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BSO3 > acute/chronic inflam mm, ligament tendon healing > Flashcards

acute/chronic inflam mm, ligament tendon healing Flashcards

1
Q

Acute Inflammation

A

rapid host response lasting mins hours or days that serves to deliver leukocytes and plasma proteins such as antibodies to sites of infection or tissue injruy

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2
Q

Granuloma Formation:
Outcome of acute inflammation

then Progession to chronic inflammation

A

Some bacteria cant broken don and remain cenclosed within their macrophage host

Commonly occurs: substantial tissue damage, inability if the tissue to regenerate, extensive fibrinous exudate

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3
Q

Abscess formation: acute inflammation

A

a creamy yellow pus may accumulate in the wound or site of injury

Dead, dying neutrophils, broken down cells tissues & dead pathogens

Inflammation fails to clear this area of debris, collagen fibres may be laid down to wall off the sac of pus

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4
Q

Outcomes of inflammation:
Complete resolution

A

Healing: clearance or cessation of injurous stimuli

removal of exudate, fibrin, debris

Revascularisation

Remodelling

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5
Q

Cardinal Signs

A

redness, swelling, heat, pain

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6
Q

Complement

A

stimulates histamine release which attracts neutrophils and promotes phagocytosis

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7
Q

Leuoktrienes

A

are produced by mast cells and basophils and help phagocytes attach to pathogens

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8
Q

Prostaglandins

A

assist with inducing chemotaxis. They can intensify and prolong the pain caused by inflammation

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9
Q

Kinins

A

induce chemotaxis of leukocytes and prompt neutrophils to release lysosomal enzymes.
Kinins are responsible for much of the pain associated with inflammation

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10
Q

Chemical Mediators of Inflammation:
Histamine

A

promote vasodilation of local arterioles increasing blood flow to injured area

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11
Q

Removal and Repair stage of acute inflammation
step 3

A

Monocytes follow neutrophils to the injured area

Monocytes are poor phagocytes, after entering the tissues they swell and develop a large number of lyosomes becomig macrophages

Macrophages are the central cells in the disposal of cell debris as acute inflammation subsides

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12
Q

Recruitment: Phagocyte mobilisation
step 2

A

Leucocytosis: increase in neutrophils (WBC”S)

Margination: phagocytes’ cling to inner walls of endothelium.
Endothelium sprouts cell adhesion molecule’s that signal that is site of inflammation

Diapedesis: Chemical signalling prompts neutrophils (wbc’s) to squeexe b/w the endothelial cells of capillary walls

Chemotaxis: inflammatory chemicals released active the neutrophils,
within an hour neutrophils are collected at the stie and are devouring the foreign material

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13
Q

Events that occur during inflammation
(Recognition)
Step 1

A

Recognition:
1. Inflammatory chemical release
chemical alarm
INfmamaotry chemicals are released such as Histamine, kinins, Prostaglandins, Sedentary macrophages
Vascular events: Vasodialation, Increased vascular permeability(capillaries)

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14
Q

Chronic Inflammation

A

Prolonged duration (weeks or months) in whcih inflammation, tissue injury and attempts at repair co-exist, in varying combinations

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15
Q

Tissue Repair Ability, regenerative capacity

A

Extremely Well: Epithelial tissues, bone, areolar connective tissue, dense irregular connective tissue, blood forming tissue

Moderate: dense regular connective tissue, smooth muscle

Limited: skeletal mm, cartilage

None: cardiac muscle, nervous tissue in brain and spinal cord

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16
Q

Acute Inflammation

A

rapid host response lasting mins hours or days that serves to deliver leukocytes and plasma proteins such as antibodies to sites of infection or tissue injruy

17
Q

Systemic Manifestations signs and symptoms

A

Malaise: tissue malnutrition due to higher overturn of proteins in chronic inflammatory process
Fever: due to presence of inflammatory mediators
Leukocytosis: greater number of white blood cells in blood due to persistent inflammation
Lymphadenitis: inflammation of lymph nodes
Depression: due to continuous pain associated with chronic inflammation
Frequent infections: due to compromised immune system

18
Q

Chronic Inflammation:
duration, weeks months years,
Caridnal signs same however reduced

Predominant cells:

Outcome:

A

Marcophages, b and T lymphocytes, plasma cells and fibroblasts

chronicn inflammtion will be ongoing, unless the intial cause is removed
mechanincal stress, antiboides, foregin obect bacteria or chemical agent

19
Q

Granuloma

A

Nodular lesion formed by collection of macrophages, lymphocytes, mononuclear cells and fibroblasts that constitutes a special form of chronic inflammation.

20
Q

Chronic Inflammation morpholgical features

A

Infiltration with immune cells:
macrophages (innate immune system)
lymphocytes and plasma cells (adaptive immune system)
Progressive tissue destruction caused by the offending agent as well as the inflammatory cells
Fibrosis (scar tissue) formation by fibroblasts, in an attempt to heal the tissues
New blood vessel proliferation (angiogenesis) to assist blood supply to healing tissues

21
Q

Aeitology of chronic inflammtion

A

persistent infections
Persistent mechanical injury
Prolonged exposure to toxic agents
Presence of a foreign body eg talc, splinter
Autoimmune diseases (self antigens)

22
Q

Chronic Inflammation

A

prolonged inflammatory response, tissue destruction and repair proceed simultaneously

23
Q

Granuloma

A

Nodular lesion formed by collection of macrophages, lymphocytes, mononuclear cells and fibroblasts that constitutes a special form of chronic inflammation.

24
Q

Chronic Inflammatory cells

A

Plasma cells, macrophages, lymphocytes, fibroblasts

25
Q

Tendon & Ligament Repair
Inflammation Stage (hours-days)

A

Haemostasis- bleeding is ceased
Acute inflammtion, stets stage for repair,
Inflammotry cells release cyotkines and growth factors

26
Q

Ligament Strain Grades info

A

Grade 1, 0-50% fibre disruption, normal range
Grade 2- 50-80% fibre disruption, increase laxity however end point
Grade 3, compete tear of ligament, excessive joint laxity no firm end point.

27
Q

Remodelling Phase (weeks to months)
Muscle Strain

A

Formation of mature contractile apparatus which fuse with existing myofibers

Attachment of new myofibre to intervening scar tissue

28
Q

Repair Phase (days to weeks)

of muscle strain

A

Clearance of necrotic tissue by macrophages

Fibroblasts produce collagen which later develops into scar tissue

Myogenic reserve cells differentiate into myoblasts and begin repair of myofibre

29
Q

MM strain, repair to myofibers Inflammation Phase (hours to days)

A

Haematoma fills the gap b/w the torn myofibers

Ruptured myo-fibres contract & sealed by a new sarcolemma

Infiltration by acute inflammatory cells
I

30
Q

Muscle Strains grading

A

Grade 1: small no. fibres affected localised pain but no loss of strength
Grade 2: greater no. fibres affected with associated pain and weakness
Grade 3: complete tear of mm, considerable pain and complete loss of function

(biarthrodial Mm) hammies, quads, gastrocs

31
Q

Acute vs Chronic Musclotendious injuries

A

Acute Mm, strain/tear
contusion

Acute Tendon, tear (partial/complete

Chronic: mm strain,
Chronic tendon injuires: tendionopathy, tendinits tendinosis, tensosynovitis

32
Q

Osteopathic Implications of Mm, tendon and Ligament Injuries
Acute soft tissue
treatemtn within the first week

A

Acute Soft Tissue Injury Management- R.I.C.E

treatment within the first week -effleurage to reduce swelling, soft tissue, mechanical loading, examination and treatment of biomechanically related region, if bad after 5-7, consider MRI

33
Q

Tendon & Ligament Repair
Remodelling Phase (weeks and months)

A

Collagen maturation beings: collagen type 3- collagen type 1
Alignment continues as ligament/tendin undergoes mechanincal loading
Cross-linking, increase strength of connective
becomes stronger but never at pre-injury strength

34
Q

Repair Phase (days[weeks)
tendon and ligament repair

DENSE REGULAR

A

Proliferation of fibroblasts- synthesise new extracellular matrix and collagen fibres

Collagen formation consists of collagen type 3 which is smaller diameter than collagen type 1.
within few weeks collagen being to align along the long axis of the ligament in response to loading

35
Q

Tendon & Ligament Repair
Remodelling Phase (weeks and months)

A

Collagen maturation beings: collagen type 3- collagen type 1
Alignment continues as ligament/tendin undergoes mechanincal loading
Cross-linking, increase strength of connective
becomes stronger but never at pre-injury strength

36
Q

Osteopathic Implications

Return to daily activities or Sport- Specific Training

Clincal features if present 3-5 days post injury, recovery period greater than 4 weeks

A

Brusiing/haematoma, tenderness to palape, lack of complete ROM

Pain during isometric mm contraction

37
Q

Osteopathic Implications
Risk Factors that predispose soft tissue injury

A

History, inappropriate training program
Overloading, freq, intensity
poor warm, cool down

ADLS, technique, equipment

38
Q

Osteopathic Implications of Mm, tendon & Ligament Injures
Rehab

A

Rehab- tissue loading results in remodelling, maturation and alignment of connective and scar tissue

Mm strain, rehab, include strengthening, lengthening, speed and agility training

Ligament strain, joint rang emotion, proprioception, balance training and mm strength to increase joint stability

39
Q

Osteopathic Implications of Mm, tendon and Ligament Injuries
Acute soft tissue
treatemtn within the first week

A

Acute Soft Tissue Injury Management- R.I.C.E

treatment within the first week -effleurage to reduce swelling, soft tissue, mechanical loading, examination and treatment of biomechanically related region, if bad after 5-7, consider MRI

BSO3 (12 decks)

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