CH 2: Abnormal Cell Bio Flashcards
What are 5 adaptive changes in cells?
Atrophy: Decrease in cell size
* Hypertrophy: Increase in cell size
* Hyperplasia: Increase in cell number
* Metaplasia: Reversible replacement of one mature cell type by another less mature cell type
* Dysplasia: Deranged cellular growth; is not a true cellular adaptation but rather an atypical hyperplasia
What are 5 adaptive changes in cells?
Atrophy: Decrease in cell size
* Hypertrophy: Increase in cell size
* Hyperplasia: Increase in cell number
* Metaplasia: Reversible replacement of one mature cell type by another less mature cell type
* Dysplasia: Deranged cellular growth; is not a true cellular adaptation but rather an atypical hyperplasia
Which of the following
statements is correct
regarding pathologic
hyperplasia?
1. Produces abnormal
proliferation of abnormal
cells.
2. Is an adaptive
mechanism that enables
organ regeneration.
3. Increases cell size.
4. May occur in response to growth factors.
ANS: 4
* Pathologic hyperplasia can occur in response to hormones and growth
factors.
1. Pathologic hyperplasia produces an
abnormal proliferation of normal cells. Dysplasia refers to abnormal
changes in the size, shape, and organization of mature cells.
2. Compensatory hyperplasia enables
organ regeneration and is a normal process. Pathologic hyperplasia is
not normal.
3. Pathologic hyperplasia increases cell number. Hypertrophy is an increase
in the size of cells and, consequently in the size of the affected organ.
Discuss Cellular Injury
Leads to injury of tissues and organs, determining
structural patterns of disease.
Injured cells may recover (reversible injury)
or die (irreversible injury).
Causes cell stress.
Is acute or chronic and reversible or irreversible.
Can involve necrosis, apoptosis, accumulation, or pathologic calcification.
Causes of Cellular Injury?
Lack of oxygen (hypoxia)
* Free radicals
* Toxic chemicals (lead, etoh, CO, drugs)
* Infectious agents
* Physical and mechanical factors
* Immunologic reactions
* Genetic factors
* Nutritional imbalances
* Physical trauma
Biochemical mechanisms
1. Adenosine triphosphate (ATP) depletion
2. Mitochondrial damage
3. Accumulation of oxygen and oxygen-derived free radicals
4. Membrane damage (ATP depletion)
5. Protein folding defects
6. DNA damage defects
7. Calcium level alterations
Cellular injury can lead to cell death by:
* Decreased ATP production
* Failure of active transport mechanisms (sodium-potassium [Na+/K+] pump)
* Cellular swelling
* Detachment of ribosomes from endoplasmic reticulum
* Cessation of protein synthesis
* Mitochondrial swelling from calcium accumulation
* Vacuolation
* Leakage of digestive enzymes from lysosomes; autodigestion of
intracellular structures
* Lysis of the plasma membrane
* Death
A nurse practitioner knows that free radicals may be produced by:
1. protein peroxidation.
2. metabolism of
exogenous chemicals
or drugs.
3. spontaneous decay of
superoxide.
4. vitamins E and C
supplements.
ANS: 2
* The metabolism of certain drugs like carbon
tetrachloride results in breakdown products
that include free radicals.
* 1. Lipid peroxidation is a response to free
radicals whereby unsaturated fatty acid
molecules are destroyed. Free radicals are
produced when alterations of proteins cause fragmentation of polypeptide
chains.
* 3. Superoxide may spontaneously decay into
water and hydrogen peroxide, ridding the
body of free radicals.
* 4. Vitamins E and C are antioxidants and
may inactivate or terminate the actions of
free radicals.
Carbon monoxide (CO)
* Is colorless and odorless.
* Produces hypoxic injury.
* Directly reduces the oxygen-carrying capacity of blood, and promotes tissue hypoxia. (carboxyhemoglobin curve)
* When carbon monoxide (CO) binds to hemoglobin, it forms carboxyhemoglobin (COHb). This has two main effects:
CO binds to hemoglobin with a much higher affinity (200-250 times) than oxygen, reducing hemoglobin’s ability to bind and transport oxygen.
The binding of CO shifts the oxygen-hemoglobin dissociation curve to the left, decreasing the release of oxygen from hemoglobin to tissues.
* CO’s affinity for hemoglobin is much greater than that of oxygen; it quickly binds with the hemoglobin, preventing oxygen molecules from doing so.
Lead
* Exposure in children can result in learning/behavior
problems, speech/hearing problems, brain/nervous
system damage, and slowed growth and development.
* Most common source is paint in older homes (children), the environment, and at work (adults).
* Toxicity affects central and peripheral nervous systems.
* Prevention is the key.
* Treatment may include chelation therapy.
Ethanol (alcohol)
* Results in major nutritional deficiencies, especially folate.
* Is metabolized in the liver.
* Has a protective effect with the cardiovascular system, up to a point.
* Acute alcoholism affects the central nervous system (CNS).
* Chronic alcoholism affects primarily the liver and stomach.
* Alcohol-induced liver disease (fatty liver, alcoholic hepatitis, cirrhosis)
* Acute gastritis
* Can cause fetal alcohol syndrome.
Mercury
* Two major sources are fish and healthcare equipment.
* Recommendation: Pregnant women, nursing mothers, and young children should avoid eating fish with a high
mercury content.
Social or street drugs
* Most popular and dangerous drugs include
methamphetamine (“meth”), marijuana, cocaine, and
heroin.
Which of the following is true about alcohol (ethanol)?
1. Is metabolized via the
microsomal P-450.
2. Is primarily metabolized and
excreted by the kidneys.
3. Increases activation of
methionine, an essential
amino acid.
4. Can produce
hypermagnesemia with
chronic use.
ANS: 1
* This is the primary pathway for oxidation of
ethanol. Most of the alcohol in blood is
metabolized to acetaldehyde in the liver by three enzyme systems: alcohol dehydrogenase (ADH), the microsomal
ethanol-oxidizing system (MEOS; CYP2E1), and catalase. The major pathway involves
ADH, an enzyme located in the cytosol of
hepatocytes. The microsomal ethanol oxidizing system (MEOS) depends on cytochrome P-
450 (CYP2E1), an enzyme needed for cellular
oxidation.
* 2. Ethanol is metabolized in the liver.
* 3. Methionine activation is decreased by ethanol.
* 4. Chronic alcohol use is associated with a number
of nutritional deficiencies including
hypomagnesemia. A large intake of alcohol has
enormous effects on nutritional status. Major
nutritional deficiencies include magnesium,
vitamin B6, thiamine, and phosphorus
Immunologic and inflammatory injuries
* Phagocytic cells
* Immune and inflammatory substances
* Histamine
* Antibodies
* Lymphokines
* Complement
* Proteases
* Cause membrane alterations
Injurious genetics and epigenetic factors
* Nucleus alterations
* Alterations in the plasma membrane structure, shape,
receptors, or transport mechanisms
* Example:
* Sickle cell anemia
Temperature extremes and climate change
* Hypothermic injury
* Slows cellular metabolic processes.
* Produces reactive oxygen species.
* Hyperthermic injury
* Heat cramps, heat exhaustion, heat stroke
* Malignant hyperthermia, neuroleptic malignant syndrome
* Drug-induced hyperthermia
* Burns
* Overheating, sudden infant death syndrome
Sudden increases or decreases in atmospheric pressure
* Blast injury
* Decompression sickness or caisson disease
* “The bends,” diver disease
* High-altitude illness
* High-altitude pulmonary edema (HAPE)
* High-altitude cerebral edema (HACE)
* Acute mountain sickness (AMS)
Manifestations of Cellular accumulations (infiltrations)
* Cells attempt to catabolize “stored” substances that cause metabolite accumulation in cells.
* Water
* Cellular swelling
* Lipids and carbohydrates
* Usually affect the liver (e.g., fatty liver).
* Glycogen
* Observed in genetic disorders: Glycogen storage diseases
* Accumulation: Excessive vacuolation of the cytoplasm
Systemic manifestations
* Fatigue and malaise
* Loss of well-being
* Altered appetite
* Fever
* Leukocytosis
* Increased heart rate
* Pain
* Other signs and symptoms
What are two types of cell death?
- Necrosis
* Includes inflammatory changes.
* Autolysis
*Process: Pyknosis (shrink), Karyorrhexis (fragmentation), and Karyolysis (nuc. dissolution) - Apoptosis
* No inflammatory changes
* Type I—programmed cell death
* Type II—autophagic cell death
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Types of Necrotic Cellular Death
**Coagulative necrosis
* Kidneys, heart, and adrenal glands
* Protein denaturation
* Changes protein albumin
Liquefactive necrosis
* Neurons and glial cells in the brain
* Hydrolytic enzymes form liquid-filled cyst or form pus.
**Caseous necrosis
* Tuberculosis pulmonary infection
* Combination of coagulative and liquefactive necrosis
* Cheese-looking substance that is walled off
Fat necrosis
* Breast, pancreas, other abdominal structures
* Action of lipases
Gangrenous necrosis
*Clinical term
*Dry vs wet
* Gas gangrene
What is Apoptosis?
- Is programmed cellular death.
- ER stress results in apoptotic cell death.
- Is the active process of cellular destruction.
- Can occur normally or pathologically.
- Dysregulated apoptosis
- is excessive or insufficient.
- can lead to cancer, autoimmune disorders, neurodegenerative diseases, and ischemic injury.
