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171 Cards in this Set
- Front
- Back
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Precision:
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The values obtained can be reproduced
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accuracy:
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The extent that the results are around the true value
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SOAP: laboratory studies in diesease
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Subjective, objective, assement, and plan
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Green tube
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heparin
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dark brown tube
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Heprin- whole blood analysis of trace metals
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red tube
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May contain a serum seperator- general biochemistry
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dark blue
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Nothing added - Serum; look at trace mineral
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mauve
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EDTA- anticaogulant- general hematology- preserves cells
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grey
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oxalates anticoagulant- used for blood glucose
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light blue
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citrate -coagulation facotors
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sensitivity equation
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True positive/ true positive + false positive
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specificity equation
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true negative/ false postive + true negtive
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prevalance
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true positive + false negative/ TP+ FP+FN+TN
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Predicative value +
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TP/ TP+ FP
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Predictive value -
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TN/ TN + FN
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Efficiency:
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TP+ TN/ TP+TN+FP+FN
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Definition: prevalance
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The number of diseased patients in a population
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defintion: sensitivity
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The number of patients with disease
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Definition: Specificity
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The number of healthy patients without disease
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Definition Predictive + and _
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+ - the frequency of true results that are true; the frequency of negative results that are negative
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Definition : efficiency
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How well the test works to determine whether or not someone has a disease or not
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What are some inter individual biological variables
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gender, race, age, body size
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What are some intra individual biological variables:
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circadian rythm, mensus, diurenal variation, seasonal, aging
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Four major endocrine glands? action?
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pituitary, thyroid, parathyroid, and adrenal; ductless glands- release hormone into circulation and acts at a distance.
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Location of the pitutary gland?
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indentation of the base of the cranium- sella turica; 2 parts; posterior and anterior- connected to the hypothalmus
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What are the 5 cell types in the anterior pituitary?
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Adenohypophysis: gonadotrophs ( FSH and LH)), Thyrotrophs ( TSH), lactotrophs ( PRL), growth (GH), adenotrophs ( ATCH)
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Site of action: GH
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Live- somatomedien synthesis- growth; and others - increase metabolic regulation
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site of action: Prolactin
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breast- milk production - lactation
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Site of action: FSH
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ovaries - estrogen synthsis and OOgenis ; Testis - spermatogenesis
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Site of action- LH
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Ovary - ovulation; corpeus leutum - progesteron produciton; testis- sysnthesis of testosterone
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Site of action TSH
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follicular cells of the thyroid- synthesis and release of T3 and T4
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Site of action ACTH
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Adrenal Cortex- sysnthesis and release of glucocrticoids
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How is the release of hormones of the anterior pituitary regulated
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+ feed back - cells in the hypothalmic centers; - from the target cells hormone release
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Posterior pituitary: type of cells
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neurohypohysis: secretory cells; release oxytocin and vassopressin. ARE not TROPIC
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Function of oxytocin
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Acts to increase estrogen receptors - utrin contraction adn milk ejection
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Function of vassopressin
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Acts on the collecting ducts: increase in number of aqua porin 2- increase absorption of water
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Thyroid gland: function
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Store ( in colliod) and release T3 and T4
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Types of cells in the tyroid and what they release
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Follicular cells release and store- T3 and T4- metbolism; C- cells - store and release calcitonin- calcium homeostasis
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Anatomy of the parathyroid:
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located behind the thryoid- usually comprised of 4 glands- secrete Parathyroid hormone which helps to regulate calcium serum levels- homeostasis.
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Primary disease:
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caused within the gland
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secondary disease:
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caused by something extrinsic to the gland
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Tertiary diesease
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2nd becomes autonomous - no feedback
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syndrome
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group of symptoms commo to several dieases
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disease
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specific cause of disease
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Lack of stimulating releasing factors can cuase what at target endocrine gland
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Atrophy
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Thryoid: hyposecretion
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Aplasia- no formation fo the gland; atropy- decrease in size; destruction- results in no or little secretion of T3 and T4
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Thyroid- hypersectrions
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Tumor; hyperplasia- results in hyper secretion of T3 and T4
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Over stimulation of thyroid- excess TSH will cause what
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Enlargment of the thyroid - goiter- hypertrophy
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Hyperactive endocrine gland are usually enlarged; what two factors cause enlargement
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hyperplasia or tumor ( benign or malignant)
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Hypofunctionning endocrine gland causes what to happen to the gland
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Atrophy, loss of cells, destruction- tumor, inflammation, or medical removal
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Neoplastic or hyperplastic enlargment of a endocrine gland could present with what other symptoms?
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Enlargment of the pituitary - press on the optic chiasm - visual destruction = bitemporal hemianopsia; bulging of the thryoid - cut of blood flow. Local symptoms are most evident when there is enlargment
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What is multiple endocrine neoplasia
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Men- heriditary syndrome ( MEN1,2,3); MEN1: origin pituitary, parathyroid, and islets in pancrease. MEN 2: origin c cells of thryoid show up in medulla carcinoma; MEN 2B = similar to MEN 2A - also includes- skin leisons, and mucosal nerve turmoes
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What are the 3 common diseases of the pituitary?
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hypofunciton, hyperfuncito, localized mass leison - compression in local area.
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What are some features of hyperfucntion
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All cells may be enlarged(macro) or only some ( micro are enlarged)
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What is the most common hyperfunction pituitary
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increased size of the lactotrophs - prolactinomas
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What is the least common hyperfuntion pituitary
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somatotrophs - and corticotrophs- TSH, LH, FSH - tumors are rare
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Is hypofunctionning of the pituitary common
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No, but is encountered in all age groups
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Hypo secretion of GH
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dwarfism
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Hypo secrecretion of ADV
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diabetes insipudus
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What is Panhypopituitarism in adults:
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Simmonds disease- women will not menstrate; men may become impotent; weakness , cold intolerance and lack of apeptite, hypotension.
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What are some causes of hypopituitarims?
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tumor ( cranial or pituitary); Vasular disease ( ischemia- postpartum, infarction, hypotension, cranial arteritis), trama, infection(meningitis, syphalis), and Iotrogenic ( surgery or irradiation), miscellanous and hypothalmic disorders ( tumor, funcitonal, anorexia, starvation)
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STimulation and suppresion TEst:
What do you do if you suspect hypo functioning? |
stimulation test - water deprevation - ADH, hypoglycemia- insulin
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Stimulation and suppression test: hyper functionning
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you want to depress the function -
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Children- hyposecrition of GH
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Dwarfism
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Alduts- single deficiency
multiple defiency |
nothing- hypotit syndrom
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Excess GH in children and ADults
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Acromegaly in adults; gigantism in children
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Excess Prolactin in wowmen
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Increased secretion of milkyh substance; lack of menstral periods and or irregular
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Excess prolatin in men
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gynocomastia- impotencen, visual field imparied- children- delayed or arrested puberty
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Hypo and hyper sectrions of ADH
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diabetes insipidus - hypo; syndrom inappropriate adh release
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agenisis
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the cell itself is not working
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How do thyroid dieses present
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hypo,hyper funcitonning presence of a mass leison- goiter
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Hyperthyroidism: 3 principles
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1. thyroid overactivity- graves, 2) thyroid destruction- hashimotos thyroiditis
3) ectopic thryoid |
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Casues of low T4- hypothyrodism
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1) loss of thyroid tissue, abnormal organ development, iatorgenic thyroidectomy, Iodine therapy. Goitrous- lack of iodine- decrease in TSH or hypothalmus
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Clinical symptoms of hyperthyroidims
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heat intolerance, increased apeptite, increased weight loss, increased persperation, muscle loss and weakness
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Clinical Sympotoms of hypothyrodism
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cold intolerance, weight gain, generalized weakness, dry and pale skin ( peaches and cream), decrease food intake
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Symptoms and signs of hyper thyroidism
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Restlessnes, hypermotility, nervousness
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symptoms adn signe of hypthyroidsim
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decreased mental alertness, constaption, depressed relfexes
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What is the most common endocrine problem
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thyroid disprders
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betwen men adn women who are most common to develop a thryoid problem?
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Women
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Serum levels of T3, T4 and TSH in primary hypothyroidims
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High TSH, low T$
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Serum levels of T4 and TSH in hyperthyroidsim:
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High T4, low TSH
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Serum levels of T4 and TSH in secondary hypothyroidims
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low T4 and low TSH
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Serum levles of T4 adn Tsh in secondary hyperthyrodism
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High T4 and High TSH
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Goiter is a primary clinical observation in what diease?
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Graves disease - hyperthroidism
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bulging eyes - increased fluid behind the eyes is a clinical feature of what type of thryoid problem
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hyperthyroidism
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Benign or malagnant- which is most common in the thryoid?
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Benign
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Thyroid Carcinoma decribe
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Ocurs in several forms- papillary, collicular, medually and anaplastic; All except meduallary arise in the follicular cell. MOST Common in WOMEN
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Papillary Carcinoma
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Good prognosis: Most common,Low grade malignant, presents as a cold nodule- will spread to lymph nodes later in the disease. Most common in women
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Follicular Carcinoma
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More common in older patients, grows faster, presents as a nodule, still a favroable prognosis
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Medullary carcinoma
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Derived from C cells!!!- produce calcitonin- calcium regulation - groups of neuroendocrin cells arranged in nests- can be inherited can occur with other endocrin tumors - MEN2. Less favroable prognosis
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Anaplastic carcinoma
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Worst, rare tumor, unfavorable prognosis- undifferenciated cells, do not resemble normal thyroid cells.
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Disease of the adrenal gland include
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hyper, hypo functioning, tumor ( functional or non funcitonal)
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Cushing disease.... what type of malfunctionning of the adrenal glands
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hyposecretion
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conns syndrom.... what type of malfunctionning fo the adrenal
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hyperfunctionning
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androgenital syndrom
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enzyme deficiency
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What are the three zones of the adrenal cortex adn what they secrete?
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glomerulosa- aldosterone
fasciculata- gluccorticoids reticularus- gluccotocoids and andriogens |
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Adrenal medulla secretes what ?
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Epinephrine
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are the disease of the zones of the adrenal all the same?
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NO
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What is the function of cortisol
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Released in times of stress; opposite effects of insuline
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What are some cuases of hypercortisolism?
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increases secretion of aTCH from the pituitary; lung carcinoma increase ACth, adrenal carcino
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hyper sectrions of aldosterone are caused by what?
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Tumor; cured surgically but is not easily diagnosised because 2nd aldosterone is common to kidney disease
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Adrenocortical hypofunctions include:
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ACCUTE adrenal insufficiency- infection of the whole body - waterhouse fiderichsen syndrom or chronic adrenal insufficiency - addison- autoimmune disease, tumors or TB
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symptoms of hypofunctions of the adrenal gland
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hypoglycemia, hyper pigmnetation, anorexia, pain in the joints, hypotension
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Sympotoms of hyperfunctions of the adrenal gland
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Cushins- increased cortisol; increased fat deposits in the abdonmin- moon shaped face, thinning of hair and the bufffalo hump
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Adrenal medulla releases what in response to what?
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Epinephrine- stress response input from the sympatheitic nervouse systme- increases heart rate as well it stimulates the release of glucose at times of hypoglycemia
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What are two types of tumors of the adrenal meduall and a urin maker, and common clincal symptom?
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Neuroblastoma- children malignant; pheochromocytoma0 adults, benign mostly
Increase secretion of VMA - vanilylmandelic acid and increased BP |
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location of parathyroid and function
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posterior to the thryoid- 4 pea like sized glands- release a polypeptide that maintains serum calicum and phosphate levele
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hyper function of the parathyroid cuase what most commonly?
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hypercalcemia = problems with osteoporosis, renal calculi, cardiac neurological adn psychiatric sympotoms
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Describe some characteristics of the parathyroid hormone
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large polypeptide- pTH
activated in circulation; 5 min half life role in CA metbolism |
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signs and symptomes of parathyroid problems
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Stones- renal; Bones- painful; groans- abdominal; moans- phsychic, overtones- fatigue
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Disease of the parathyroid include
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hyperparathyroidism hypercalcemia, and hypoparathyroidism- hypocalcemia
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Prevalance of hypercalcemia assocatiated with primary Hyperparathyroidism
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tumor- most common
increased 10 fold most assymptomatic |
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How might primary hyper parathyrodism present
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assymptomatic, hypercalcemia onset- headach weight loss; and renal colic
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What are some metabolic consequences of hyper parathyroidsim
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hypercalcemia; increased GI tract absorption of Ca2+, increased CA2+ loss from bones, activation of Vit D in the GI tract ( increases); increased secretion of phosphate
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Common sympton of primary hyper parathyroidims
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assymptomatic
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What are some other cuases of hypercalcemia
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High bone tunronver, Vit D intoxification, tumor of the parathyroid, renal disorder
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Hypo parathyroidism
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Very rare, present with hypocalcemia- may be due to ianogenic removel or autoimmnue
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Causes of hypocalcemia
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insufficient vit D intake ( malabsorption or renal failure), parathyroid- magnesium deficiency, iatrogenic- massive transfusion, other- accute pancreatitis
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Pancrease composition
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90% acinar cells- secretion 2% islet beta cells; located in the know between teh jejunum and duedenom
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diabetes mellitus
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improper mamnagement of glucose levels
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What are some of the major diseases fo the panrease?
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Type I diabetes, pancreatitis acute and chronic, tumors in teh exocrine and endocrine cells in the pancrease
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What are some internal consequances of hyperglycemia assocaiated with diabetes
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high glucose levles- toxic = can cause atherosclerosis and neuropathies
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What are the primary and secondary causes of diabetes mellitus
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primary: type 1 and 2 diabetes; secondary- pancreatic disease, endocrine release, drug, genetic
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What are some characteristical features of type 1 diabetes
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onset- child hood; caused by a viral infection, onset is fast, rare family history, rare in twins, autoimmune, complete loss of beta cells. require insuline for treatement
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What are some characteristic features of type 2 diabetes:
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onset later in life, correlation to obesity, slow onset, no anitobodies to receptors, normal beta cells, normal serum levels, treatment oral hypoglycemics and insulin
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Complications with diabetes:
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accelerated athersclerosis, stroke , gangrene, Heart attack, infarction, peripheral nerve damage, kidney failue glomerulsclerosis, and retinal damage ( retinopathy and cataracts), Nervous system -cerebrovascular disease
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Between accute and chronic which is a medical emmergency?
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Accute- inflammation- due to alchol, bile stones, infections, truama etc.... Most common Bile stones>alcholol> over eating or drug use>viruses> etc...
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Features and complications of pancreatitis accute
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FAt necrosis, calcifications,a dn hypocalcemia
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Causes of Chronic pancreatitis
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Alchol, trauma, sutemic metabolic or endocrine disease. ONset is slow, uppper abdomen pain that radiates to the back, malabsorption ( enzymes from kidneys), calcificaiton deposits, 2nd diabetes mellitus
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Chronic pancreatitis pathlogy
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fibrosis of the pancreas, atrophy, intraductal stones, iselts of langerhans preserved but in late stage reduce becuase they are filled with firbous tissue
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General characteristics of pancreatic neoplams:
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Solid, usually in exocrine cells, occur in ducts, malginant, and are functionally silent rather than hormonally active
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Adenocarcinomas of the pancreas- features
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4th major cancer in men 5th in women. Smoking increases your risk 3 times, chronic pancreatitis in crease risk2 X; increases with age over 40. prognosis poor
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location of pancreatic carcinomas
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25%-diffuse
5% tail 10% body 60% head |
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Clinical features of carcinoma in pancrease
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weight loss - lack of enzymes for digestion; jaundice- if in head, pain if in tail, metastases common to lympe nodes- diagnosised with endoscopic retrograde
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tumors of the endocrine pancrease ( islet cells)
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insulinoma - insuline releasing tumor- hypoglycemia; gastrinoma- increased secreations of HCL- zollinger-ellison syndrome; glucagoma- increased secretion of glucagon- hyperglycemia
Vipoma- gastric enzyme |
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What are some clinical signs of nephrotic syndrome?
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edema, hyperlipidemia, hypoalbumenia, proteinuria
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What are the three subcatogories of nephrotic syndrome
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1) minimal change- lipoid nephrosis 2) focal segemental glomeruloscelrosis - diabetes 3) membranous neurophathy
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minimal change nephrosis
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most common in children, minial change in glomeruli- fusion of foot processes of podocytes- lipid depostits damage of negative charge barrier- responds to steroid treatment
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What are the three filtration barriers
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1_ endothelial linnin
2_ glomerular basement membrane 3_ podoctes adn slit diagphram |
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Membranous nephropathy
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Neprotic syndrom: increased deposit of immune complexes, non inflammation, immune mediated , thickening of the glomerular basement membrane, proteinuria, 30-40% unresponsive to treatment, 30-40% progress to renal failure- common in adults- 85% time unkown other times infection.
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Features of nephritic syndrom
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edema, hypertension, hematuria, increased creatine levles, proteinuria
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Nephritic syndrom: accute glomeulonephritis
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Caused_ 1-2 weeks after strep throat. Ag-ab complex deposit into the glomerular basement membrane and attrack immune complexes ( macrophages, neutrophils, etc...); there is an increase in cells in the glomeruli - including mesangial cells. Decrease urine outflow; increased water and NA retention: the macula densa cells send signals to release renin- increase water and Na absorption - increased blood pressure. There is loss of albumin- edema, increased proteinuria and hematuria- recovery most recover soon less then 10 % kidney failure- mostly seen in adults
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Nephritic syndrome: Crescentic glomerulonephritis
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Occurs after focal nephrosis of capilliaries in goodpastures syndrome ( lung and renal disease); Ab in the basement membrane cause there to be holes: there is anuria; capillaries are compressed- decreased blood flow - prognosis not good- dialysis
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Diabetis mellitus
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Glomerulos: protein sugar complex deter the basement membrane- inside they irretate the mesangium - secretes collagen. There is a thickened basement memebrane- glomeruloscleoris. Mesangial expansion - Kimmelsteil wilsons disease. Vascular_ arteriols walls thicken, lumen narrows, ischemia and atrophy. Bacterial infection - pyelonephritis- kidney- Proteinuria. this usually takes 10-20 years to develop in a diabetic
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Pyelonehritis
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caused by: ascending infection fron the ureter and bladder (common in women), or hematogenous ( spread of -ve bacteria from GI tract or spesis).
accute pyelonephritis- supprative infection, abcess in kidneys ( pus permeates throughout kidney into renal pelvis), Chronci - evloved from accute results in destruction of kidney, scar tissu, shrinkages - loss of function. |
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Renal cell carcinoma
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85% of cancers, cause unkown
nodules or masses demarcated from normal parenchymal cells, invades through the capsule and into the surrounding tissues, usually obstructs the renal vein, will be yellow in color from lipid deposits. Triad- flank pain, hematuria, and abdominal mass Can diagnosis with CT. Not a good cancer |
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Most common renal carcinoma
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wilms tumor- common in infants
mutation in the WT-1 gene tumor supressor. Mass growa uncontrollably- it presents like a small kidney with immature glomeruli, meschyme and tubles. Usually found on palipiation, very malignant requires surgery and chemo |
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Renal stones: types
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Calcium: most common; improper metabolism of Ca2+ thryroid and parathyroid- or kidney problem; sturvite- largets type of stones; poor converion of urea to ammonia; Uric acid- patients with have gout, Cycstein not very common associated with cystonosis.
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Pathology of kidney stones
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Urinary bladder or renal pelvis; less then 3 mm size except struvite stones, more common in men ages 20-30, sympotoms hematuria and renal colic; bladder stones- chronic infeciton
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Cystitis
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Infection of the urinary bladder:usually caused by ground negatice bacteria. Accute- there is visible congestion, hemorrage somtimes pus- treat with antibiotics. Chronic- hemorrage, ulcers, fibrosis, scarring- resistant to antibiotice ( diabetes, stones, or prostate), common in youger women and older men
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Benign prostatic hypertrophy ( BPH)
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Cause- increase in E/T ratio with age: estrogen potentiates the growth the prostate. while present with soft pliable nodules and hyperplasia. Symptoms- increased frequency of urination, pain while urination (dysuria), increased urgency, chronic cystitis, hydrouretor. Prostate may become trabeculated ( grow into the bladder) and increased in fibromuscular stroma around the prostate.
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What is the most common cause of vaginal bleeding?
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DUB- dysfunctional uterine bleeding- occurs at puberty and again at menopause- no ovulation
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What is the most common benign tumor of uterus?
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Fibroids- leiomyoma- almost always benign. Depends on location of the tumor. Small tumors are assymptomatic, Large tumors mass effect- pressure on the retum and bladder- constapation, menstral irregularities and heaviness in the abdomin
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Endometrial hyperplasia
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Due to excess estrogen present but responds to progesterone: causes anovulatory cycles, polycistic ovulatory dises, and exogenous estrogen. Type of PCO: simple, complex- no atypis and complex with atypis- carcinoma need to remove the uterus does not repsonde to progesteron
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Two types of endometrial carcinomas
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Endometroid- responds to estrogen and there is hyperplasia. Serous carcinoma does not respond to estrogen occurs in atrophic endometrium there is a mutation in the P53 occurs in older women and there is a poor prognosis
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What increases your risk to endometrial carcinomas
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obesity, diabetes, hypertension, age ( 55-60), infertility.
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Achondroplasia
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defect in endochondral ossification - dwarfisim; growth of long bones are retarded not trunk- autosomal dominant
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osteogenesis
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defective bone formation; mutation in the gene coding fro collagen: dominant or recessive- show up with blue sclera, thin skinn and thin enamel
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Osteomylitis
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bacterial infection- staph, TB or mixed flora in drug addicts. metaphysis is the area where the blood supply comes- pain in joints- presure and increased exudate
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sequestra versus involucrum
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S - dead bone
I- new bone formation to protect against infection |
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Osteoporosis
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bone normal but thinned out- big pores. reduction in mass; more prevalent in women. Due to changes in hormones; decreased estrogen, increased thyroig, increased coritsol, diet
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osteomalacia
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Adults- soft bone- demineralization of the organic portion of the bone- due to Vit deficiency and decrease phosphate. In young people rickets. New bone formed without minerals- osteoid. Adults- muscle spasm (tetany) adn fractures; children bow legs
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simple fracture
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one line fracture bone not exposed
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compound fracture
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one line fracture- bone exposed
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comminuted
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multple fracturs bone not exposed
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complete
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fracture right through the bone not exposed
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partial complete
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half way through- green stick
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cause of fracture
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trauma or disease- tumor etc..
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Osteosarcoma
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Most common bone cancer- young people metaphysis- long bones- knees; srugery chemo 5 year survival mimics bone remodelling
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osteoarthritis
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Primary cuases - unknown; 2nd cuased abnormal weight barring on joints. Cracks in the cartilage- bones don't slide smoothly over one another
Wear and tear. Mechanical stress moves down the bones- causing remodelling0 ostephytes- new bone grows like spkies- pain |
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rheumatoid arthritis
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Autoimmune; associated with other systemic features ( fibrosis in the pleural space of the lungs), deformed joints, ulnar drift, immobilization of joints ( destruction of cartilage and bone), increased Ab ( change in blood composition), symmetrical change, increased risk in women
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