Cell Injury Adaptation and Death Flashcards

1
Q

Incidence - define and how to calculate

A

number of new cases occurring in a given population within a given time period- usually 1 year.

calculate- incidence of down syndrome in the US is 1 in 690 births (1/690 x 100 = 0.14%)

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2
Q

Prevalence- define and calculate

A

number of old and new cases in a given time period.

prevalence of down syndrome in the US is 400,000 for a population of 314 million.
ex. 400,000/314,000,000 x 100 = 0.13%

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3
Q

define pathogenesis-

A

involves the sequence of events that occurs between the stimulus event/s and the manifestations of the disease

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4
Q

clinical manifestations-

A

includes symptoms, results of physical and mental assessment, and results of diagnostic studies in general.

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5
Q

primary prevention vs. secondary and tertiary prevention-

A

primary prevention- is to prevent the initial occurrence of a disorder.
secondary- is to reduce the impact of a disease that has already occurred.
tertiary- is to slow down the progression of a disease.

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6
Q

ATP depletion-

A

causes 1. Na/K+ ATPase pump fails. Sodium and calcium flow inward. Potassium flows out freely. Water follows sodium and cell swells.
2. anaerobic respiration occurs-> increase in prod of lactic acid-> lower pH-> pyknosis, karyorrhexis, and karyolysis. along with rupture of lysosomes and disruption of cell membrane-> increased calcium influx and activation of proteases, endonucleases, and phospholipase that proceed to destroy the cell and contents

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7
Q

oxygen and oxygen derived free radicals-

A

lipid peroxidation- free radicals are unstable and avidly combine with phospholipid bilayer. which leads to dissolution of the membrane.

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8
Q

intracellular calcium and loss of ca steady state

A

causes 1. increased mitochondrial permeability 2. activation of multiple cellular enzymes

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9
Q

defects in membrane permeability-

A

caused by 1. free radicals and 2. lysis by enzymes or lysis by viruses.

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10
Q

how does the body handle free radicals and ROS?

A

Antioxidants such as vitamin e, C, cysteine, glutathione, albumin, ceruloplasmin, and transferrin.

Enzymes- like catalase, glutathione peroxidase, can modulate the cellular destructive effects of free radicals which are also released in inflammation.

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11
Q

describe the pathophysiological basis of repercussion injury-

A

increased amounts of ROS, Superoxide, and hydrogen peroxide-> membrane damage and mitochondrial calcium overload.

rapid restoration of intracellular pH-> opening of pore in mitochondrial membrane called the mitochondrial permeability transition pore (MPTP) with massive escape of ATP and solutes-> apoptosis.

tx- use of antioxidants, blockage of inflammatory mediators, and inhibition of apoptotic pathways

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