

57
Q

describe peripheral pulses

A

contraction of left ventricle results in volume of blood ejected into arterial tree
systolic heart contraction results in pressure wave
pulse represents palpable arterial palpation after each heartbeat
felt where artery can be compressed against bone

58
Q

femoral pulse

A

mid inguinal point - halfway between anterior and superior iliac spine and pubic symphysis

59
Q

popliteal pulse

A

above knee in the popliteal fossa - hold knee bent to find

60
Q

dorsalis pedis pulse

A

top of the foot, immediately lateral to the tendon of the extensor hallucis longus

61
Q

posterior tibial pulse

A

medial side of ankle, 2cm inferior and 2cm posterior to medial malleolus

62
Q

axillary pulse

A

inferior on the lateral wall of axilla

63
Q

brachial pulse

A

medial aspect of arm near elbow

64
Q

ulnar pulse

A

medial aspect of wrist

65
Q

radial pulse

A

lateral aspect of wrist and also anatomical snuff box

66
Q

carotid pulse

A

medial to anterior border of sternocleidomastoid muscle

above hyoid bone and lateral to thyroid cartilage

67
Q

ABPI - ankle brachial pressure index

A

measures systolic pressure of arteries in upper and lower limb - allows comparison

68
Q

buergers test

A

assesses arterial sufficiency

when leg is elevated or drops it goes pale from the red state

69
Q

are the iliac arteries easy to find

A

no - only felt if the person is skinny or has an aneurysm

70
Q

atherosclerosis

A

arterial disease characterised by calcification and plaque formation
arterial wall thickening, elasticity loss
can be blockage of artery

71
Q

risk factors for atherosclerosis

A

increasing age, sex (male), family history

hyperlipidaemia, hypertension, cigarette smoking, diabetes, obesity and pro-thrombotic tendencies

72
Q

atherosclerosis hypothesis

A

chronic inflammation response of the vascular wall to endothelial injury or dysfunction
activation of endothelial cells
recruitment of monocytes/macrophages (chronic inflammatory cells)
formation of foam cells and fatty streaks
proliferation of smooth muscle cells
deposition of ECM proteins

73
Q

major components of plaque

A

cellular - SMCs, macrophages, WBCs
ECM - collagen, elastin and prostaglandins
lipid - cholesterol

74
Q

major process of plaque formation

A

intimal thickening - SMC proliferation and ECM synthesis

lipid accumulation

75
Q

altered vessel function in athersclerosis and their consequence

A

plaque narrows lumen - ischaemia, turbulence
weakening of wall - aneurysms and rupturing
thrombosis - narrowing, ischaemia, embolisation
plaque disruption - athero-embolisation

76
Q

intermittent claudication

A

“leg angina”
exertional leg pain - typically in the calf
assessment includes - walking distance, level of disability, risk factors, medical comorbidity - imaging after

77
Q

critical limb ischaemia

A

rest pain, ulceration, gangrene

limb-threatening and life-threatening

78
Q

arterial reconstruction methods

A

endovascular - balloon angioplasty or stent to keep artery open
open surgery - endarterectomy or bypass

79
Q

angioplasty procedure

A

needle into lumen
wire into artery
balloon over the wire is inflated
lumen is widened

80
Q

endarterectomy

A

open artery, remove plaque and close artery

81
Q

peripheral bypass

A

bypass graft added to artery - blood flows around and separate to blockage
blockage too lengthy for other methods

82
Q

two types of peripheral bypass

A

reroutes blood supply from blockage in artery
anatomical - bypass alongside
non-anatomical - blood supply from a completely different site eg. arm to groin

83
Q

embolism

A

blockage of blood vessel by a solid, liquid or gas at a site distant from its origin
>90% of emboli are thrombo-emboli

84
Q

carotid artery stenosis

A

internal carotid artery supplies brain
common carotid bifurcation is a common site of atherosclerosis - causes luminal narrowing and potential embolisation to brain
subsequent cerebral ischaemia can result in transient ischamic attack of thromboembolic stroke

85
Q

ECM change from embryo to adult

A

early embyro - 80% cells, 20% ECM

adult - 20% cells and 80% ECM

86
Q

ECM functions

A

provides a scaffold for tissue development
provides a mechanical basis for cell attachment and movement
transmits force eg. tendon, ligament cartilage, bone
can withstand compression in cartilage and intervertebral disc
provides survival signals to cells and differentiation signals to stem cells
reservoir for growth factors

87
Q

ECM components

A

water, proteins, glycoproteins, proteoglycans, glucosaminoglycans

88
Q

glycoproteins

A

protein with carbohydrate side chains

attached by glycosylation in golgi by glycosyltransferase

89
Q

proteoglycan

A

subclass of glycoprotein
heavily glycosylated protein with GAG side chain
acid group provides negative charge
attracts water and protection against compressive forces

90
Q

is collagen always arranged in the same way

A

organisation is related to the function

tendons, skin and a cornea all have different collagen fibril arrangement

91
Q

types of collagen and the disease their mutant phenotype

A

type 1 - severe bone defects, fractures
2 - cartilage deficiency, dwarfism, vitreous humor of the eye
3 and 5 - fragile skin, loose joints, blood vessels prone to rupture
4 - kidney disease, deafness
6 - myopia, blindness
9 - osteoarthritis
12 and 17 - skin blistering
18 - myopia, detached retina, hydrocephalus

92
Q

describe triple helix structure of collagen

A

types I, IV, V, IX and XI have 2 or 3 types of alpha chain (hetrotrimer) whereas II, III, VII, XII and XVIII have only one type of alpha chain each (homotrimer)

93
Q

collagen structure

A

glycine-x-y repeating unit - glycine residue located at the centre of the triple helix - x is sometimes proline and y can be hydroxyproline
triple helical structure - 3 alpha polypeptide chains - each chain is a polyproline helix

94
Q

intracellular steps of collagen maturation

A

transcription of mRNA in the nucleus, translation, post translational modification

95
Q

extracellular steps of collagen maturation

A

propeptide cleavage

collagen fibril assembly

96
Q

describe transcription and translation in collagen maturation

A

transcription - genes for pro-a2 and pro-a2 chains are transcribed
translation - mRNA moves into the cytoplasm and interacts with ribosomes for translation
it is now referred to as a pre-pro-polypeptide and it travels to ER

97
Q

post translational modification in collagen maturation

A

pre-pro-polypeptide undergoes post translational processing - 3 major modifications for it to become pro-collagen
1. signal peptide on N terminal is removed
2. lysine and proline residues get additional hydroxyl groups added to them via hydroxylase enzymes which require vitamin C as a cofactor - catalysed by prolyl-4-hydroxylases, prolyl-3-hydroxylase and lysul hydroxylases
3. glycosylation of the selected hydroxyl groups on lyosine with galactose and glucose b
three of the hydroxylated and glycosylated pro-a-chains fold into a triple helix and are then secreted into vesicles

98
Q

propeptide cleavage in collagen maturation

A

enzymes known as collagen peptidases preform propeptide cleavage and remove the ends of the procollagen molecule and the molecule becomes tropocollagen

99
Q

collagen fibril assembly

A

lysyl oxidase acts on lysine and hydroxlysines

covalent bonding between tropocollagen molecules forms a collagen fibril

100
Q

describe c-proteinase and n-proteinase

A

the C-propeptides of the fibril-forming collagen, and the N-propeptides of type I and II, partially also of type III collagen are cleaved by these proteases
c-proteinases are of the BMP1 type
n-proteinases are ADAMTS family members - a disintegrin and metalloproteinase with thrombospondin repeats

101
Q

describe the collagen turn-over-half life

A

in adulthood - no collagen turnover in healthy state

about 120 years meaning collagen will stay for life - even defective proteins will stay for life

102
Q

describe osteogenesis imperfecta

A

brittle bone disease
range of clinical severity from fractures to lethality
autosomal recessive and dominant forms
collagen type 1 related disorder - mutation in COL1A1 or COL1A2

103
Q

describe the structure of collagen type 1

A

major fibrillar collagen

COL1A1 and COL1A2 heterotrimeric protomer - 2 alpha 1 chains and 1 alpha 2 chain

104
Q

OI type 1

A

less severe, no symptoms at birth
early onset osteoporosis, few fractures
null mutations - gene not being transcribed into RNA and/or translated into a functional protein
reduced collagen

105
Q

how does mild OI impact procollagen

A

normally 8 molecules of pro-alpha1 chains and 4 molecules of pro-alpha2 chains which combine to make 4 procollagen proteins
OI means you only have 4 molecules of pro-alpha1 chains and so only 2 procollagen proteins are produced

106
Q

mutations in mild OI

A

stop codons
promoter mutations - impacts amount of collagen being produced
mRNA instability
consequences always the same - not enough collagen made - quality of collagen is fine

107
Q

role of HSP47 in collagen maturation

A

prevents aggregation of collagen by coating the procollagen

HSP47 can be recycled

108
Q

mutations in severe forms of OI

A

80% glycine missense mutations - quality of the protein is impacted
dominant negative
effect on modification due to delay in folding - disruption of gly-x-y sequence slows rate of folding resulting in overmodification of the chains N-terminal to the disruption
mutant chains are secreted
potential effects on protein binding

109
Q

3 joints of the elbow

A

humeroulnar
humeroradial
proximal radioulnar joint - not involved in flexion/extension - passively moves

110
Q

where does the humerus articulate

A

with two forearm bones - laterally with radius at the rounded capitulum and medially with ulna bone at the trochlea

111
Q

epicondyles on distal end of humerus

A

medial and lateral epicondyles
located proximal to capitulum and trochlea
they site muscle attachment

112
Q

describe the proximal end of ulna

A

trochlear notch
2 processes:
larger processes is called olecranon and is posterior - elbow prominence
smaller process is the coronoid process which is anterior
both processes together receive the trochlea of humerus

113
Q

describe the distal end of ulna

A

head is anterior and articulates with radius
styloid process is posterior and medial - wrist ligaments
ulnar does not articulate with carpal bones - fibrocartilaginous ligament prevents this
ulnar articulates with radius instead

Medicine phase 2 limbs and back (6 decks)

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