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Hypoxia - literally means a "deficiency in oxygen."
- Blood donation
- Hemorrhage - bleeding
smokers.
Examples are:
- Carbon monoxide
- Cyanide poisoning
- Certain narcotics
- Chewing tobacco
blocking of blood vessels). The oxygen supplied to the region of the body is
Examples are:
- cerebral ischemia
- cold temperatures
Stagnant hypoxia usually experienced when sitting for hours in a boring class.
7. Mixed form of hypoxia develops when several systems responsible
for O2 supply to cells and tissues are affected e.g. at traumatic shock
develop simultaneously:
- Circulatory hypoxia
- Respiratory hypoxia
- Hemic hypoxia (if bleeding is accompanied).
Respiratory
Circulatory
Hypoxic Tissue
Overload
Hemic
5. The body produces more of a particular enzyme that causes the release of
oxygen from hemoglobin to the body tissues.
Immediate reactions of adaptation at acute Hypoxia
Acute Hypoxia
R
Passage of concentrated
Increase in Volume of Systolic ejection
blood from depot organs e
and Heart rate
and bone marrow Activation of tissue a
respiration and c
Increase in
glycolysis, t
Dilatation of increases
number of capillaries or
Coronary and brain processes of
i
Increase in
density in tissues
supplying blood oxidation o
dissociation of
vessels
oxy-hemoglobin
and n
phosphorilation
The depth of
respiration
Increases volume
Centralization of R
of alveolar
ventilation and O2 blood supply e
Increases efficacy
delivery of biological
s
Increases volume of systolic oxidation u
Increases oxygen
ejection, cardiac output, carrying capacity of the
l
Increases tissues
oxygenation
arterial Pressure, tissue blood t
perfusion
Compensatory reactions at c h r o n i c
Hypoxia
Chronic Hypoxia is a pathological condition in which the body as a whole (generalized hypoxia) or region of the
body (tissue hypoxia) is deprived of adequate oxygen supply.
R
Quantitative
Increase in Increase in e
increase in
pulmonary Myocardial capillary density in a
mitochondria, Activation of
their crists, and
capillarity hypertrophy, tissues, increase in c
density increase in number of erythropoesis, tissue blood supply
ferments, erythrocytosis, t
mitochondria in
facilitation of
cardiomyocytes acceleration of i
oxydation / oxyhemoglobin o
phosphorilation dissociation
n
s
E
Increased volume f
of systolic ejection
Increased
Increased tissue f
Increased oxygenation of Increased oxygen
efficacy of blood in lungs carrying capacity of
perfusion, e
oxigenation and
biological the blood c
nutrition
oxidation t
s
Cellular Injury and
Adaptation
THE CELL AND ITS FUNCTIONAL ORGANIZATION
Composition:
- Mitochondria,
itochondria which supply the energy needs of the cell.
- Ribosomes,
ibosomes which synthesize proteins and other materials needed for cell function.
- lysosomes,
ysosomes which function as the cells digestive system
- Golgi bodies modify materials synthesized in the ER and package them into secretory granules for
transport within the cell or for export from the cell.
- Microtubules are slender, stiff tubular structures that influence cell shape, provide a means of
moving organelles through the cytoplasm, and effect movement of the cilia and of chromosomes during
cell division.
The cell membrane encloses the cell and provides for intracellular and intercellular communication, transport of
materials into and out of the cell, and maintenance of the electrical activities that power cell.
When confronted with stresses that affect its normal structure and function,
the cell undergoes ADAPTIVE changes that permit survival and
maintenance of function.
Adaptation Injury
Reversible Irreversible
changes changes
Keep in mind that any Reversible changes can become irreversible when taken
to the extreme
A normal cell and the changes in reversible and irreversible cell injury (necrosis).
Injurious Stimulus
Time scale of reversible and irreversible cell injury.
The relationship between normal, adapted, reversibly injured, and dead myocardial cells.
The cellular Adaptation depicted here is Hypertrophy, the type of Reversible injury is Ischemia and the
Adaptive cellular responses
- Atrophy
- Hypertrophy
- Hyperplasia
- Metaplasia
- Dysplasia
1. Hypoxia
2. Infection
3. Immunologic reaction
4. Congenital disorders
5. Chemical injury
ER, Endoplasmic
reticulum.
2. Infections Viruses, Bacteria, Parasites, and Fungi (and probably prions)
Mechanism of injury:
Production of toxins
- Cytogenetic disorders
Pollution
Burns
Frostbite
Radiation
Pressure changes
7. Nutritional or Vitamin imbalance
Or
Hypervitaminosis
Cellular changes during injury
1. General
Cellular responses to injury:
- Adaptation
- Reversible injury
(necrosis/apoptosis)
DNA
Cell membranes
Protein synthesis
Generation of free radicals
Free Radical Scavengers
O 2
Superoxide dismutase
Catalase
H2O2 H 2O
Fenton
Reaction
Fe
2+/3+
OH- Vitamin E
Vitamin C
-caroten
Important mechanism of cell injury
2. ATP depletion
4. Mitochondrial dysfunction
- Decreased oxidative phosphorylation
- Formation of mitochondrial permeability transition (MPT) channels
5. Influx of Calcium
- Second messenger
- Activates a wide spectrum of enzymes
2. Denervation
6. Aging
Atrophy
Atrophy
A, Normal brain of a young adult.
B, Atrophy of the brain in an 82-year-old male with atherosclerotic disease. Atrophy of the brain is
due to aging and reduced blood supply. Note that loss of brain substance narrows the gyri and
widens the sulci. The meninges have been stripped from the right half of each specimen to reveal the
surface of the brain.
Hypertrophy
long-standing hypertension.
(From Rubin E., Farber J.L. [1999]. Pathology [3rd ed., p. 9]. Philadelphia: Lippincott- Raven)
Hyperplasia
It occurs in tissues with cells that are capable of mitotic division, such as the:
- Epidermis
- Intestinal epithelium
- Glandular tissue.
Nerve cells and Skeletal and Cardiac muscle DO NOT divide and
It has been suggested that the replacement cell is better able to tolerate
the environmental stress.
Fatty liver
A - The possible mechanisms leading to accumulation of triglycerides in fatty liver. Defects in any of the steps of uptake,
catabolism, or secretion can lead to lipid accumulation.
B - High-power detail of fatty change of the liver. In most cells the well-preserved nucleus is squeezed into the displaced
rim of cytoplasm about the fat vacuole.
(B, Courtesy of Dr. James Crawford, Department of Pathology, University of Florida School of Medicine, Gainesville,
Florida.)
Accumulation of intracellular lipofuscin.
A photomicrograph of the liver of an 80-year-old man shows golden
cytoplasmic granules, which represent lysosomal storage of lipofuscin.
(From Rubin E., Farber J.L. [1999]. Pathology [3rd ed., p. 13]. Philadelphia: Lippincott-Raven)
Hemosiderin granules in liver cells.
A - H&E section showing golden-brown, finely granular pigment.
B - Prussian blue reaction, specific for iron.
Lipofuscin granules in a
cardiac myocyte.
A - Light microscopy (deposits
indicated by arrows).
B - Electron microscopy. Note
the perinuclear, intralysosomal
location.
Cell Death
Necrotic cell death is a pathologic form of cell death resulting from cell injury.
- DNA fragmentation
2. Activation of Caspases
3. Activation of endo-nucleases
5. DNA fragmentation
8. Cell shrinking
Necrosis is death due to unexpected and accidental cell damage. A number of toxic chemical
or physical events can cause necrosis:
- Toxins
- Radiation
- Heat
- Trauma
As necrotic cells begin to die, they swell holes appear in the plasma membrane and
intracellular materials spill out into the surrounding environment.
Necrosis
As the cell dies, its ability to maintain the integrity of the plasma membrane and to pump
ions is lost.
Ca2+ acts as an allosteric effector of many proteins, drastically altering their activity.
Unregulated Ca2+ induces the generation of toxic chemicals and activates enzymes that lead
to the degradation of cellular molecules.
As the cell is disassembled, various breakdown products are produced and released into the
neighborhood.
Among these are derivatives of membrane phospholipids, such as arachidonic acid, which is a
free fatty acid or FFA.
The FFAs generated by damaged and dying cells are themselves substrates for enzymes, in
particular the cyclooxygenases.
These enzymes transform FFAs into prostaglandins and other molecules, known collectively
as eicosanoids, which mediate inflammatory responses.
and
Apoptosis (right).
Necrosis Apoptosis