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Week 5 Flashcards

1
Q

what are 4 ways to calissfy bone fracures

A

complete/incomplete
open/close
numebr of frcatur elines
direction of fracture liens

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2
Q

true or false - boen fractures are a complete break in bone?

A

false - cna eb complerte oe rpartial

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3
Q

what is difference betwene complete an incomplete fracture

A

complete- broke into 2 piecs

incompelte - bone partiallys evered -eg greenstick

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4
Q

open vs closed frcture

A

open - skin is broken - hgiher risk of infection
closed- not broken

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5
Q

what are the 3 ways to classifyf ractures based on number of fraction liens

A

simple - bone broekn in one places
cominuted - multiple fracture lines/fragement
compression - rushed into tiny pieces + collapses

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6
Q

what is a cominuted fracture

A

mutiple fracue liens/fragemnts

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7
Q

what is a compresssion fracture?

A

bone shatterd +collapse s

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8
Q

what are the 4 ways to classify fracture based on diretion of fracture line

A
  1. transverse -a cross bone
  2. spiral (angles) - rotaional (spirals around bone)
  3. longitudinal(Linerat) - along axis of bone
  4. oblique - bone breask at angle (diagnoal fractur)
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9
Q

what is an impacted fracture?

A

one end forced into anotehr end of bone

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10
Q

what is a stress fracure

A

excessive stress

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11
Q

what are spontanous fractures?

A

not a blunt force - usually from wakenss in bone due to condition

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12
Q

what is a colles fracture? who is it comon in

A

bone bends backwards - usualyl due ot hyerpextended in wrist - common in athletes or osteoperotic elderly

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13
Q

Maria is 86 years old with complaints of chronic back
pain. X-ray displayed microfractures within a lumbar
vertebral body. This fracture looks characteristic of

A

compression frature

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14
Q

Geoff fell hard while mountain biking and landed with full force on
his forearm. The force was so strong that the fracture pierced
through the soft tissues and broke the skin. Upon X-ray it became
clear that the bone is fractured in multiple regions

A

open, cominuted fracture, complete

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15
Q

signs and symtoms of fracture

A

pain, swelling bruising, inability to move, altered sensation
- msialigned shortened, deformed limb

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16
Q

treatment of fracture?

A

immobilization of joint
surgery if neeeded
reallign,ment of bones
inseriton o rods, plates, screws
exercise to maintain rom, muscle mas circulation

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17
Q

what are the 4 steps of boen haling process?

A
  1. hematoma formation
  2. inflammatopry phase
  3. reparative phase
  4. remodelling phase
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18
Q

what is the fist step of bone healing - explai. it

A

heamtoma formation
- blood from vessels in and around bone and tissue
- clot in medullary cavity, under periosteum and between bone fragements
- fibrin mesh forms to seal off fracture site and act as scaffolding for next steps

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19
Q

after hematoma formation in bone healing what happens

A

inflammtory phase and begining of reparitve phase

  • inflammation
  • due to cell damge/necrosis + debris prescense (infiltration of immune cells)
  • growth of granualtion tissue (new conn tissue) in fibrin mesh
  • new cappilaires infiltrate
  • fibroblasts and chondroblasts migrate here and form procallus (fibrocarilagenous callus)
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20
Q

explain the whole process of bone healing

A

. Hematoma Formation
Bone break
Bleed from blood vessels in/around bone/tissues
Clot in medullary cavity, under periosteum and between bone fragments
Fibrin mesh forms to seal off fracture site and act as scaffolding for next steps
2. Inflammatory Phase
Inflam response due cell damage/necrosis and presence of debris at the cite (infiltration of immune cells)
Growth of granulation tissue (new conn tissue) within fibrin mesh network
New capillaries infiltrate area
Fibroblasts and chondroblasts migrate here - form the procallus (fibrocartilaginous callus)
Formation of procallus usually complete by week 3 post injury
3. Reparative Phase - bony callus formation
Osteoblasts generate generate new bone over the fibrocartilage model (procallus)
Procallus is replaced by bone (bony callus)
4. Remodeling Phase
During following months in response to mechanical stresses on the bone, repared bone is remodeled by osteoblast and osteoclast activity - excessive callus removed and more compact bone laid down

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21
Q

what is granualtion tissue?

A

new connectiv tissue fomrs in healing

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22
Q

whta does the inflammatory response lead to in bone healing?

A

growth of new connn tissue - forms procallus

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23
Q

what two cells form the procallus?

A

chondroblastsa and fibroblasts

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24
Q

when is formation of procallus usually omplte after a fracture?

A

3 weeks

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25
what happens after the inflmmatory resposne and formation of procallus?
Repartaive phase osteoblasts come in and replace the fibrocartilagenosu callus (procallus) with bone (bony callus)
26
once the boen callus has frome din the reparative phase what happens in the bone healing process?
the remoddling phase - mechanical stress on bone - repaire dbone is remodeled with osteoblast/lst acitivty - excessive callus removed and more compact boen laid don
27
what facors impair bone healing?
age - kids fastser extent of damage, complciated breaks systemic factors -0 aging circultory issues, anemia, diabtese, nutitional deficits, cofritcosteroids, smoking
28
what are some shrot term complications of ractures
1 . broken ends damge surrounding stutures 2. comaprtment synrom 3. fracture of longbone 4. iscehmia due to cast 5. infection
29
how can fracrures damage surroudning strcuture?
blood vessels leading ot bleeding nerves - altering sensation tears to msucles and tendons
30
what is compartment syndrome?
blleding or edema leads to increased presure in limb and this can impait blood supply + potential for tisuse necrosis pressure build up - squeeze blood vessles/nerves - damge msucle and nderce - necrosis fo tissue
31
what can happen with adipose in long bone fractures? is this common?
no -rare - release of adipose from fractured area enters blood and obsructs blood flow (to brain and lungs)
32
what is ischemia and how is this a complication of bone healing?
ischemia is due to the cast compression - edema occurs within casted area so must monitor distal protion of limb fo rpal, cold numbness
33
anoher name for open fracture is _____
compound
34
what is a compound fracture?
open rcature - peirces skin
35
What is complication that could occur in a compund fracture?
infeciton - specifically ostemyelitis - bacteria enters the bone and local andsytemic manifesations
36
what is common infection in bone fractures?
ostemyelitis - bacteria enters the bone and local andsytemic manifesations
37
what is malunion healing?
bone heals out of allignment
38
what ar 3 long terms complications of bone fractures ?
1. ehaing abnormalieties - 3 types 2. mobility complciation - stiffness, limtied ROM, instabiity 3. side effect of long term immobilization - pressure injury, deep vein thrombosis
39
what are the three types of healing abnormalities in fractures?
malunion - boen heals out of allignment delayed union - more time needed to heal non-union - failur to heal
40
what are 2 side effects of long term immobilzaation after fracture?
pressure injury + deep vein thrombosis - blood clots
41
Matt fractured his clavicle, Breaking the bone into 4 separate pieces. He was initially treated without surgery. The bone healed, but in a displaced and abnormal position as seen on the X-ray image. Healing in this way is described as:
malunion
42
abnormla curvature of spine often due to ____
osteoperosis or arthritis
43
main differnce between osteoperosis and oasteroarthritis
osteroperosis affects bone and bone density - osteoarthritis is innjoint (catilage breakdown_)
44
what are the three types of abnormal curavtures of the spine?
lumbar lordosis - inward curve (0besity pregnant) kyphosis - ourword hunchback scoliosis - s shape sideqays
45
what is a concussion
midl brain injury by biomachnical foce - traumatic blow to head or body
46
is concucussion obcuious on brain trauma imagin?
no
47
what are the most commoncaues of concussion
contact spo, motor vehicle, falling downs tairs, doemestic violence
48
what are the 2 main types of conussions -describe each
1. coup-countercoup injury - contusion formpact (coup) -causes movemtn of the brain to impact opposit side of skull (countercoup) - stretching + shearing of neurons 2. torque (rotational) injury - head and neck twists, causing brain to rotatie - strethcing and shearing of neurons
49
a concussion is essentially what?
stretch and shearing of neurons
50
describe the pathophys of concussion starting from neurons..
stretch/shear of neruons 2. axons leak ions, spontaneous AP firing 3. excess excitatory NT release(glutamate) 4.many neurons stimulated (EPSP) 5. increase metabloic activity 6. increase demand for blood (glucose) - transient decrease inblood to brain after convussion 7. imbalnce nutrient supply/demand 8. neurons dmaged: inter into lwo matbloc state for epriod of time
51
what is the neurotransmitter athat is excitatory in ap? what happens to this neurotransitter during concussion?
excess of it - glutatmate -
52
during a concussion excess__ enteres whic ___
excess ca2+ slows down effectiveness of Mito
53
when axons leak in concsusion the ___ is needed to compensate which means more ___ is needed
sodum potassium pump needs to be acivatd more whcih meakns more atp is needed by mito- but... atp impaired because of CA2- enternc einto mito - slows down effectiveness
54
what are the 4 domains of concussion symp?
somatic, cognitie, mood, sleep
55
acute symtoms of consusion
confsuion, memory loss, loss of conscoiusneess
56
chronic symptoms of concussion
headahce, dizzness, mood changes, nasueas, light/noise sentiicity,faitgue, sleep distubances
57
what does recent evidence suggeset in terms of PA and concussions?
early mild-mod PA cna recue time-to symptom free avoid actiivties with exesive brain movement avoid repeated concussion
58
why are repeated concussion dangerous? what can it lead to?
chronic traumatic encephalopathy - damge due to misfolding of structural protein in neurons - TAU protein - clusteing and buildup aorun dbloodvessels in brain - neuron death - brain atrophy - dmentia
59
what is chronic traumatic encephalopathy
damge due to misfolding of structural protein in neurons - TAU protein - clusteing and buildup aorun dbloodvessels in brain - neuron death - brain atrophy - dmentia
60
what structural protein in neurons is damged in repeated consusions. what happens to it in repeated concussions and what does this lead to?
Tau portein - misfolding - lead to neuronal death - brain atophy + demntial
61
what does evidenc show for exrcise as acute treatment for concussion?
those who walk caysaully, light acitivyt or even moderate activity had less days till symptom free _ return to play
62
what does spincal chord injury do to neural messges?
obstructs transmission thru SC - loss f somatic an dautonmoic control of tunk, libs and viscera below site of injury
63
differcen between tetaplegia and apraplegia?
tetraplegia - C1- T1 paprplegia - below T2
64
why might tetraplegia be more fangerous?
can impair upper bdoy funcitons like rebathing + brain
65
what is the differnc ebetween complete and incomplte spincal injury
compelte - loss of all sensory ad motor funciton icnompelte -some
66
explain the diffenrt nervous sytem disruption caused by spinal injurues
somatic NS - motor +seneory pathway disruption ANS - SNS +PNS disruption SNS nerves found at T1-L5 PNS nerves at s1-s2- cranial nerves intact
67
where are SNS nerves found? Pns?
T1-L5 PNS - S1-s2
68
the PNS is often distubed in ____plegia. Why?
PNS dsiturbed in paraplegia - affexts nerves below T2 and PNS nerves ar s1 and S2
69
the SNS can be dsiturbed in ___Plegia why?
tetra and para tetra - C1-T1 Para >t2 SNS nerves are located between T1 and L5
70
what are the 2 pahes of SCI?
primart and secondary injury
71
explain. primary SCI in 3 steps
1. suden trauma to spine 2. acute compresion of SC - shear stress, severing 3. acure imapct to neurons, lgial cells + nerual parenchyma (functional tissue of the nervous system, specifically the tissue that is involved in transmitting electrical signal)
72
s seconadary SCI always form primary?
yes - cascade of proceses
73
what does secondary SCI arise form? what are the subphases?
priamry triggers secondary - cascade of biochemical/metabolic + machnical changes in neural tissues - consequenc eof downstram effects - homorahe an inflmation 3 subphaess 1.Acute phase 2. sub-acute phase 3. chronic phase
74
how long is ht acute phase of secondary SCI?
0-48 hours
75
how long is acut ephase of SCI and what happens?
0-48hrs . hemmorage, inflammation + local ischemia neural excitoxicity (too much excitiation of neruons - crazy signals like concussion) - leads to cellualr damge - celld death begins
76
when is the sub-acute pahes of secondary SCU? what happns heere/
first 2 weeks - neurotxiciity contonues, inflmamation + cell death SCAR TISSUE forms - undamged tracts continue fucntion (incomplete)
77
what subphase does scar tissue form in secondary SCI?
sub-acute phase
78
when is the chronic phase of secondary SCI? what happens?
days to years. conrinued celld eath + scar tissue fomation axonal dgenration + cyst development
79
what phase do axons start to degenerate in seocndary SCI?
chronic
80
when is hemmoraging in seocndary sci? what phase?
0-48hrs - acute phase
81
what are the 5 classifcaiton of american spinca chord injury calssificaiton brief explaine axh
complete A - no sensorynmotor function in sacral (s4-s5) incomplete B - soem sensation belwo injury - sensory but no motor incomplete C - motor + sensory - half of musscles work incomplte D - most msucles work (muscle grad >3) Normal E - fucntions normal
82
what are some CV effects from SCI?
HR + BP regualtion - due to loss of ANS funcitons
83
some pulmonary effects of DCI?
ventialtion imapored above c5 injuries
84
some bowel and bladd of SCI?
fucntion likel imapcted +Secual ucntion
85
name 5 systemic effects of SCI?
Cardiovascular: issues with regulation of HR and BP due to loss of autonomic NS signals below the injury * Pulmonary: Ventilation severely impaired in injuries above C5 (ventilator assistance required) * Bowel and bladder function, sexual function all likely affected * Thermoregulation (harder to regulate below the level of the SCI) * Hyperreflexia (Spasticity): due to central disinhibition of spinal reflex arcs --> leads to inappropriate activation of the stretch reflex within skeletal muscle * Autonomic Dysreflexia (see next slide)
86
waht is autonomic dysreflexia?
usncontroleld SNS repsone to afferent stimulus below loeveloof the SCI (eg ulle bladder, cut, fracture, pressure sore)
87
autonomic dysreflexia is uncosntoleled ___ repsosne to ___ sitmulus __ SCI
SNS response to affernt stu=imul below SCI
88
what is the result of autonomic dysreflexia?
widesprad vacosntiction below level of injruy - incrased BP - baroreceptors signal medulla - PNS reposne (abvoe oinjury - decreased HR + vasodilation - life threatneign results - sudden acute hypertension bradychardia
89
autonomic dysreflexia?
when the body’s automatic systems (which control things like blood pressure, heart rate, and breathing) go out of balance, often in response to a noxious stimulus (like a full bladder, constipation, or skin irritation) below the level of the injury. What happens: The body can't sense the problem below the injury (due to the SCI), but the brain still gets signals from the upper body, causing a sudden spike in blood pressure. The nervous system tries to lower the blood pressure by slowing the heart rate, causing symptoms like: Severe headache Sweating Flushed skin (usually above the injury) Nausea Blurred vision Increased blood pressure that can be dangerous if not treated. Why it happens: The injury to the spinal cord interferes with the normal signaling between the brain and the body, so the body’s automatic response (like controlling blood pressure) doesn’t work properly.
90
what are some consideraiton for exrcise for thsoe with SCI?
multidisciplinary team (CPT, physio and physciain) adapt based on ability genral health _+ fitnes + sternght consider autonomic limiations mediactiosn? comorbidiites - - CVS, repsiration, rpessure injruies , osterperosis
91
what are PA guidleines for those with SCI? for strnegh + aerobic
aerobic: start at 20 mins 2x/week MVPA progress to exeed 30 mins 3x/week sterngtj start: 3 sets 10 reps 2x/weel exceed; 3 sets 10 reps 2x/week

Pathophysiology (11 decks)

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