Porth's Essentials of Pathophysiology, 4e - page 67

C h a p t e r 2
Cellular Responses to Stress, Injury, and Aging
47
R E V I EW E X E R C I S E S
1.
A 30-year-old man sustained a fracture of his leg
2 months ago. The leg has been encased in a cast
and he has just had the cast removed. He is amazed
at the degree to which the muscles in his leg have
shrunk.
A.
Explain.
2.
A 45-year-old woman has been receiving radiation
therapy for breast cancer.
A.
Explain the effects of ionizing radiation in
eradicating the tumor cells.
B.
Why is the radiation treatment given in small
divided, or fractionated, doses rather than as a
single large dose?
C.
Partway through the treatment schedule, the
woman notices that her skin over the irradiated
area has become reddened and irritated. What is
the reason for this?
and free radicals, promotion of cell hypoxia,
or impaired regulation of intracellular calcium
levels. Free radicals are an important cause of cell
injury in hypoxia and after exposure to radiation
and certain chemical agents. Lack of oxygen,
which underlies the pathogenesis of cell injury in
hypoxia and ischemic, can result from inadequate
oxygen in the air, cardiopulmonary disease,
cardiorespiratory disease, anemia, or the inability
of the cells to use oxygen. Increased intracellular
calcium activates a number of enzymes with
potentially damaging effects.
■■
Injurious agents may produce sublethal and
reversible cellular damage or may lead to
irreversible cell injury and death. Cell death can
involve two mechanisms: apoptosis or necrosis.
Apoptosis involves controlled cell destruction
and is the means by which the body removes and
replaces cells that have been produced in excess,
developed improperly, have genetic damage, or
are worn out. Necrosis refers to cell death that is
characterized by cell swelling, rupture of the cell
membrane, and inflammation.
■■
A number of body functions decline with age,
including muscle strength, cardiac reserve,
vital capacity, nerve conduction time, and
glomerular filtration rate. At the cellular level,
oxidative phosphorylation by the mitochondria is
reduced, as is the synthesis of nucleic acids and
transcription factors, cell receptors, and structural
and enzymatic proteins.
3.
People who have had a heart attack may experience
additional damage once blood flow has been restored,
a phenomenon referred to as
reperfusion injury.
A.
What is the proposed mechanism underlying
reperfusion injury?
B.
What factors might influence this mechanism?
4.
Every day blood cells in our body become senescent
and die without producing signs of inflammation,
yet massive injury or destruction of tissue, such
as occurs with a heart attack, produces significant
signs of inflammation.
A.
Explain.
R E F E R E N C E S
1. Strayer DS, Rubin E. Cell adaptation, cell injury, and cell death.
In: Rubin R, Strayer CS, eds.
Rubin’s Pathology: Clinicopathologic
Foundations of Medicine
. 6th ed. Philadelphia, PA: Wolters
Kluwer Health/Lippincott Williams & Wilkins; 2012:1–46.
2. Kumar V, Abbas AK, Fauusto N, et al.
Robbins Basic Pathology
.
8th ed. Philadelphia, PA: Saunders Elsevier; 2010:3–42.
3. Heszele MFC, Price SR. Insulin-like growth factor 1: the yin and
yang of muscle atrophy.
Endocrinology.
2004;145:4803–4805.
4. Heineke J, Molkentin JD. Regulation of cardiac hypertrophy
by intracellular signalling pathways.
Nat Rev Mol Cell Biol.
2006;7:589–600.
5. Hunter JJ, Chien KR. Signaling pathways in cardiac hypertrophy
and failure.
N Engl J Med.
1999;341:1276–1283.
6. Anastassios C, Koumbourlis MD. Electrical injuries.
Crit Care
Med.
2002;30(suppl):S424–S430.
7. Strayer DS, Rubin E. Environmental and nutritional
pathology. In: Rubin R, Strayer CS, eds.
Rubin’s Pathology:
Clinicopathologic Foundations of Medicine
. 6th ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2012:293–328.
8. Centers for Disease Control and Prevention.
Preventing Lead
Poisoning in Young Children: A Statement by the Centers for
Disease Control and Prevention
. Atlanta, GA: U.S. Department
of Health and Human Services, Public Health Service; 2005.
9. Warniment C, Tsang K, Galazka SK. Lead poisoning in children.
Am Fam Physician.
2010;81(6):751–760.
10. Chandran L, Cataldo R. Lead poisoning: basics and new
substances.
Pediatr Rev.
2010;31(10):399–405.
11. Canfield RL, Henderson CR Jr, Cory-Slechta DA, et al.
Intellectual impairment in children with blood lead concentrations
below 10
μ
g per deciliter.
N Engl J Med.
2003;348:1517–1526.
12. Clarkson TW, Magos L, Myers GJ. The toxicity of mercury—
Current exposures and clinical manifestations.
N Engl J Med.
2003;349:1731–1737.
13. McCord JM. The evolution of free radicals and oxidative stress.
Am J Med.
2000;108:652–659.
14. Poljsak B. Strategies for reducing or preventing the generation of
oxidative stress.
Oxid Med Cell Longev.
2011(H):1–15.
15. Chuyanyu CL, Jackson RM. Reactive species mechanisms of
cellular hypoxia-reoxygenation injury.
Am J Physiol Cell Physiol.
2002;282:C227–C241.
16. Lagouge M, Larsson NG. The role of mitochondrial DNA
mutations and free radicals in disease and ageing.
J Intern Med.
2013;273:529–543.
17. Finkel T. Oxidant signals and oxidative stress.
Curr Opin Cell
Biol.
2003;15:247–254.
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