just like the other day, i have summed up the tutorial done - until we were interrupted, that is.
MSK
Osteomyelitis
· Inflammation of bone and marrow
o Pathways of transmission
§ Posttraumatic osteomyelitis accounts for as many as 47% of cases of osteomyelitis.
§ Other major causes of osteomyelitis include vascular insufficiency (mostly occurring in persons with diabetes; 34%) and hematogenous seeding (19%).
§ Motor vehicle accidents, sports injuries, and the use of orthopedic hardware to manage trauma also contribute to the apparent increase in prevalence of posttraumatic osteomyelitis.
o Presenting signs/symptoms - how to differentiate bet. Septic arthritis?
§ Arthritis is a joint problem, whereas OM
o Salmonella osteomyelitis -> very common in Sickle cell trait / sufferers.
o Bone and marrow -> limited space -> when inflammation and exudation, limited space -> cause a Necrosis around the area due to high pressure and lack of blood -> opening established (absess) to release the pus -> through a “pointing” in the skin surface, the necrotic and infective material is relaeased -> sequastrum (dead bone) ->new bone formation using the dead bone as support / buttress. New bone called involucrum
o How to look at a microscopic bone tissue and say its dead or alive?
§ Non-viablity of bone
· Absence of osteoblastic rimming at surface
· Empty lacunae devoid of osteocytes
· Learn how to describe an ulcer.
o Malignant?
o Ischemic?
· Tuberculous osteomyelitis - differences from Brody’s absess
o Cold absess
o Usually no remodeling
o Preferance for spine (pott’s spine)
Avascular necrosis
· Causes
o Fracture / dislocation
o Embolic phenemona
o Vascular occlusion:
§ This is characterized by the interruption of the extraosseous blood supply via factors such as direct trauma (eg,fracture, dislocation), nontraumatic stress, and stress fracture.
o Altered lipid metabolism:
§ Animal studies have led to the hypothesis that increased levels of serum lipids leads to lipid deposition in the femoral head, causing femoral hypertension and ischemia.[2] Lipid-level–lowering drugs in animals reverse this process. Corticosteroid administration was associated with fat emboli in the femoral heads of rabbits.[3]
§ Disorders of the coagulation system have been implicated in the pathogenesis of AVN. Typically, it is a secondary event triggered by a familial thrombophilia, hypercholesterolemia, allograft organ rejection, other disorders (eg, infection, malignancy), or pregnancy.
o Healing process:
§ Necrotic bone triggers a process of repair that includes osteoclasts, osteoblasts, histiocytes, and vascular elements. Osteoblasts build new bone on top of the dead bone, leading to a thick scar that prevents revascularization of the necrotic bone, with resultant abnormal joint remodeling and joint dysfunction.
o Primary cell death:
§ Osteocyte death without other features of AVN has been seen in renal transplant patients, as well as in patients receiving steroids and those who consume significant amounts of alcohol.
o Mechanical stress:
§ Animal studies have shown an association between increased weight bearing and an increased incidence of AVN of the femoral head.
o Infarctions are divided into 2 types according to the amount of blood present:
o White infarctions (anemic infarcts) affect solid organs such as the spleen and kidneys wherein the solidity of the tissue substantially limits the amount of nutrients (blood/oxygen/glucose/fuel) that can flow into the area of ischemic necrosis. Similar occlusion to blood flow and consequent necrosis can occur as a result of severe vasoconstriction as illustrated in severe Raynaud's phenomenon that can lead to irreversible gangrene.
o Red infarctions (hemorrhagic infarcts), generally affect the lungs or other loose organs (testis, ovary, small intestines). The occlusion consists more of red blood cells and fibrin strands. Characteristics of red infarcts include: occlusion of a vein; loose tissues that allow blood to collect in the infarcted zone; tissues with a dual circulatory system (lung, small intestines); tissues previously congested from sluggish venous outflow; and reperfusion (injury)[3] of previously ischemic tissue that is associated with reperfusion-related diseases[4] such as - Myocardial infarction, stroke (cerebral infarction), shock-resuscitation, replantation surgery, frostbite, burns and organ transplantation.
Osteoarthritis
· Consequences of OA
Osteoporosis
· Why is it important to discuss OP?
o Preventable
o Common
o Ageing population
· Etyology of OP
· Screening of OP
o T-score
o Z-score
§ Cut variables of race, sex, age
§ More reliable
· What happens to the IVD in OP?
o Nuclear pulposis
§ May become herniated out
o Annulus fibrosis
§ As people age, the annulus becomes thin and slit-opening will appear, frail and break
Tumours of the bone
osteochondroma
o most common tumour!
o Exostoses - bony core, cartilaginous cap!
o Can occur anywhere.
o Lilac coloured
o When cartilage is >1cm, may become chondrosarcoma (rare but possible)
Giant cell tumour - osteoclastoma
o Osteoclast + spindle cells
o Behavior of GCT is determined by ratio of osteoclast and spindle cells
o Usually epiphyseal
o It it benign
o Fusiform dilatation of lower end of epiphyses
o Eggshell crackling on palpation. (cystic spaces filled with haemorrhage)
o Eccentric expansile tumour
Paget’s disease
· Hats don’t fit!
· Loss of bone -> loss+formation -> formation
· Osteoid Osteoma
Osteoblastoma
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