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  /Title (6002-general-ll.pdf)
  /Creator (Cheatography)
  /Author (bee.f (bee.f))
  /Subject (6002 General LL Cheat Sheet)
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    \vspace{-2pt}\large{\bf{\textcolor{DarkBackground}{\textrm{6002 General LL Cheat Sheet}}}} \\
    \normalsize{by \textcolor{DarkBackground}{bee.f (bee.f)} via \textcolor{DarkBackground}{\uline{cheatography.com/180201/cs/42418/}}}
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  \vspace{-2pt}bee.f (bee.f) \\
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  \mymulticolumn{1}{p{5.377cm}}{\bf\textcolor{white}{Cheat Sheet}}  \\
   \vspace{-2pt}Published 4th March, 2024.\\
   Updated 4th March, 2024.\\
   Page {\thepage} of \pageref{LastPage}.
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Muscle Strains}}  \tn
% Row 0
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
% Row Count 1 (+ 1)
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• {\bf{Intro:}} & - Muscle / tendon strain is equivalent to ligament sprain in terms of injury type\{\{nl\}\}- Happens when muscle fibres are overworked, resulting in fibre tearing \tn 
% Row Count 9 (+ 8)
% Row 2
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• {\bf{Aetiology (risk factors):}} & - ↑ incidence in athletes\{\{nl\}\}- Commonly occurs when there's sudden ↑ in duration, intensity, or frequency of activity\{\{nl\}\}{\bf{3 types of muscles at risk:}}\{\{nl\}\}- {\bf{Two-joint muscles:}} motion at one joint can ↑ passive tension, leading to overstretching injuries\{\{nl\}\}- {\bf{Eccentric contractions:}}. common during deceleration phase, may change muscle tension \& cause myofibril overload injuries\{\{nl\}\}- {\bf{Muscles w/ ↑ \% of type II fibres:}} fast-twitch muscles w/ high-speed contractions, making them more prone to injury (running \& sprinting)\{\{nl\}\}→ Hamstrings, gastrocnemius, quadriceps, hip flexors, hip adductors, ES, deltoids, \& rotator cuff \tn 
% Row Count 39 (+ 30)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Muscle Strains (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Contraction induced injury caused by extensive mechanical stress\{\{nl\}\}- Often occurs due to powerful eccentric contractions or over-stretching of the muscle\{\{nl\}\}{\bf{Muscle lesions are classified as grade I, II, \& III}}\{\{nl\}\}{\bf{Grade I (mild):}}\{\{nl\}\}- Affect a limited number of muscle fibres\{\{nl\}\}- No decrease in strength\{\{nl\}\}- Full AROM \& PROM\{\{nl\}\}- Px \& tenderness may be delayed to the next day\{\{nl\}\}{\bf{Grade II (moderate):}}\{\{nl\}\}- Nearly half of muscle fibres torn\{\{nl\}\}- Acute \& significant px\{\{nl\}\}- Accompanied by swelling\{\{nl\}\}- Minor decrease in muscle strength\{\{nl\}\}{\bf{Grade III (severe):}}\{\{nl\}\}- Complete rupture of the muscle\{\{nl\}\}- Tendon separated from the muscle belly or muscle belly torn in 2 parts\{\{nl\}\}- Severe swelling \& px\{\{nl\}\}- Complete loss of function \tn 
% Row Count 36 (+ 36)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Muscle Strains (cont)}}  \tn
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• {\bf{Sx \& Ssx:}} & - Swelling, bruising, or redness\{\{nl\}\}- Px at rest\{\{nl\}\}- Inability to use the muscle at all\{\{nl\}\}- Weakness of muscle or tendons \tn 
% Row Count 6 (+ 6)
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\SetRowColor{white}
• {\bf{Management:}} & - {\bf{First phase:}} protection, rest, ice, compression, elevation (PRICE) \& NSAIDs\{\{nl\}\}- {\bf{Second phase:}} mobilisation should occur ASAP but gradually \& within limits of px, Mobs/Drops, low impact exercises\{\{nl\}\}- 3-6 weeks for the muscle fibres to recover = full ROM, pain free, \& 90\% strength bilaterally\{\{nl\}\}- {\bf{Third phase:}} proprioceptive \& endurance, SMT / STW, TrPs \tn 
% Row Count 24 (+ 18)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.physio-pedia.com/Muscle\_Strain"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{AVN / Osteonecrosis}}  \tn
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
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\SetRowColor{white}
• {\bf{Intro}} & - Degenerative bone condition resulting from the death of bone cells due to disruption in the subchondral blood supply\{\{nl\}\}- Also known as AVN, aseptic necrosis, \& ischemic bone necrosis\{\{nl\}\}- Typically affects the epiphysis of long bones at WB joints, w/ severe cases potentially causing subchondral bone destruction or joint collapse\{\{nl\}\}- Common sites include femoral head, knee, talus, \& humeral head\{\{nl\}\}- Less common occurrences in other bones like the carpus \& jaw \tn 
% Row Count 25 (+ 24)
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• {\bf{Aetiology (risk factors):}} & - 30-65 yrs\{\{nl\}\}- M\textgreater{}F\{\{nl\}\}- Females more at risk w/ PMHx of lupus\{\{nl\}\}{\bf{6 groups of risk factors:}}\{\{nl\}\}- {\bf{Direct cellular toxicity:}} chemo/radiotherapy, thermal injury, smoking\{\{nl\}\}- {\bf{Extraosseous arterial fracture:}} hip dislocation, femoral neck fracture, iatrogenic post-surgery, congenital arterial abnormalities\{\{nl\}\}- {\bf{Extraosseous venous:}} venous abnormalities, venous stasis\{\{nl\}\}- {\bf{Intraosseous extravascular compression:}} haemorrhage, elevated bone marrow pressure, fatty infiltration of bone barrow due to prolonged high-dose corticosteroid use, cellular hypertrophy \& marrow infiltration (Gaucher disease), bone marrow oedema, displaced fracture\{\{nl\}\}- {\bf{Intraosseous intravascular occlusion:}} coagulation disorders (thrombophilias \& hypofibrinolysis), sickle cell crises\{\{nl\}\}- {\bf{Multifactorial}} \tn 
% Row Count 67 (+ 42)
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{AVN / Osteonecrosis (cont)}}  \tn
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• {\bf{Pathophysiology:}} & {\bf{1.}} Reduction in subchondral blood supply\{\{nl\}\}{\bf{2.}} Induces hypoxia\{\{nl\}\}{\bf{3.}} Loss of cell membrane integrity\{\{nl\}\}{\bf{4.}} Necrosis of cells (osteonecrosis) \tn 
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• {\bf{Clinical \& physical exam presentation:}} & {\bf{Non-traumatic cases:}}\{\{nl\}\}- Mechanical px w/ variable onset \& severity\{\{nl\}\}- Difficult to localise\{\{nl\}\}- Normal physical exam in early disease (causing delay in Dx)\{\{nl\}\}- {\bf{Focused Hx considerations:}} recent trauma, steroid use, autoimmune disease, Sickle cell, alcoholism, tobacco use, manual labour, change in gait, connective tissue disorders, insidious onset px, decreased ROM\{\{nl\}\}{\bf{AVN of the hip:}}\{\{nl\}\}- Early stages often asymptomatic\{\{nl\}\}- Hip \& groin px\{\{nl\}\}- Late-stage. progression indicated by px at rest\{\{nl\}\}- {\bf{Associated Ssx:}} referred px in buttock \& thigh, stiffness, changes in gait\{\{nl\}\}{\bf{AVN of the knee:}}\{\{nl\}\}- Acute onset knee px while WB \& at night\{\{nl\}\}- Typical responses in Hx: osteoporosis or osteopenia, no recent trauma\{\{nl\}\}- {\bf{Physical exam findings:}} px w/ palpation over medial femoral condyle, decreased ROM\{\{nl\}\}{\bf{AVN of the talus:}}\{\{nl\}\}- Associated w/ polyarticular disease \& trauma\{\{nl\}\}- Complaints of px \& difficulty ambulating beyond expected recovery time post-trauma \tn 
% Row Count 61 (+ 52)
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{AVN / Osteonecrosis (cont)}}  \tn
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• {\bf{Diagnosis:}} & {\bf{MRI findings:}}\{\{nl\}\}- Osteosclerotic changes\{\{nl\}\}- Decreased bone resorption due to disrupted osteoclast function\{\{nl\}\}- Low on T1 (fat is white)\{\{nl\}\}- High on T2 (fat is dark) \tn 
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• {\bf{Complications:}} & {\bf{Postoperative complications:}}\{\{nl\}\}- Surgical site infection\{\{nl\}\}- Prosthesis malfunctions\{\{nl\}\}- Neuromuscular compromise \tn 
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• {\bf{Management:}} & - Pharmacological therapy in early stages\{\{nl\}\}- Surgery\{\{nl\}\}- Exercises to maintain joint mobility \& strengthen muscles around\{\{nl\}\}- Later in therapy implement endurance \& coordination training\{\{nl\}\}- Post-surgery \& recovery full conservative care \tn 
% Row Count 30 (+ 13)
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{AVN / Osteonecrosis (cont)}}  \tn
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• {\bf{Ddx:}} & - OA\{\{nl\}\}- Osteoporosis\{\{nl\}\}- Osteomyelitis\{\{nl\}\}- Neoplastic bone conditions\{\{nl\}\}- Inflammatory synovitis\{\{nl\}\}- CRPS\{\{nl\}\}- Soft tissue trauma \tn 
% Row Count 8 (+ 8)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK537007/"\}\}link text\{\{/popup\}\}; \{\{popup="https://www.physio-pedia.com/Avascular\_Necrosis?utm\_source=physiopedia\&utm\_medium=search\&utm\_campaign=ongoing\_internal"\}\}link text\{\{/popup\}\}}  \tn 
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Bursitis}}  \tn
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
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• {\bf{Intro:}} & - Swelling or inflammation of a bursa\{\{nl\}\}- Bursae are found near bony provinces \& between bones, muscles, tendons, \& ligaments (approx. 150 facilitate MSK movement)\{\{nl\}\}- Bursitis causes the bursa to enlarge w/ fluid, resulting in px w/ movement \& pressure\{\{nl\}\}- Not all forms of bursitis are due to 1° inflammation, some result from swelling due to a noxious stimulus \tn 
% Row Count 18 (+ 17)
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• {\bf{Aetiology (risk factors):}} & - Overuse of the joint\{\{nl\}\}- Repetitive strain: picking up \& lifting heavy loads\{\{nl\}\}- Trauma: falling / bumping against things\{\{nl\}\}- Pressure: "student's elbow" \& "housemaid's knee"\{\{nl\}\}- Bacterial infection: unattended wound (causing septic bursitis)\{\{nl\}\}- Other inflammatory disease: e.g. Gout (crystals can form in the bursa \& cause inflammation)\{\{nl\}\}- Immunocompromised individuals: diabetes, rheumatological disorders, alcoholism, or HIV, are at risk of septic bursitis \tn 
% Row Count 40 (+ 22)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Bursitis (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Bursa is a synovial lining sac\{\{nl\}\}- Collapses upon itself until triggered, leading to irritation \& filling with synovial fluid\{\{nl\}\}- Px occurs when the inflamed bursa is compressed against bone, muscle, tendon, ligaments, or skin\{\{nl\}\}- Not all bursitis is linked to an overt inflammatory process\{\{nl\}\}- Subacromial bursa examination shows ↑ inflammatory mediators \tn 
% Row Count 17 (+ 17)
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• {\bf{Clinical presentation:}} & - ↓ ROM due to px in involved joint\{\{nl\}\}- Px with AROM, but not w/ PROM in some cases\{\{nl\}\}- Two forms of bursitis: acute \& chronic\{\{nl\}\}{\bf{Acute:}}\{\{nl\}\}- Caused by trauma, infection, or crystalline joint disease\{\{nl\}\}- Pts experience px on palpation of bursa\{\{nl\}\}- Px w/ FX, but no px w/ EXT in certain types (e.g. prepatellar \& olecranon bursitis)\{\{nl\}\}{\bf{Chronic:}}\{\{nl\}\}- Often results from inflammatory arthropathies \& repetitive pressure/overuse\{\{nl\}\}- Often painless\{\{nl\}\}- Bursa has had time to expand to accommodate increased fluid, resulting in significant swelling \& thickening of the bursa \tn 
% Row Count 45 (+ 28)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Bursitis (cont)}}  \tn
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• {\bf{Physical examination:}} & - Evaluate skin for trauma, erythema, \& warmth\{\{nl\}\}- Temperature increase of 2.2°C over affected bursa compared to unaffected indicative of {\emph{septic bursitis}}\{\{nl\}\}- Deep bursitis may not show tenderness or obvious skin changes\{\{nl\}\}- Normal ROM in septic bursitis \tn 
% Row Count 13 (+ 13)
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\SetRowColor{white}
• {\bf{Diagnosis:}} & - {\bf{Plain radiography:}} recommended w/ Hx of trauma, concern for foreign body, or fracture causing swelling or px\{\{nl\}\}- {\bf{MRI:}} for evaluating deeper bursa\{\{nl\}\}- {\bf{US:}} helpful in differentiating cellulitis from infectious bursitis\{\{nl\}\}- {\bf{Bursa fluid punction:}} can rule out infections \tn 
% Row Count 27 (+ 14)
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• {\bf{Management:}} & {\bf{Bursitis w/o infection:}}- Most often self-limiting\{\{nl\}\}- RICE\{\{nl\}\}- NSAIDs\{\{nl\}\}- Injections\{\{nl\}\}- Mobs\{\{nl\}\}- Gradual ↑ in exercise\{\{nl\}\}- Immobilising is a risk towards adhesive capsulitis\{\{nl\}\}{\bf{Septic bursitis:}}\{\{nl\}\}- Antibiotics\{\{nl\}\}- Aspiration (needle)\{\{nl\}\}- NEVER inject w/ steroids\{\{nl\}\}- Surgical removal of bursa (in case of tuberculous bursitis)\{\{nl\}\}- Surgical incision \& drainage \tn 
% Row Count 46 (+ 19)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Bursitis (cont)}}  \tn
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• {\bf{Ddx:}} & - OA\{\{nl\}\}- RA\{\{nl\}\}- Can mimic other conditions in specific locations (e.g. shoulder - rotator cuff / labral tear)\{\{nl\}\}- Pathologies can coexist w/ or precipitate bursitis (e.g. gout)\{\{nl\}\}- Ischial bursitis can mimic sciatica (sitting-induced px distinguishes it from sciatica)\{\{nl\}\}- Trochanteric bursitis differs from ITB syndrome, w/ tenderness in IT band more distal compared to proximal location of trochanteric bursa\{\{nl\}\}- Iliopsoas bursitis can resemble arthritis, overuse injuries, synovitis, labral tears, or AVN\{\{nl\}\}- Knee bursitis typically doesn't cause effusion, aiding in differentiation from other knee pathologies\{\{nl\}\}- Retrocalcaneal bursitis may initially resemble achilles tendinitis, enthesopathy, px from bone spurs, or plantar fasciitis \tn 
% Row Count 35 (+ 35)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK513340/"\}\}link text\{\{/popup\}\}; \{\{popup="https://www.physio-pedia.com/Bursitis"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Calcific Tendonitis}}  \tn
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
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• {\bf{Intro:}} & - Self-limiting disorder characterised by deposition of calcium in the tendon / muscle\{\{nl\}\}- Leads to px \& reduced ROM \tn 
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• {\bf{Aetiology (risk factors):}} & - 30-50yrs\{\{nl\}\}- F\textgreater{}M\{\{nl\}\}- Occupational risk (construction, agriculture, certain sports)\{\{nl\}\}- Metabolic conditions (e.g. diabetes)\{\{nl\}\}- Mechanical stress: repetitive microtrauma or overuse of tendons\{\{nl\}\}- Vascular factors: poor blood supply (reduced clearance of metabolic waste)\{\{nl\}\}- Genetic predisposition \tn 
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• {\bf{Pathophysiology:}} & - Repetitive trauma → tendon degeneration → calcification\{\{nl\}\}- Tendon necrosis → intracellular calcium accumulation\{\{nl\}\}- Active process mediated by chondrocytes arising from metaplasia → calcium deposition\{\{nl\}\}- Phagocytosis of metaplastic areas reforms normal tendon \tn 
% Row Count 35 (+ 13)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Calcific Tendonitis (cont)}}  \tn
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• {\bf{Clinical presentation:}} & - Px w/ or w/o loss of ROM\{\{nl\}\}- Stiffness, usually after periods of inactivity (morning)\{\{nl\}\}- Swelling\{\{nl\}\}- TTP \tn 
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• {\bf{Physical examination:}} & - Limited ROM\{\{nl\}\}- Crepitus\{\{nl\}\}- Muscle weakness\{\{nl\}\}- Warmth \& redness\{\{nl\}\}- Palpable calcium deposits \tn 
% Row Count 11 (+ 5)
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• {\bf{Diagnosis:}} & - {\bf{X-ray:}} identify calcifications in the tendon or adjacent soft tissue\{\{nl\}\}- {\bf{US:}} visualise extent \& characteristics of calcifications \& assess tendon thickness\{\{nl\}\}- {\bf{MRI:}} may be used to evaluate soft tissue involvement \& inflammation \tn 
% Row Count 23 (+ 12)
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• {\bf{Complications:}} & - Chronic px\{\{nl\}\}- Tendon rupture\{\{nl\}\}- Compression of adjacent structures\{\{nl\}\}- Bursitis\{\{nl\}\}- 2° OA\{\{nl\}\}- Functional impairment\{\{nl\}\}- Psychosocial impact\{\{nl\}\}- Recurrence \tn 
% Row Count 32 (+ 9)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Calcific Tendonitis (cont)}}  \tn
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• {\bf{Management:}} & - Pts w/ chronic calcific tendonitis often don't respond to conservative care\{\{nl\}\}- Anti-inflammatory NSAIDs (ibuprofen)\{\{nl\}\}- Injections\{\{nl\}\}- Surgery \tn 
% Row Count 7 (+ 7)
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• {\bf{Ddx:}} & - Adhesive capsulitis\{\{nl\}\}- Tendinopathy\{\{nl\}\}- Bursitis\{\{nl\}\}- Arthritis\{\{nl\}\}- Ossifying tendinitis \tn 
% Row Count 12 (+ 5)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteoarthritis}}  \tn
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
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• {\bf{Intro:}} & - Non-inflammatory, degenerative joint disease\{\{nl\}\}- Characterised by loss of articular cartilage \& marginal hypertrophy of bone\{\{nl\}\}- Accompanied by px \& stiffness that is aggravated by prolonged activity\{\{nl\}\}- Most prevalent type of arthritis \tn 
% Row Count 13 (+ 12)
% Row 2
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• {\bf{Aetiology (risk factors):}} & - Higher age\{\{nl\}\}- F\textgreater{}M\{\{nl\}\}- Hx of joint trauma\{\{nl\}\}- Obesity\{\{nl\}\}- {\bf{1° OA:}} most common subset of OA; absence of predisposing trauma or disease\{\{nl\}\}- {\bf{2° OA:}} occurrence w/ pre-existing joint abnormality; Ssx\{\{nl\}\}- Modifiable environmental factors: repetitive movements, obesity, metabolic syndrome, smoking, vitamin D deficiency, muscle weakness, low bone density\{\{nl\}\}- Commonly affects hands, knees (most common), feet, facet joints, \& hips \tn 
% Row Count 34 (+ 21)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteoarthritis (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
• {\bf{Pathophysiology:}} & - Multifactorial \& involves 3 major processes: mechanical degeneration (wear \& tear), structural degeneration, \& joint inflammation\{\{nl\}\}- Overuse \& aging of the joint are believed to be the main contributors, but inflammatory processes indicated by ↑ cytokines are also present\{\{nl\}\}- Firstly, OA involves cartilage damage, including surface fibrillation, irregularity, \& focal erosions\{\{nl\}\}- Then, cartilage damage prompts chondrocyte proliferation, \& outgrowths can ossify, forming osteophytes\{\{nl\}\}- Later, subchondral bone sclerosis \& bone cyst formation occur, potentially increasing joint stiffness \& px\{\{nl\}\}- Advanced OA may lead to episodic synovitis, \& in rare cases, bony erosions can occur in erosive OA \tn 
% Row Count 33 (+ 33)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteoarthritis (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
• {\bf{Clinical presentation:}} & - Joint px worse w/ use \& improves w/ rest\{\{nl\}\}- Px peaks in late afternoon or early evening, also present in the early morning\{\{nl\}\}{\bf{Two types of px:}}\{\{nl\}\}- Dull, aching, throbbing px (predictable \& constant over time)\{\{nl\}\}- Intense, unpredictable px for short periods\{\{nl\}\}{\bf{Classified into three stages based on px types:}}\{\{nl\}\}- {\bf{Early OA:}} sharp, predictable px limiting high-impact activities\{\{nl\}\}- {\bf{Mid OA:}} constant px, unpredictable joint px or locking, affecting ADLs\{\{nl\}\}- {\bf{Advanced OA:}} constant dull-aching px w/ intermittent intense episodes, limiting recreational activities\{\{nl\}\}{\bf{Additional joint Ssx:}}\{\{nl\}\}- Tenderness, stiffness, crepitus\{\{nl\}\}- Limited ROM\{\{nl\}\}- Joint swelling, deformity, or instability \tn 
% Row Count 34 (+ 34)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteoarthritis (cont)}}  \tn
% Row 5
\SetRowColor{LightBackground}
• {\bf{Physical examination:}} & - Bony enlargement (commonly in DIP \& PIP joint of fingers \& toes)\{\{nl\}\}- Crepitus\{\{nl\}\}- Effusions (non-inflammatory)\{\{nl\}\}- Joint line tenderness\{\{nl\}\}- Limited ROM due to px, swelling, or joint deformity\{\{nl\}\}{\bf{Specific bony enlargements:}}\{\{nl\}\}- {\emph{Heberden's nodes:}} posterolateral bony swelling of DIP joints\{\{nl\}\}- {\emph{Bouchard nodes:}} posterolateral bony swelling of PIP joints\{\{nl\}\}- OA involving the base of the thumb is described as a "shoulder appearance" or "squaring" \tn 
% Row Count 22 (+ 22)
% Row 6
\SetRowColor{white}
• {\bf{Diagnosis:}} & {\bf{Plain radiographs to grade OA:}}\{\{nl\}\}- {\bf{0:}} no OA\{\{nl\}\}- {\bf{1:}} Doubtful narrowing of joint spaces \&/or possible osteophytes\{\{nl\}\}- {\bf{2:}} Definite osteophytes \& possible narrowing of joint spaces\{\{nl\}\}- {\bf{3:}} Multiple osteophytes, definite narrowing of joint space \& some sclerosis \& deformity of bone ends\{\{nl\}\}- {\bf{4:}} Large osteophytes, marked narrowing of joint space, severe sclerosis \& definite deformity of bone ends \tn 
% Row Count 42 (+ 20)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteoarthritis (cont)}}  \tn
% Row 7
\SetRowColor{LightBackground}
• {\bf{Complications:}} & - Chronic px\{\{nl\}\}- Long-term analgesics use\{\{nl\}\}- Reduced joint mobility\{\{nl\}\}- Decreased stability \& increased fall risk\{\{nl\}\}- Joint malalignment\{\{nl\}\}- Deformity\{\{nl\}\}- Stress fractures\{\{nl\}\}- Hemarthrosis\{\{nl\}\}- Osteonecrosis\{\{nl\}\}- Joint infection\{\{nl\}\}- Gout \& pseudogout\{\{nl\}\}- Depression \tn 
% Row Count 14 (+ 14)
% Row 8
\SetRowColor{white}
• {\bf{Management:}} & - Exercise program\{\{nl\}\}- STW\{\{nl\}\}- Mobs/drops\{\{nl\}\}- SMT\{\{nl\}\}- NSAIDs (preferably topical) \tn 
% Row Count 19 (+ 5)
% Row 9
\SetRowColor{LightBackground}
• {\bf{Ddx:}} & - RA\{\{nl\}\}- Gout\{\{nl\}\}- Pseudogout\{\{nl\}\}- Septic arthritis\{\{nl\}\}- Hemochromatosis\{\{nl\}\}- Fibromyalgia\{\{nl\}\}- Lyme disease\{\{nl\}\}- Ankylosing spondylitis\{\{nl\}\}- Psoriatic arthritis\{\{nl\}\}- Neuropathic arthropathy\{\{nl\}\}- Parvovirus-associated arthritis \tn 
% Row Count 31 (+ 12)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK557808/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Inflammatory arthropathies}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Painful inflammation \& stiffness of the joints\{\{nl\}\}- Inflammatory arthritis is typically associated w/ classic Ssx of inflammation\{\{nl\}\}- Can have various factors - inc. infectious / non-infectious factors\{\{nl\}\}- Inflammatory arthritis may or may not be associated w/ systemic features related to the underlying condition causing the inflammation \tn 
% Row Count 17 (+ 16)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - Increasing age\{\{nl\}\}- F \textgreater{} M (autoimmune inflammatory arthritis)\{\{nl\}\}- M\textgreater{}F (gout \& seronegative spondyloarthritis)\{\{nl\}\}- Smoking (strongest environmental factor)\{\{nl\}\}- Caucasian, FHx\{\{nl\}\}- W/ juvenile idiopathic arthritis presenting before 10 yrs of age \tn 
% Row Count 29 (+ 12)
% Row 3
\SetRowColor{white}
• {\bf{Pathophysiology:}} & - Varies depending on the underlying etiology\{\{nl\}\}- External or self-antigens trigger an immune-mediated inflammatory response\{\{nl\}\}- Inflammatory cells migrate from the bloodstream into synovial membrane\{\{nl\}\}- Hyperplasia of synovial fibroblasts is associated with inflammatory response\{\{nl\}\}- Cartilage \& bone damage can occur, leading to joint destruction in some cases\{\{nl\}\}- Infectious arthritis results from the direct invasion of the joint by infectious organisms\{\{nl\}\}- Infectious agents may trigger an immune response, leading to inflammatory arthritis\{\{nl\}\}- Autoimmune inflammatory arthropathies involve an interplay of environmental \& genetic factors activating the immune system\{\{nl\}\}- Crystalline arthropathies involve crystals in the synovial acting as antigens, triggering a neutrophil-mediated inflammatory cascade \tn 
% Row Count 67 (+ 38)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Inflammatory arthropathies (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
• {\bf{Clinical presentation:}} & - Disease progression can be chronic \& progressive, leading to joint damage, deformity, \& disability if left untreated\{\{nl\}\}- Joint px\{\{nl\}\}- Joint stiffness\{\{nl\}\}- Joint swelling\{\{nl\}\}- Warmth \& redness\{\{nl\}\}- Fatigue\{\{nl\}\}- Malaise\{\{nl\}\}- Low-grade fever\{\{nl\}\}- Inflammatory arthritis often follows a pattern of flares \& remissions \tn 
% Row Count 16 (+ 16)
% Row 5
\SetRowColor{white}
• {\bf{Physical examination:}} & - Inflammatory eye conditions: uveitis or iritis, common in various types of IA\{\{nl\}\}- Skin rashes: commonly in connective tissue diseases (systemic lupus or psoriatic arthritis)\{\{nl\}\}- Enthesitis: inflammation in the sites where tendons \& ligaments insert into bones (common in seronegative spondyloarthropathies)\{\{nl\}\}- Dactylitis: swelling of an entire digit (common of certain spondyloarthropathies)\{\{nl\}\}- Symmetry: common in RA \tn 
% Row Count 36 (+ 20)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Inflammatory arthropathies (cont)}}  \tn
% Row 6
\SetRowColor{LightBackground}
• {\bf{Diagnosis:}} & {\bf{Labs:}}\{\{nl\}\}- Elevated inflammatory markers: erythrocyte sedimentation rate (ESR) \& C-reactive protein (CRP)\{\{nl\}\}- Positive autoantibodies: such as rheumatoid factor (RF) \& anti-cyclic citrullinated peptide (anti-CCP) antibodies in RA\{\{nl\}\}{\bf{Plain radiographs:}}\{\{nl\}\}- Initially normal in early inflammatory arthritis\{\{nl\}\}- May show periarticular osteopenia at the disease progresses\{\{nl\}\}- Periarticular erosions are seen in inflammatory arthritis like RA\{\{nl\}\}- Gout erosions are typically \seqsplit{juxta-articular/rat-bite} erosions w/ overhanging edges\{\{nl\}\}- Chondrocalcinosis or CPPD deposition can be easily visualised\{\{nl\}\}- Axial spondyloarthropathies can later show 'bamboo' spine \& SIJ function \& erosions\{\{nl\}\}{\bf{MRI:}}\{\{nl\}\}- Beneficial, especially when radiographs are nondiagnostic\{\{nl\}\}- More sensitive than plain film in evaluating synovitis, erosions, sacroiliitis\{\{nl\}\}- Higher sensitivity than X-rays \tn 
% Row Count 42 (+ 42)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Inflammatory arthropathies (cont)}}  \tn
% Row 7
\SetRowColor{LightBackground}
• {\bf{Complications:}} & - Arise from delay in treatment or mass Dx\{\{nl\}\}- May lead to aggressive \& permanent joint damage\{\{nl\}\}- Associated conditions w/ joint damage: chronic gout, RA, seronegative spondyloarthritis\{\{nl\}\}- Erosive changes in joints\{\{nl\}\}- Interference w/ ADLs \tn 
% Row Count 12 (+ 12)
% Row 8
\SetRowColor{white}
• {\bf{Management:}} & - Inflammation is reversible, while joint destruction is not\{\{nl\}\}- Antibiotic therapy\{\{nl\}\}- NSAIDs\{\{nl\}\}- Education\{\{nl\}\}- Manual therapy\{\{nl\}\}- Diet\{\{nl\}\}- Lifestyle modification \tn 
% Row Count 21 (+ 9)
% Row 9
\SetRowColor{LightBackground}
• {\bf{Ddx:}} & - RA\{\{nl\}\}- AS\{\{nl\}\}- Psoriatic arthritis\{\{nl\}\}- Lupus arthritis\{\{nl\}\}- Gout\{\{nl\}\}- Juvenile idiopathic arthritis\{\{nl\}\}- Reactive arthritis\{\{nl\}\}- Spondyloarthritis \tn 
% Row Count 29 (+ 8)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK507704/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Septic arthritis}}  \tn
% Row 0
\SetRowColor{LightBackground}
• {\bf{YELLOW}} & - Same day referral \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Inflammation of joints 2° to an infectious etiology\{\{nl\}\}- Usually monoarticular, however polyarticular also occurs\{\{nl\}\}- Although rare, septic arthritis is considered an orthopaedic emergency \tn 
% Row Count 10 (+ 9)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & {\bf{In children:}}\{\{nl\}\}- Diverse casues\{\{nl\}\}- Staphylococcus is the 1° pathogen\{\{nl\}\}- Kingella king affects children under 2-3 yrs\{\{nl\}\}- Neonates face streptococcus, staphylococcus, gonorrhea\{\{nl\}\}- Adolescents: gonorrhoea concern\{\{nl\}\}- Salmonella links w/ sickle cell disease\{\{nl\}\}- Prolonged antibiotic use raises fungal infection risk\{\{nl\}\}- Pseudomonas from puncture wounds/drug use\{\{nl\}\}- Hip joint commonly affected in children\{\{nl\}\}{\bf{In adults:}}\{\{nl\}\}- Staphylococcus major in adults\{\{nl\}\}- Streptococcus pneumonia significant\{\{nl\}\}- Gonorrhoea causes non-traumatic mono-arthritis\{\{nl\}\}- Fungal/mycobacterial organisms challenging to Dx\{\{nl\}\}- SCJ/SIJ infections involve pseudomonas, common in IV drug abusers\{\{nl\}\}- Damaged joints, especially in RA, prone to infection w/ cartilage damage, effusions, \& px\{\{nl\}\}{\bf{Epidemiology:}}\{\{nl\}\}- Incidence peaks at 2-3 yrs \& elderly\{\{nl\}\}- M\textgreater{}F (2:1)\{\{nl\}\}{\bf{Risk factors:}}\{\{nl\}\}- Age \textgreater{}80\{\{nl\}\}- Diabetes mellitus\{\{nl\}\}- RA\{\{nl\}\}- Recent joint surgery\{\{nl\}\}- Joint prosthesis\{\{nl\}\}- Previous intra-articular injection\{\{nl\}\}- Skin infections \& cutaneous ulcers\{\{nl\}\}- HIV infection\{\{nl\}\}- OA\{\{nl\}\}- Sexual activity (gonorrhoea) \tn 
% Row Count 64 (+ 54)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Septic arthritis (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
• {\bf{Pathophysiology:}} & - Bacterial invasion of synovial, followed by inflammatory processes\{\{nl\}\}- Common pathogens change throughout lifetime (viz. aetiology)\{\{nl\}\}- Damaged joints through RA are highly susceptible to infection\{\{nl\}\}- Synovium lacks limiting basement membrane → systemic infection can spread to bones\{\{nl\}\}- Contagious spread from osteomyelitis (hip \& shoulder are prone) \tn 
% Row Count 17 (+ 17)
% Row 4
\SetRowColor{white}
• {\bf{Clinical presentation:}} & {\bf{In children}}\{\{nl\}\}{\emph{Local Ssx:}}\{\{nl\}\}- Px, joint swelling, warmth\{\{nl\}\}- Limited ROM\{\{nl\}\}- Limp, refusal to use or move the affected joint (pseudoparalysis)\{\{nl\}\}{\emph{Systemic Ssx:}}\{\{nl\}\}- Ill appearance\{\{nl\}\}- Fever\{\{nl\}\}- Tachycardia\{\{nl\}\}- Fussiness/irritability\{\{nl\}\}- Decreased appetite\{\{nl\}\}{\bf{In adults:}}\{\{nl\}\}- Acute onset monoarticular (large joints) joint px\{\{nl\}\}- Fever (40-60\% of pts), swelling, reluctance or refusal to move the affected joint\{\{nl\}\}- LL (hip, knees, ankles) commonly affected\{\{nl\}\}- Knee most affected joint \tn 
% Row Count 42 (+ 25)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Septic arthritis (cont)}}  \tn
% Row 5
\SetRowColor{LightBackground}
• {\bf{Physical examination:}} & - Palpation may elicit px\{\{nl\}\}- Limited ROM\{\{nl\}\}- Effusions are common \tn 
% Row Count 4 (+ 4)
% Row 6
\SetRowColor{white}
• {\bf{Diagnosis:}} & - Synovial WBC count\{\{nl\}\}- ESR \& CRP\{\{nl\}\}{\bf{Imaging}}\{\{nl\}\}{\emph{Plain radiographs:}}\{\{nl\}\}- May reveal widened joint spaces\{\{nl\}\}- Soft tissue bulging\{\{nl\}\}- Subchondral bony changes (late finding)\{\{nl\}\}- Normal plain radiograph doesn't rule out septic arthritis\{\{nl\}\}{\emph{US:}}\{\{nl\}\}- Useful for identifying \& quantifying joint effusion\{\{nl\}\}- Aids needle aspiration\{\{nl\}\}{\emph{MRI:}}\{\{nl\}\}- Sensitive for early detection of joint fluid\{\{nl\}\}- Reveals abnormalities in surrounding soft tissue \& bone\{\{nl\}\}- Cartilaginous involvement \tn 
% Row Count 28 (+ 24)
% Row 7
\SetRowColor{LightBackground}
• {\bf{Complications:}} & - Osteomyelitis\{\{nl\}\}- Chronic px\{\{nl\}\}- Osteonecrosis / AVN\{\{nl\}\}- Leg length discrepancies\{\{nl\}\}- Sepsis\{\{nl\}\}- Death \tn 
% Row Count 34 (+ 6)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Septic arthritis (cont)}}  \tn
% Row 8
\SetRowColor{LightBackground}
• {\bf{Management:}} & - Same day referral to GP\{\{nl\}\}- Antibiotics\{\{nl\}\}- Aspiration of joints \tn 
% Row Count 4 (+ 4)
% Row 9
\SetRowColor{white}
• {\bf{Ddx:}} & - Infections\{\{nl\}\}- CPPD\{\{nl\}\}- OA\{\{nl\}\}- Fractures\{\{nl\}\}- AVN/osteonecrosis\{\{nl\}\}- Other inflammatory arthropathies\{\{nl\}\}- Systemic infections\{\{nl\}\}- Tumour \tn 
% Row Count 12 (+ 8)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK538176/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Tendinopathies}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Tendinopathy is an umbrella term to describe tendon px, w/ unknown cause\{\{nl\}\}- {\bf{Tendinosis}} describes the degenerative state of tendons (more applicable) \tn 
% Row Count 9 (+ 8)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - Not fully understood\{\{nl\}\}- Mechanical stressors, repetitive overloading, or toxic chemical exposure ca initiate tendinosis\{\{nl\}\}- Age, genetic predisposition, \&/or comorbidities can increase susceptibility to healing failure leading to tendinosis \tn 
% Row Count 21 (+ 12)
% Row 3
\SetRowColor{white}
• {\bf{Pathophysiology:}} & - Decreased simplistically in 3 stages, but actually occurs on a continuum\{\{nl\}\}{\bf{Stage 1:}}\{\{nl\}\}- Begins w/ tendon experiencing the initial insult, stress, or injury\{\{nl\}\}- Causes: acute overload, repetitive stress, or chemical irritation\{\{nl\}\}- Linked to the death of tenocytes (tendon cells)\{\{nl\}\}{\bf{Stage 2:}}\{\{nl\}\}- Characterised by failed healing of the tendon\{\{nl\}\}- Unclear cause, but believed to result from an altered tendon environment (steroids/NSAIDs may alter natural healing cascade)\{\{nl\}\}- Improper cell recruitment \& a cascade of healing issues may occur\{\{nl\}\}{\bf{Stage 3:}}\{\{nl\}\}- Characterised by apoptosis (death) of cells, disorganisation of the matrix, \& neovascularisation\{\{nl\}\}- Pts often present at this stage, experiencing mechanical weakness or increased px\{\{nl\}\}- Neovascularisation theorised to supply neonerves, contributing to px (neurogenic inflammation) \tn 
% Row Count 62 (+ 41)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Tendinopathies (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
• {\bf{Clinical presentation:}} & - Identify potential stressors\{\{nl\}\}- Impact on ADLs\{\{nl\}\}- Recent changes in medication, inc. antibiotics (may influence treatment) \tn 
% Row Count 6 (+ 6)
% Row 5
\SetRowColor{white}
• {\bf{Physical examination:}} & - Tenderness\{\{nl\}\}- Swelling\{\{nl\}\}- Other abnormalities\{\{nl\}\}- Special tests based on the specific tendon \tn 
% Row Count 11 (+ 5)
% Row 6
\SetRowColor{LightBackground}
• {\bf{Diagnosis:}} & - Labs: CRP \& ESR (aid in identifying inflammatory processes)\{\{nl\}\}- {\bf{X-ray:}} if bone injury is suspected\{\{nl\}\}- {\bf{US:}} increased spacing of fibrillar lines, reduced echogenecity, tendon thickening, neovascularisation (via colour Doppler)\{\{nl\}\}- {\bf{MRI:}} valuable for evaluating tendinosis \tn 
% Row Count 25 (+ 14)
% Row 7
\SetRowColor{white}
• {\bf{Complications:}} & - Tendon rupture (if untreated)\{\{nl\}\}- Contractures of the tendon, w/ reduced tendon liability\{\{nl\}\}- Tendon adhesions\{\{nl\}\}- Atrophy of muscles\{\{nl\}\}- Loss of functionality, even up to \& including disability \tn 
% Row Count 35 (+ 10)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Tendinopathies (cont)}}  \tn
% Row 8
\SetRowColor{LightBackground}
• {\bf{Management:}} & - Healing as long as 3-6 months\{\{nl\}\}- STW\{\{nl\}\}- SMT\{\{nl\}\}- Mobs/drops\{\{nl\}\}- RICE\{\{nl\}\}- NSAIDs \tn 
% Row Count 5 (+ 5)
% Row 9
\SetRowColor{white}
• {\bf{Ddx:}} & - Acute compartment syndrome (ACS)\{\{nl\}\}- Ankle injury\{\{nl\}\}- Bursitis\{\{nl\}\}- Carpal tunnel syndrome\{\{nl\}\}- Gout \& pseudogout\{\{nl\}\}- Hand infections\{\{nl\}\}- Reactive arthritis\{\{nl\}\}- Rotator cuff injuries\{\{nl\}\}- Soft tissue knee injury \tn 
% Row Count 16 (+ 11)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK448174/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{LL nerve entrapments / Tunnel syndromes}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Umbrella term for conditions characterised by compression or entrapment of nerves, blood vessels, or tendons within anatomical tunnels in the LL\{\{nl\}\}- Can lead to various Ssx inc. px, numbness, tingling, \& weakness, affecting the function \& sensation of the LL\{\{nl\}\}{\bf{Common LL tunnel syndromes inc.:}}\{\{nl\}\}- Sciatica\{\{nl\}\}- Tarsal tunnel s.\{\{nl\}\}- Common peroneal n. entrapment\{\{nl\}\}- Anterior compartment s. (ACS)\{\{nl\}\}- Popliteal artery entrapment s. (PAES) \tn 
% Row Count 23 (+ 22)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - Age-related degeneration\{\{nl\}\}- Obesity\{\{nl\}\}- Sedentary lifestyle\{\{nl\}\}- Trauma\{\{nl\}\}- Arthritis\{\{nl\}\}- Tumours\{\{nl\}\}- Diabetes\{\{nl\}\}- Pregnancy\{\{nl\}\}- Tight clothing\{\{nl\}\}- Occupation-related factors \tn 
% Row Count 33 (+ 10)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{LL nerve entrapments / Tunnel syndromes (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
• {\bf{Pathophysiology:}} & - Increased pressure within confined spaces leads to nerve or vascular compression\{\{nl\}\}- Inflammation, fibrosis, or space-occupying lesions contribute to compression\{\{nl\}\}- Repetitive use or trauma can exacerbate Ssx\{\{nl\}\}- Individual anatomical variations may predispose individuals to specific tunnel syndromes \tn 
% Row Count 15 (+ 15)
% Row 4
\SetRowColor{white}
• {\bf{Clinical presentation:}} & - Px or discomfort in the affected LL\{\{nl\}\}- Numbness or tingling\{\{nl\}\}- Weakness in the muscles of the affected area\{\{nl\}\}- Altered sensation or hypersensitivity\{\{nl\}\}- Px may worsen w/ specific activities or movements\{\{nl\}\}- Swelling in the affected area\{\{nl\}\}- Impaired coordination or balance \tn 
% Row Count 29 (+ 14)
% Row 5
\SetRowColor{LightBackground}
• {\bf{Physical examination:}} & - Tenderness or px upon palpation of the affected nerve pathway\{\{nl\}\}- Muscle atrophy in severe or chronic cases\{\{nl\}\}- Limited ROM in affected joint\{\{nl\}\}- Positive {\bf{Tinel's sign}}: tingling or px elicited by tapping on the nerve\{\{nl\}\}- Positive {\bf{Nerve tension tests}}: straight leg raise / slump test to assess nerve mobility \& irritation\{\{nl\}\}- Changes in reflexes, such as diminished or exaggerated reflexes \tn 
% Row Count 48 (+ 19)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{LL nerve entrapments / Tunnel syndromes (cont)}}  \tn
% Row 6
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• {\bf{Diagnosis:}} & - {\bf{MRI}}: provides detailed soft tissue visualisation, helping identify nerve compression \& surrounding structures\{\{nl\}\}- {\bf{US:}} useful fro dynamic imaging, assessing nerve movement during various joint positions\{\{nl\}\}- {\bf{CT:}} may be used in specific cases, especially fro bony abnormalities contributing to nerve compression \tn 
% Row Count 15 (+ 15)
% Row 7
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• {\bf{Complications:}} & - Nerve compression \& damage\{\{nl\}\}- Ischemia (reduced blood supply)\{\{nl\}\}- Muscle atrophy \& weakness\{\{nl\}\}- Chronic px\{\{nl\}\}- Motor dysfunction\{\{nl\}\}- Sensory abnormalities\{\{nl\}\}- Functional limitations\{\{nl\}\}- Trophic changes (skin, hair, nail condition)\{\{nl\}\}- Risk for 2° injuries (risk of falls)\{\{nl\}\}- Psychosocial impact\{\{nl\}\}- Surgical complications \tn 
% Row Count 32 (+ 17)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{LL nerve entrapments / Tunnel syndromes (cont)}}  \tn
% Row 8
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• {\bf{Management:}} & - Rest \& activity modification\{\{nl\}\}- NSAIDS \& neuropathic px medication\{\{nl\}\}- Injections\{\{nl\}\}- Occupation \& ergonomic modifications\{\{nl\}\}- Weight management\{\{nl\}\}- Surgery\{\{nl\}\}- Pt education\{\{nl\}\}- SMT \& STW\{\{nl\}\}- Strengthening \& mobilising \tn 
% Row Count 12 (+ 12)
% Row 9
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• {\bf{Ddx:}} & - Peripheral neuropathy\{\{nl\}\}- Lx radiculopathy\{\{nl\}\}- MFPD\{\{nl\}\}- Complex regional px s. (CRPS)\{\{nl\}\}- Tarsal tunnel syndrome\{\{nl\}\}- Morton's neuroma\{\{nl\}\}- Stress fractures\{\{nl\}\}- Compartment s.\{\{nl\}\}- MSK injuries (ligament sprains, tendonitis etc.)\{\{nl\}\}- Inflammatory arthropathies (RA etc.)\{\{nl\}\}- Infectious causes (cellulitis, osteomyelitis etc.)\{\{nl\}\}- Neoplastic conditions (tumours)\{\{nl\}\}- Systemic conditions (diabetes, hypothyroidism etc.)\{\{nl\}\}- Iliotibial band s.\{\{nl\}\}- Popliteal entrapment s. \tn 
% Row Count 36 (+ 24)
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\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK430685/?term=nerve\%20entrapments\%20and\%20tunnel\%20syndromes"\}\}link text\{\{/popup\}\}}  \tn 
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\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Stress fractures}}  \tn
% Row 0
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{RED}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & - Fractures that occur due to an imbalance between the bone strength \& the chronic mechanical stress placed upon the bone (→ overuse s.)\{\{nl\}\}- {\emph{spondylolisthesis}} is also classified as stress fracture \tn 
% Row Count 12 (+ 11)
% Row 2
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• {\bf{Aetiology (risk factors):}} & - Abrupt increase in activity or training patterns\{\{nl\}\}{\bf{Intrinsic factors:}}\{\{nl\}\}- Poor physical conditioning\{\{nl\}\}- F\textgreater{}M\{\{nl\}\}- Hormonal disorders\{\{nl\}\}- Menstrual disorders\{\{nl\}\}- Poor bone density\{\{nl\}\}- Reduced muscle mass\{\{nl\}\}- Genu valgum kness\{\{nl\}\}- Short leg\{\{nl\}\}{\bf{Extrinsic factors:}}\{\{nl\}\}- High-impact sports\{\{nl\}\}- Abrupt increase in physical activity\{\{nl\}\}- Irregular or angled running surface\{\{nl\}\}- Poor footwear\{\{nl\}\}- Running shoe wear older than 6 months\{\{nl\}\}- Vitamin D \& calcium deficiency\{\{nl\}\}- Smoking\{\{nl\}\}{\bf{Common risk factors:}}\{\{nl\}\}- Abrupt increase in activity\{\{nl\}\}- Females\{\{nl\}\}- PMHx of stress fractures\{\{nl\}\}{\bf{Common sites:}}\{\{nl\}\}- Metatarsals, tibia, tarsals, femur, fibula, \& pelvis (in decreasing order)\{\{nl\}\}- Pelvic \& metatarsal stress \# common in females\{\{nl\}\}- UL stress \# rare but reported in gymnasts, weightlifters, \& throwing sports\{\{nl\}\}{\bf{Sports-specific risks:}}\{\{nl\}\}- Runners: tibia \& metatarsal stress \# (F may also experience pelvic stress \#)\{\{nl\}\}- Long-distance runners: association w/ femoral neck \& pelvic injuries\{\{nl\}\}- Hurdlers: patella \#\{\{nl\}\}- Gymnasts, female soccer players, certain American football positions \& weightlifters: increased risk of spondylolysis (unique stress \# related to repeated hyperEXT of the spine) \tn 
% Row Count 77 (+ 65)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Stress fractures (cont)}}  \tn
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• {\bf{Epidemiology:}} & - Stress \# are 20\% of all sports injuries\{\{nl\}\}- Common along military\{\{nl\}\}- Runners (16\% of injuries): tibia (23.6\%), tarsal navicular (17.6\%), metatarsals (16.2\%), femur (6.6\%), pelvis (1.6\%)\{\{nl\}\}- F\textgreater{}M\{\{nl\}\}- Neuromuscular factors play a role (muscle loss / fatigue decreases ability to absorb forces)\{\{nl\}\}- Rapid weight loss, particularly muscle loss, is associated w/ stress \#\{\{nl\}\}- Overtraining / relative energy deficiency s. contribute (esp. in females w/ disordered menstruation \& hormonal imbalances)\{\{nl\}\}- Male endurance athletes w/ high training volumes \& restricted calorie intake (low testosterone), leading to osteoporosis \& stress \# \tn 
% Row Count 33 (+ 33)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Stress fractures (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Wolff's law: applied force on a normal bone leads to remodelling for increased strength\{\{nl\}\}- Osteocytes: most common bone cells, orchestrate osteoclastic \& osteoblastic functions\{\{nl\}\}- Osteocyte's dendritic network: responds to biomechanical stress, secretes mediators regulating bone activites\{\{nl\}\}- Cycling loading impact: compromises osteocyte singling, hinders physiological repair mechanisms\{\{nl\}\}- Repetitive loading effect: stimulates osteoclasts for faster resorption, outpacing osteoblasts in new bone formation\{\{nl\}\}- Normal remodelling cycle: takes 3-4 months \tn 
% Row Count 29 (+ 29)
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• {\bf{Clinical presentation:}} & - Insidious onset of px after activity\{\{nl\}\}- Progressive increase in px duration post-exercise\{\{nl\}\}- Px present upon waking up following training activity\{\{nl\}\}- Important factors in Hx: recent changes in training, nutrition, intrinsic \& extrinsic risk factors, PMHx, \& medications \tn 
% Row Count 44 (+ 15)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Stress fractures (cont)}}  \tn
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• {\bf{Physical examination:}} & - Focal TTP\{\{nl\}\}- Occasional edema at the suspected stress fracture site\{\{nl\}\}- Limited clinical diagnostic tests\{\{nl\}\}- Px percussion \& vibration\{\{nl\}\}- Commonly used tests: "hop test" \& fulcrum test\{\{nl\}\}- Bony tenderness on palp, often at distal to middle third junctions I the tibia or over 3rd \& 4th metatarsal shafts \tn 
% Row Count 17 (+ 17)
% Row 7
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• {\bf{Spondylolysis \& spondylolisthesis:}} & - Require high index of suspicion\{\{nl\}\}- {\emph{Spondylolysis}} may be asymptomatic \& found incidentally on Lx films\{\{nl\}\}- Lx extension increases px in {\emph{spondylolysis}}, Stork test or single leg hyperextension test is common\{\{nl\}\}- {\emph{Spondylolisthesis}} occurs when pars defect does not heal, leading to anterior migration of the vertebral body \tn 
% Row Count 34 (+ 17)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Stress fractures (cont)}}  \tn
% Row 8
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• {\bf{Diagnosis:}} & - First is plain radiography\{\{nl\}\}- CT\{\{nl\}\}- MRI \tn 
% Row Count 3 (+ 3)
% Row 9
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• {\bf{Complications:}} & - Small for low-risk stress fractures\{\{nl\}\}- Occasional residual px\{\{nl\}\}- Higher for high-risk stress fractures\{\{nl\}\}- More likely to progress to non-union \& thus require surgery \tn 
% Row Count 12 (+ 9)
% Row 10
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• {\bf{Management:}} & - NSAIDs\{\{nl\}\}- Splinting\{\{nl\}\}- Resting / non-WB\{\{nl\}\}- Supplementation of vitamin D, magnesium\{\{nl\}\}- Potential surgery\{\{nl\}\}- Post-surgery / healing rehab\{\{nl\}\}- Strengthening /mobs \tn 
% Row Count 22 (+ 10)
% Row 11
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• {\bf{Ddx:}} & - Cellulitis\{\{nl\}\}- Osteomyelitis\{\{nl\}\}- Tendonitis\{\{nl\}\}- Tendinopathy\{\{nl\}\}- Exertional compartment syndrome\{\{nl\}\}- Tumours (benign \& malignant)\{\{nl\}\}- Nerve entrapment\{\{nl\}\}- Arterial entrapment\{\{nl\}\}- Coagulation disorders\{\{nl\}\}- Compartment s.\{\{nl\}\}- Neuropathic px\{\{nl\}\}- CRPS \tn 
% Row Count 37 (+ 15)
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\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK554538/"\}\}link text\{\{/popup\}\}}  \tn 
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\end{tabularx}
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\end{document}