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140 Cards in this Set

  • Front
  • Back
iron deficient enemia in males means
CA of GI until proven otherwise
prognostic indicator - colorectal CA
extent of tumour at diagnosis
detection, testing
digital-rectal, fecal test, enema, CT, colonoscopy, biopsy
4 chars bone disease
lesion, cavity-lytic, unusual calcium deposition, zonal or sclerotic bone, neoplasms
type I bone lesion
geographic - central - slow growth
Type II bone lesion
‘moth eaten’ intermediate growth
Type III bone lesion
permeative pattern, rapid growth
malignant bone lesions
usually type III
benign lesions
usually type I
bone structure (normal)
calcium hydroxapatite in collagen scaffold with osteocalcin and osteonectin
2 bone forming proteins
osteocalcin, osteonectin
% of bone types
70 compact, 30 cancellous
term - mature bone
lamellar (has parallel strand orientation)
main unit of bone
osteon or haversian system
cellular cycle of bone
osteoblasts -osteocytes (imbedded in bone), - osteoclasts, absorb bone
bone growth and shape change due to
modelling (formation, resorption at independent sites
bone growth type,new bone laid on existing periosteum
pattern of bone remodelling - cortical
osteoclasts lead - cutting cone, osteoblasts follow - closing cone
location of bone modelling - trabecular bone
howships lacunae
bone resp. for structure, protection
bone resp. for calcium homeostasis
complications of fracture healing
non-union, osteonecrosis
causes of non-union
other tissue trapped at site, periosteum lost
most common occur of patho fracture
lytic lesions, metastatic tumours
bone healing - three phases
inflammation (fracture callus), reparative(mineralization of callus), remodelling (endochondral bone forms, normal shape returns
stress fracture
partial break - pain (worse w/activity) caused by excessive imbal. bone remodelling
bone destroying organisms within bone
osteomyelitis survives how
relies on bone structure - cavity and blood supply
osteomyelitis agents and transport mech
S.aureus, H.Influenzae, Salmonella, via blood or joints
area of dead bone and infection - osteomyelitis
area of fracture, reactive bone
treatment osteomyelitis
chronic antibiotics
excessive remodelling of specific bones, in elderly, genetic disorder
pagets disease
3 phases pagets
lytic (hot phase, bone resorption), mixed phase - bone formation, sclerotic (cold) phase
diagnosis pagets
abnormal lamellar bone - woven look, osteoclasts, lots of nuclei
pagets complications
brittle bone, nerve impingement
bone cysts
usually evident at metaphyseal plate, proximal humerus, femur, calcaneus
bone cyst characteristics
fluid filled cavity, with histiocytes, osteoclasts
subperiosteal bone lesion with blood filled spaces
aneurismal bone cyst, usually post-trauma. multiple levels of fluid within cyst.
giant cell tumour
benign with multinucleated giant cells, fibrous stroma
location, population with giant cell tumour
women, distal femur, prox. tibia, nr. growth plate
unusual abt giant cell tumour
invasive, bone necrosis, can metastasis
giant cell reparative granuloma locations
jaw, hands, feet
giant cell rep.granuloma char
giant cells and stroma, HIGHLY vascular, zonal pattern, reactive fibrosis
failure of replacement joints
septic or aseptic. histocytic reaction at interface membrane with mechanical wear. Cells react with breakdown of mech. replacement parts and materials
most com. arthritis cause of disability
osteoarth of knee
osteoarthritis description
chronic, noninflam. joint disease, loss of articular cart., synovial changes, subchondral bony formation, can heal
contrib. factors - osteoarthritis
age, weight(knee), genetic (esp. hands)
obvious bone changes, OA
disappearance of joint space, osteophytes at margins
term for cartilage disappearing
earliest stage osteo
disruption in superficial cartilage layer
2nd stage osteo
fibrillation (cracks) in cartilage, followed by clumping of chondrocytes for repair
chg to bone surface with osteo
focal necrosis of osteocytes
synovial leak into underlying bone
subchondral bone cyst
bone fragments in osteoarthritis
necrosis and metaplasia of tips, become “loose bodies”
define rheumatoid arthritis
chronic inflammatory arthritis, primarily effecting synovial joints, autoimmune disease
effected structures - rheum arth
women 2-3x more than men, all joints, esp hands
key feature of rheum arth
pannus formation- granulation tissue, cytokines, necrosis, bone and cartilage destroyed
gout - definition
deposition of urate crystals in joints and tissues
precipitates gout attack
usually large meal or alcohol
gout usually effects
big toe MTP joint
why gout
hyperuricemia - purine metabolism error
deposit of ureic acid crystals and fibrous conn. tiss.
locations tophi
ear, achilles tendon
also effected by urea crystal deposit
most comm. cause of arthritis
define pseudogout
chondrocalcinosis - inflamm react. in cartilage caused by CPPD deposition
calcium pyrophosphate dihydrate
pseudogout usually effects
knee, hip, discs
pigmented villonodular tenosynovitis
PVNS def
synovial proliferative disorder - kids especially - neoplasia in knees
osteomyelitis usually caused by
pyogenic organisms
organisms causing osteomyelitis - in what groups
staphlococcus aureus (adults), haemophilus influenze (kids), salmonella - sickle cell patients
osteosarcoma produces and percentage
osteoid matrix 20percent of tumours,
conventional osteosarcoma effects
mainly men, around knee. Have TP53 and or Rb gene mutation
pathology osteosarcoma
metaphysis of long bone, areas of hemorrhage, necrosis: destroys cortex.
mechanism osteosarcoma
osteoblasts form osteoid - bone matrix
osteosarcoma behaviour
aggressive, hematogenous spread, usually already metastasis at diagnosis
main joint type
diarthroidal - articular cartilage, synovium, capsule, stabilized by ligaments
main cartilage type in joints
hyaline - type II collagen
articular cartilage nutrition
no vessels, no nerves, can’t perceive injury, nutrition is via synovial fluid, during movement
2 types of osteoarthritis
primary - no obvious predisposing factors, secondary - dmgd joint
imbalance causing osteoarthritis
decreased tensile strength, degenerative chgs overwhelm reparative
nodes on fingers in osteoarthritis
heberdens nodes
biochemical changes - osteoarth
more water, less proteoglycans (nutrients), less collagen synthesis - collagen breakdown incr, apoptosis, reduction in functional chondrocytes.
4 endocrine functions
homeostasis, survival, emotion, metabolism
2 thyroid hormones
T3 and T4
what are T3 and T4
tri-iodothyronine, tetra-iodothyronine
prod. of thyroid hormones requires
dietary source of iodine
thyroid purpose
metabolic pacemaker - controls rate of food conversion to energy
define goiter
enlargement of thyroid
hypothyroidism - cause
TSH reduced, iodine deficiency, T3/T4 synth. impaired
hashimotos thyroidosis
AUTOIMMUNE, mostly effects women, HYPOthyroid
cause of hashimotos
autoagressive lymphocytes attack thyroid
4 causes hyperthyroidism
adenoma, toxic goiter, thyroiditis, graves disease
graves disease
autoimmune, thyrotoxicosis
underlying mechs - graves disease
IgG antibody, is not TSH but stimulates thyroid
signs of hyperthyroidism
nervousness, restlessness, palpitations, fatigue, weakness, diarrhea, weight loss, heat intolerance
graves disease treatment
radioactivity - destroy gland, give HRT
parathyroid purpose
regulate circulating blood calcium
cause of hyperparathyroid
mechanisms hyperparathyroid
CA from bone, blood CA levels rise, phosphate levels decr
symptoms hyperparathyroidism
painful urination, hematuria, GI sounds, kidney and urine stones
dental implications - hyperparathyroid
lamina dura around teeth disappear
diabetes def
chronic persistent elevation of blood sugar
diabetes effects
chronic disorder of carb, fat, and protein metabolism
diabetes feature
impaired glucose use, hyperglycemia
mechanism of diabetes
destruction of insulin producing cells
poss.mech. for type I diabetes
CMV (cytomegalovirus), mumps?
insulin mechanism
promotes glucose transport across cell memb of musc, fat, fibroblasts
type I diabetes
childhood onset autoimmune
Bloor of type I diabetes shows
serum IgG antibody to beta cells
main reason decrease insulin in type II
fewer insulin receptors
Main reason typeI diabetes
pancreas can’t produce insulin
signs diabetes
polyuria, polydipsia, polyphagia
polyuria mechanism, type II
high glucose (diuretic) levels in urine, results in forced fluid loss
mech. tissue reactions, typeII
musc. weakness, weight loss, fatigue, glucose depleted, not replaced
iron overload
iron overload consequence
can cause diabetes
why musc. weakness in diabetes
glycogen used up, no energy
diabetic chgs in musc
musc. protein breakdown, amino acids to liver
musc. amino acids in liver undergo
fat degradation yields
3 ways acids disposed of
utilization by skin, musc. filtration through kidney (loss of electrolytes), expiration via lung buffer system
diabetic vessel problems
atherosclerosis, peripheral circ. probls, increased risk MI
diabetic kidney probs
sclerosis, glomerulosclerosis, renal failure
diabetic eye problems
retinopathy, cataracts(blindness)
cause of diabetic eye problems
retinal exudates, edema, hemorrhage
treatments of diabetes
cyclosporine, pancreas transplant, blood sug. monitor, insulin pump, DIET.
erythropoeisis where
what cytokines req. for erythropoeisis
RBC production influences
hemoglobin level, O2 content and affinity of RBS
RBC lifespan
# RBCs per ml per kilo
2000 per ml, 300 x 10 to the 9 per Kilo
percent RBCs destroyed daily
about 1 percent
Required for RBC production
erythropoetin, marrow stroma, iron, VitB12, Folate
where are iron, B12, folate producted
renal peritubular interstitium
finction of iron folate and B12 on RBCs
proliferation and maturation
anemia deficiency
decreased hemoglobin
2 types anemia (functional)
kinetic or nutritional