2022-09-02T05:32:42+03:00[Europe/Moscow] en true <p>atrophy</p>, <p>hypertrophy</p>, <p>hyperplasia</p>, <p>metaplasia</p>, <p>dysplasia</p>, <p>Adaptive hypertrophy</p>, <p>Compensatory hypertrophy</p>, <p>Dystrophic calcification</p>, <p>Metastatic calcification</p>, <p>Free radicals:</p>, <p>Reactive Oxygen Species (ROS)</p>, <p>Antioxidants</p>, <p>Oxidative Stress</p>, <p>SOD, GSH, Catalase</p>, <p>carotenes (vit A), Tocopherols (vit E), Ascorbate (vit C)</p>, <p>Hypoxia</p>, <p>hypoxia-inducible factors (HIFs), angiogenesis </p>, <p>oxidative metabolism ceases, cellular swelling</p>, <p>Ischemia</p>, <p>Reperfusion</p>, <p>hypercalcemia, increase in free radicals from damaged mitochondria</p>, <p>cellular swelling &amp; steatosis</p>, <p>steatosis</p>, <p>Extrinsic pathway</p>, <p>Intrinsic pathway</p>, <p>Extrinsic apoptosis</p>, <p>Intrinsic apoptosis</p>, <p>Necrosis</p>, <p>Liquefactive necrosis</p>, <p>Coagulative necrosis</p>, <p>Caseous necrosis</p>, <p>Dry gangrene</p>, <p>Wet gangrene</p> flashcards
Ch. 5 & 9 - Patho

Ch. 5 & 9 - Patho

  • atrophy

    decrease in cell size; reduced number and size of organelles

  • hypertrophy

    increase in cell size; common in tissue with limited mitosis (cardiac, skeletal)

  • hyperplasia

    :increase in cell number

    -activation of mitotic division

    -activation of genes controlling cell proliferation

  • metaplasia

    replacement of one fully differentiated adult cell type in a tissue into another adult cell type

  • dysplasia

    :abnormal cell growth/development causing cells to vary in size, shape, and organization

    -potentially reversible

    -strongly implicated as a precursor of cancer

  • Adaptive hypertrophy

    thickening of hollow organ walls due to obstruction/increased resistance (heart)

  • Compensatory hypertrophy

    cell size increases to take over for non-functioning cells (kidney)

  • Dystrophic calcification

    occurs in dead or dying tissue; intracellular or extracellular formation of crystalline calcium phosphate ; caused by components of calcium deposits from dead cells that flow into the circulation

  • Metastatic calcification

    occurs in normal tissue as a result of hypercalcemia:

  • Free radicals:

    highly reactive chemical species with unpaired valence shell electron

  • Reactive Oxygen Species (ROS)

    -normal redox reactions that generate free radicals

    -free radical generation is a physiological response: antimicrobial reaction, role in vascular tone, insulin and VEGF signaling

  • Antioxidants

    molecules that inhibit/prevent ROS reactions

  • Oxidative Stress

    pathophysiological condition that occurs when ROS exceeds the body's ability to neutralize

  • SOD, GSH, Catalase

    What are some enzymes that neutralize free radicals?

  • carotenes (vit A), Tocopherols (vit E), Ascorbate (vit C)

    Non-enzymatic antioxidants:

  • Hypoxia

    deprives cell of oxygen and interrupts oxidative metabolism and the generation of ATP

  • hypoxia-inducible factors (HIFs), angiogenesis

    Release of __ stimulate RBC formation, ATP production in absence of oxygen, and increased ____

  • oxidative metabolism ceases, cellular swelling

    What are some effects of hypoxia?

  • Ischemia

    a condition in which the blood flow (and thus oxygen) is restricted or reduced in a part of the body.

  • Reperfusion

    the action of restoring the flow of blood to an organ or tissue, typically after a heart attack or stroke.

  • hypercalcemia, increase in free radicals from damaged mitochondria

    What are some implications of reperfusion ?

  • cellular swelling & steatosis

    What are the 2 reversible cell injuries?

  • steatosis

    infiltration of liver cells with fat, associated with disturbance of the metabolism by, for example, alcoholism, malnutrition, pregnancy, or drug therapy.

  • Extrinsic pathway

    receptor mediated apoptosis

  • Intrinsic pathway

    mitochondria mediated apoptosis

  • Extrinsic apoptosis

    -initiated by activation of TNF TRAIL

    -form death domain

    -activate caspase cascade

  • Intrinsic apoptosis

    -initiated by ROS, DNA damage, hypoxia, low ATP, and aging

    -activate p53 causing cytochrome c release

    -activation of caspase cascade

  • Necrosis

    death of a body tissue

  • Liquefactive necrosis

    cells die but catalytic enzymes are not destroyed (abscess)

  • Coagulative necrosis

    acidosis develops and denatures enzymatic and structural proteins (hypoxic areas of infarction)

  • Caseous necrosis

    form of coagulation necrosis in which dead cells persist (granulomas)

  • Dry gangrene

    -affected tissue becomes dry and shrinks

    -skin wrinkles

    -color changes to dark brown or black

    -spread is slow

  • Wet gangrene

    -affected area is cold, swollen, and pulseless

    -skin is moist, black, and under tension

    -foul odor is caused by bacterial action

    -spread is rapid