BLD 204

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Author:
branch10
ID:
148711
Filename:
BLD 204
Updated:
2012-04-19 23:05:30
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BLD 204
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Cell, Tissue, Disease
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  1. factors that cause fluid to leave the vasculature
    • increased vasculature pressure
    • increased proteins/colloids in extravascular space
  2. factors that cause the fluids to stay in the vasculature
    • tissue tension in the intertitial tissue
    • selective vascular permeability
    • intravascular presence of albumin (protein that has largesr impact on fluid movement)
  3. compare and contrast exudates to trasudate and their cause
    • exudate: fluid leaves because of increased vascular permeability (ie. inflammation) --> proteins leave with fluid --> macromolecules (WBC)
    • trasudate: fluid leaves because of hydrostatic pressure -->proteins do not leave vasculature --> no macromolecules (WBC)
  4. three main factors causing edema
    • high/increased intracapillary pressure
    • low plasma oncotic pressure (low protien concentration in vessel)
    • retention of salt and water
  5. cardiac edema
    • fluids accumulate throughout the body due to cardiac failure, edema seen mostly in legs and ankles (gravity), poor pumping by heart leads to decrease in capillary pressure and reduction of renal perfusion which leads to the kidneys retaining salt and water
    • redistribution and general retention of fluid
    • distribution has a lot to do with gravity
    • excess retention by renal tubules--> Na+ and water
  6. renal edema/nephritic
    • swelling of glomeruli of kidneys, edema is a transudate implying no change in vessel permeability. Usually sodium excreted in urine to decrease edema, but this responce is hulted in this disorder
    • fall in flomeralar filtration rate, tubular reabsorption of sodium. Results in increasing extracellular fluid volume and followed by excretion of sodium in the urine. The acute golmerulonephritis has the characteristics of transudate, indicating there is no significant change in permeability
  7. renal edema/nephrotic
    • albumin leaves vessel faster than the liver can produce it leading to decrease in plasma oncotic pressure, edema is exudate (heavy proteinuria --> lots of protien in the urine)
    • heavy proteinuria in excess of ability of liver to synthesize albumin (leasing to hypoalbinaema)
    • losing albumin faster than liver can produce
    • decrease plasma oncotic pressure
  8. nutritional edema
    • results of prolonged starvation
    • loss of subcutaneous fat (so subcutaneous connective tissue is of much looser texture than normal and there is an associated decline in the tissue tention within it)
    • poor nutrition means inadequate protien concentration
  9. chronic liver edema
    • appears as ascites --> free fluid in peritoneal cavity
    • involves factor such as increased intracapillary pressure
    • decreased plasma albumin (leading to a lowered oncotic pressure)
    • decreased oncotic pressure
    • increased formation of hapetic lymphatics
    • Na+ retention in cirrhosis
  10. pulmonary edema
    • balance of intracapillary hydrostatic pressure versus capillary permeability
    • increasing either leads to edema
  11. three types of disturbances in fluid distribution seen in local edema
    • increased hydrostatic pressure within microcirculation (ex. due to thrombosis)
    • increased local vascular permeability (ex. acute inflammation and type I hypersensitivity)
    • lymphedema (obstruction of normal lymph flow, can be caused by tumors, surgery, inflammation)
  12. differentiate between and give examples of both exogenous and endogenous pigments
    • exogenous: come from the environment exposure by inhalation, ingestion, or contact
    • endogenous: synthesized from the body
  13. list three sorces of pigment for endogenous pigmentation
    • melanin
    • hemoglobin
    • fat
  14. generalized hyperpigmentation
    • abnormalities in melanin pigmentation
    • addison's disease
    • acromegaly (too much growth hormone)
    • chronic arsenic poisoning
    • hemochromatosis
    • high levels of iron in body (too much absorption)
    • administration of the drug chlorpromazine
    • large dose of estrogen
  15. focal hyperpigmentation
    • freckles
    • cafe au lait spots (increased number of melanocytes-found in 2 disorders--> neurofibromatosis, Albright's syndrome)
    • peutz- jeghers syndrome (autosomal dominate)
    • lentigenosis (characterized by increase in number of melanocytes)
    • melanocyte tumors (mostly benign)
  16. generalized hypopigmentation
    albinism --> deficiency of tyrosinase, no melanocytes
  17. focal hypopigmentation
    vitiligo --> spots of depigmentation due to absence of melanocytes
  18. state how iron can be involved in pigmentation and the possible outcomes
    excess iron initially stored as ferritin, with further accumulation of intracellular iron, ferritin molecules aggregate to produce a crystallin yellow-brown pigment hemosiderin). Localized deposition of hemosiderin is due to hemorrhage at site of pigmentation, commonly seen in relation to bruises. Excess hemosiderin is deposited in parenchyma and reticuloendothelial system. Accumulation of excess iron can be due to increased absorption of iron, decreased excretion, impaired utilization, excess breakdown of hemoglobin with release of iron.
  19. discuss how fats can be involved in pigmentation
    lipofuscins are yellowish-brown granular pigments that deposit in the parenchymal cells in the liver and heart of older people. As cells age, there are many vacuoles containing cell debris and the lipid portion of the membranes tend to resist lysosomal digestion and undergo auto-oxidation to form compunds with a yellowish color.
  20. discuss how bilirubin breakdown products are involved in pigmentation
    bilirubin is a byproduct of the normal breakdown of old red blood cells (an orange yellow pigment in the bile that forms as a product of Hg). Yellow pigment in blood, which gives a yellow coloring to the skin (jaundice).
  21. dystrophic calcification
    serum calcium levels normal, calcium salts deposited in dead/degenerative tissues. Seen in caseous necrosis, fat necrosis, thrombosis, hematomas (bruise), atherosclerotic plaque, inflammatory granulation tissue, various cysts, degenerative tumors
  22. metastatic calcification
    increased serum calcium levels seen with bone resorption (osteoclasts break down bone) or from excess calcium absorption from gut. Calcium deposits in kidney, lung, stomach, coronary arteries, cornea. Commonly caused by primary hyperparathyroidism (benign neoplasm), excessive calcium absortpion from diet, hypophosphatasia (error in calcium metabolism), destructive bone lesion, renal tubular acidosis.

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