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71 Cards in this Set
- Front
- Back
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1. What is cell adaptation?
What is cell injury? |
Altered state but steady state while preserving the health of the cell despite continued stress
Progressive deterioration of cell structures and functions due to environmental stress or stimuli that may be either reversible or irreversible |
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2. What is hypertrophy?
What are two causes of hypertrophy? |
An increase in the size of cells w/ an increase of cell substance and subsequently an increase in the size of the organ
1. Increased functional demand 2. Specific hormonal stimulation |
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3. What are some subcellular changes that occur with hypertrophy?
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1. Increased numbers of cytoplasmic filaments
2. Increased number of structural proteins 3. Increased number of organelles **this is all done to meet increased functional demands |
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4. When does cardiac muscle hypertrophy occur?
What type of cells undergo only hypertrophy and not hyperlasia? What are examples? What can undergo both hypertrophy and hyperplasia? |
Occurs in patients w/ high blood pressure which exerts an increased workload for the cardiac muscle
Permanent cells (do not divide after birth) Cardiac muscle fibers and skeletal muscle fibers are permanent cells Uterine smooth muscles during pregnancy caused by estrogen stimulation |
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5. What is hyperplasia?
What are two causes of hyperplasia? In what type of cells does hyperplasia occur? |
An increase in the number of cells in an organ or tissue
**esp. in CT cells 1. Increased hormonal stimulation 2. Excessive growth factor stimulation Occurs in a cell population that is capable of duplication |
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6. What is atrophy?
What are six causes of atrophy? |
Shrinkage in the size of the cell by the loss of cell substance
**entire organ or tissue diminishes in size 1. Decreased workload (conserve energy) 2. Loss of innervation 3. Diminished blood supply 4. Inadequate nutrition 5. Loss of endocrine stimulation 6. Aging |
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7. What is the pathogenesis of atrophy?
How does protein degradation occur? How is the function of atrophic cells? |
Atrophy results from decreased protein synthesis and increased protein degradation
1. Ubiquitin-proteosome pathway 2. Loss of cell substance/structures by autophagy Atrophic cells have decreased functions |
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8. What is metaplasia?
What are three causes of metaplasia? |
Replacement of one adult cell type by another adult cell type that is a reversible change
1. Chronic irritation 2. Nutritional deficiency 3. Injury |
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9. What is the pathogenesis for metaplasia?
How does squamous metaplasia of respiratory columnar epithelium occur? Where does osseous metaplasia of fibrous CT occur? |
Altered differentiation pathway of stem cells
Occurs in cigarette smokers and in vitamin A deficient subjects **cigarette smoke is irritant Occurs at injured site |
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10. What is reversible cell injury?
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In the early stages or mild forms of injury, the functional and morphological changes of cells are reversible if the damaging stimulus is removed
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11. When does cell death occur?
What are the two pathways of cell death? |
With continuing damage, the cell membrane breaks and the nucleus is fragmented or dissolves
**injury becomes irreversible and cell dies 1. Necrosis 2. Apoptosis |
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12. What are eight causes of cell injury?
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1. Hypoxia
2. Chemical agents 3. Infectious agents 4. Immunologic reactions 5. Genetic defects 6. Nutritional imbalances 7. Physical agents 8. Aging |
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13. What is hypoxia?
What are three causes of hypoxia? What does hypoxia interfere with? |
Lack of oxygen supply
1. Ischemia 2. Inadequate oxygenation of the blood (i.e. pneumonia) 3. Reduction in oxygen carrying capacity of the blood (i.e. anemia, CO poisoning) Interferes w/ oxidative phosphorylation |
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14. How can toxic chemicals (poisons) damage cells?
Three things they can alter.... What are examples of chemical agents that can cause cell damage? |
1. Membrane permeability
2. Osmotic homeostasis 3. Integrity of an enzyme or cofactor Alcohol - hepatocytes; neurons Mercury - systemic poisoning Aspirin - mucous membrane in mouth/GI |
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15. What are some infectious agents that can cause cell injury?
What are some immunologic reactions that can cause cell injury? What are some genetic defects that can cause cell injury? |
Viruses, rickettsiae, bacteria, fungi, protozoa, parasites
Anaphylactic reaction, autoimmune reactions, AIDS Congenital malformations, sickle cell anemia, enzyme deficiency |
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16. What are some nutritional imbalances that can cause cell injury?
What are some physical agents that can cause cell injury? Why can aging cause cell injury? |
Protein-calorie deficiencies, avitaminosis, atherosclerosis, obesity
Trauma, thermal changes, atmospheric pressure changes, radiant energy, electrical energy Aging cells have encountered long-term stress/stimuli so their ability to respond to environmental stress and injury is diminishes |
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17. What are two patterns of reversible injury?
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1. Cellular swelling
2. Fatty change |
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18. What is cellular swelling?
When does it occur? |
Enlargement of cells due to shift of extracellular water into cells, small vacuoles in the cytoplasm due to accumulation of water in ER
Occurs whenever cells are incapable of maintaining ionic and fluid homeostasis |
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19. What is fatty change?
When does it occur? |
Intracellular accumulation of lipid droplets
Occurs in cells involved in and dependent on fat metabolism **hepatocytes and myocardial cells |
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20. What two phenomena characterize irreversible cell injury (cell death)?
What do damaged cell membranes form? What are these? |
1. Inability of mitochondria to perform oxidative phosphorylation and produce ATP
2. Disruption of cell membrane and organelle membranes Myelin figures Phospholipid masses which are altered membranous structures resembling myelin sheath of nerves |
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21. What are the three hallmarks of cell death found in the nucleus?
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1. Karyolysis
-loss of chromatin due to digestion by DNAases 2. Phyknosis -nuclear shrinkage and condensation of chromatin 3. Karyorrhexis -fragmentation of the pyknotic nucleus |
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22. What is necrosis?
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Cell death recognized by the sequence of morphological changes cause by enzymatic digestion and denaturation of proteins in the irreversibly injured cell
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23. When dose coagulative necrocsis develop?
Why do structural and enzymatic proteins denature in coagulative necrosis? What is coagulative necrosis characteristic of? |
If denaturation of proteins prevails
Due to increasing intracellular acidosis Characteristics of... 1. Hypoxic death of cells in all tissues except the brain 2. Occurs in injuries by certain chemicals and toxins |
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24. What leads to liquefactive necrosis?
Where are these enzymes derived from? (two places) |
Prominent enzymatic digestion of dead cells
1. Lysosomes of the dead cells (autolysis) 2. Lysosomes of immigrant leuokocytes (heterolysis) |
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25. What is liquefactive necrosis characteristic of?
(two things) What does the enzymatic degradation of dead cells usually create? |
1. Focal bacterial infections of all types of tissues
2. Hypoxic death of the brain Abscess |
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26. What is an abscess
What does pus consist of? (three things) |
A localized collection of pus in a cavity formed by the disintegration of tissues
1. Necrotic cell debris 2. Neutrophils 3. Bacterial colonies (sometimes) |
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27. What is gangrenous necrosis?
Where does gangrenous necrosis often occur? |
Coagulative necrosis is infected by bacteria
**coagulated tissues may be liquefied by lysosomal enzymes of leukocytes In infarcted lower legs of diabetic patients |
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28. What is caseous necrosis?
How does the necrotic tissue appear? What is caseous necrosis characteristic of? |
Coagulation and fragmentation of dead cells
Tissue appears white and cheesy (not solid or firm) Tuberculous infection |
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29. What is fat necrosis?
What is this type of necrosis seen with? |
Destruction of adipose tissue due to release of pancreatic enzymes into the adipose tissue in the pancreas and the peritoneal cavity
Free FA combine w/ Ca to produce chalky white substances (soaps - which are hard) Acute pancreatitis |
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30. What is fibrinoid necrosis characterized by?
When is fibrinoid necrosis seen? |
Deposition of immune complexes and fibrin around blood vessels
Seen in some immune reactions |
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31. What is dystrophic calcification?
Where does dystrophic calcification occur most commonly? |
Calcification of necrotic cell debris
**cell debris attracts Ca salts and becomes calcified if not removed or reabsorbed Seen in atherosclerosis most commonly then in the lungs |
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32. What is autophagy?
What are the lysosomes involved in autophagy called? When is autophagy prominent? |
Process in which cell organelles and substances are engulfed and digested by primary lysosomes of the injured cell itself
Autolysosomes Prominent in cellular atrophy |
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33. What happens to lysosomes w/ undigested debris?
(two things) |
1. Extruded to the outside of the cell by exocytosis
2. Persist w/in cell as residual bodies (lipofuscin pigment granules) |
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34. What induces the synthesis of more SER and the associated P-450 oxidase system in hepatocytes?
What is the SER and oxidase system responsible for? Why can this system render chemical more injurious? |
Barbiturates and other compounds (alcohols, steroids, insecticides)
Responsible for detoxification of chemical compounds Can be more injurious b/c has oxidase system which converts chemicals into free radicals **free radicals can be injurious to other cells |
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35. What mitochondrial alterations can cells have?
What diseases can cause changes in mitochondria number, size, and shape? |
1. Increase in number - hypertrophy
2. Decrease in number - atrophy Alcoholism Nutritional Deficiencies Myopathies Neoplasms |
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36. What does the cytoskeleton consist of?
Four components.... What is the function of the cytoskeleton? |
1. Microtubules (25 nm diameter)
2. Thin actin filaments (7 nm) 3. Thick myosin filaments (15 nm) 4. Intermediate filaments (10 nm) Establishes cell form so cell can preform proper function |
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37. What is Chediak-Higashi syndrome or "lazy leukocyte" syndrome?
What are Mallory bodies or "alcoholic hyaline" characteristic of alcoholic liver disease? What are neurofibrillary tangles and in what type of patients are they seen? |
A defect in microtubule polymerization resulting in impaired phagocytosis of leukocytes
Abnormal accumulation of keratin filaments in hepatocytes (cytoskeleton becomes clumped) Tangles of abnormally cross-linked neurofilaments seen w/ Alzheimer's disease |
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38. What are the major causes of ATP depletion?
Three things... |
1. Reduced supply of oxygen and nutrients
2. Mitochondrial damage 3. Some toxins |
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39. What are some results of ATP depletion?
Four things... |
1. Cellular swelling and dilatation of ER
*Na pump activity is reduced 2. Intracellular lactic acid accumulation and inactivation of enzymes *due to anaerobic glycolysis increase 3. Ca influx & resulting cell damage *due to failure of Ca pump 4. Disruption of protein synthetic apparatus |
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40.What three things can cause mitochondrial damage?
What three things does mitochondrial damage result in? |
1. Increase in cytosolic Ca ions
2. Increase in reactive oxygen species 3. Oxygen deprivation 1. Oxidative phosphorylation failure 2. Depletion of ATP 3. Leakage of mitochondrial proteins |
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41. What can cause an increase in cytosolic [Ca]?
(two things) What initially causes an increase in cytosolic [Ca]? What later causes in the increase? What does increased cytosolic Ca do? |
1. Ishcemia
2. Certain toxins Initially be release of Ca from mitochondria and ER Later from influx of Ca across cell membrane Activates cellular enzymes which degrade cellular structures and induce apoptosis |
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42. By what three major reactions do free radicals cause cell injury?
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1. Lipid peroxidation of membranes
2. Cross-linking of proteins *seen in Alzheimer's disease 3. DNA fragmentation **can cause mutations |
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43. How are free radicals generated?
Six ways.... How does radiation energy work? |
1. Redox rxn in mitochondria
2. Fenton reaction 3. Absorption of radiation energy 4. Enzymatic metabolism of exogenous chemicals 5. Leukocytes in inflammation 6. NO Ionizes water molecules into hydroxyl and free radicals |
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44. Even though free radicals decay spontaneously what cellular systems work to inactivate or remove free radicals?
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1. Superoxide dismutase
**form water and oxygen by reaction superoxide free radicals w/ H 2. Glutathione peroxidasse **convert hydroxyl free radicals to water 3. Catalase **degrade H2O2 to water 4. Antioxidants **block formation or remove **antioxidants include vitamins E, A, and C and beta carotene |
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45. What are the most important sites of membrane damage?
(three sites) What can damage cell membranes and membranes of organelles? |
1. Mitochondrial membrane
2. Cell membrane 3. Lysosomal membrane Ischemia Microbial Toxins Lytic Complement Components Physical/Chemical Agents |
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46. What can cause damage to DNA and proteins?
What happens if cells are unable to repair damaged DNA and/or improperly folded proteins? |
Caused by free radicals
Apoptosis |
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47. What happens to aerobic respiration in hypoxic cells?
As a result what happens to ATP generation? In hypoxic cells what happens to the sodium pump? As a result what occurs? |
Aerobic respiration (oxidative phosphorylation) is decreased
ATP production slows or is stopped Sodium pump fails so water fluid accumulates in cytoplasm Accumulate Na, influx of K and Ca producing cellular swelling |
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48. In hypoxic cells why is anaerobic glycolysis stimulated?
What does this result in? (two things) |
Stimulated due to decreased production of ATP
1. Depleted glycogen stores 2. Production of lactic acid and inorganic phosphates |
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49. Why is protein synthesis decreased in hypoxic cells?
Where can Blebs form in hypoxic cells? What are Blebs? |
Ribososomes detach from ER and polysomes dissociate into single ribosomes
Blebs may form at cell surface Weak points in the membrane due to swelling that become microblisters |
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50. What happens if ischemia/hypoxia persist?
What happens if the cell membrane and membranes of organelles break? What happens to the dead cell? How are they removed? (two ways) |
Irreversible injury ad necrosis occur
Exit of cell enzymes into EC spaces and blood flow Become large masses of phospholipids which appear a myelin figures 1. Phagocytized by leukocytes 2. Degraded into FA that may be calcified |
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51. Why can the restoration of blood flow to ischemic tissues result in exacerbated and accelerated damage?
Where does this process contribute significantly to tissue damage? |
1. Increased generation of ROS from parenchymal and endotheial cells and from leukocytes
2. Inflammation may increase w/ reperfusion b/c of increased influx of leukocytes and plasma proteins In myocardial and cerebral infarcations |
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52. What two mechanisms are involved in chemical injury?
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1. Chemical binds directly to a critical molecular component or cellular organelle
**i.e. mercury, aspirin 2. Chemicals are converted to reactive free radicals to cause cell injury **metabolic activation |
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53. How is apoptosis activated?
What happens to the apoptotic bodies (fragments of apoptotic cells that break off)? |
Activation of caspases enzyme system will cause individual or small cluster of cell death
Removed by phagocytes and do not elicit an inflammatory reaction |
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54. What is the purpose of apoptosis in pathological conditions?
What are some examples of cell death through apoptosis? |
Eliminates cells that genetically altered or injured beyond repair w/o eliciting a severe host reactions
1. Councilman bodies in liver in toxic or viral hepatitis 2. Death of cancer cells 3. Civatte bodies in oral epithelium and in epidermis in lichen planus |
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55. What is the fundamental event in apoptosis?
What does these enzymes do? |
Activation of caspases
Activate nucleases that degrade DNA and other enzymes that destroy nucleoproteins and cytoskeletal proteins |
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56. What is fatty change (steatosis)?
What can cause fatty change of heptocytes? (five things) What can cause fatty change in the heart muscle? (two things) Is fatty change reversible? |
Any abnormal accumulation of lipids in the cytoplasm of parenchymal cells of an organ
1. Alcohol 2. Carbon tetrachloride 3. Protein malnutrition 4. Diabetes 5. Obesity Hypoxia or myocarditis Is reversible **cells w/ severe fatty change may die |
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57. What is fatty ingrowth?
Where does it occur frequently? |
An overgrowth of mature adipocytes in the CT stroma of an organ between parenchymal cells
**not result of injury of parenchymal cells Heart, pancreas, and parotid in atrophy and obseity |
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58. What are foam cells (foamy macrophages)?
Why does their cytoplasm appear foamy? Where does this occur commonly? (two places) |
Scavenger macrophages that engulf lipid debri of necrotic cells or abnormal plasma lipids and become stuffed
Due to presence of numerous minute vacuoles of lipids 1. Atherosclerosis 2. Periapical inflammation of non-vital tooth |
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59. What are two examples of accumulation of proteins?
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1. Proteinuria
2. Russell bodies |
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60. What can proteinuria lead to?
How does proteinuria appear? Where do these droplets occur? |
Leads to reabsorption of the lost protein
Appears as hyaline droplets In proximal convoluted tubular cells of the kidney |
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61. What are Russell bodies?
Where are Russell bodies commonly seen? |
Rounded, eosinophilic bodies resulting from accumulations of immunoglobulins in degenerating plasma cells
1. Chronic periodontal inflammation 2. Periapical inflammation |
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62. In what two diseases does accumulation of glycogen in parenchymal cells occur?
How does the accumulated glycogen appear? Where are the three most common sites for glycogen accumulation? |
1. Diabetes mellitus
2. Glycogen storage diseases Appears as clear vacuoles Major large organs -heart -kidney -liver |
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63. In errors of metabolism due to genetic deficiency of enzymes what happens to mucopolysaccharides and complex lipids?
What cells does this mainly happen in? What are some results of this? |
Cannot be metabolized and accumulate w/in cells
Reticuloendotheliay systems **line sinusoid space of liver/spleen 1. Hepatomegalia or enlargement of spleen 2. Mental retardation (Tay sach disease) *neurons accumulate glycolipids and loss star shape morphology --> ovoid or circular shape 3. Cell death |
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64. What is anthracosis?
What does it lead to? |
Accumulation of black carbon dust in the lung
Leads to emphysema and/or fibrosis |
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65. What are other names for lipofuscin?
What color is lipofuscin? What is it a result of? In what two type of patients is it usually seen? |
Lipochrome, ceroid, "wear and tear", and aging pigment
Yellow-brown Results from free radical injury and lipid peroxidation 1. Seen in atrophic organs (brown atrophy) of aging patients 2. Patients w/ severe malnutrition |
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66. What color is melanin?
What produces it? What are freckles of the skin due to? When is excess production of melanin seen? What is the purpose of smoker melanosis? |
Brown-black pigment
Produce by melanocytes Due to focal overproduction of melanin Excess production seen in adrenal insufficiency Protect underlying tissue from smoke |
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67. What color is hemosiderin?
What is it derived from? When are hemosodierin granules found? (two scenarios) |
Golden yellow to brown pigment
Hemoglobin 1. Local hemorrhage 2. Systemic hemosiderosis |
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68. What is dystrophic calficiation?
In what types of areas does it occur? Where does intracellular dystrophic calcification initiate? Where does extracellular dystrophic calcification occur? |
Deposition of Ca salts in dead or dying tissues and cells
Occurs in areas of coagulative necrosis, caseous necrosis, liquefactic necrosis, fat necrosis, and in atheromas Initiates in mitochondria of dying or dead cells Occurs in membrane vessicles of degenerating or aging cells |
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69. What does Ca have an affinity for?
How are Ca levels in dystrophic calcification? |
Has affinity from membrane phospholipids
Serum Ca levels are normal **no derangement in Ca metabolism |
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70. What is metastatic calcification?
What does it always reflect? Where does it principally occur? |
Deposition of Ca salts in normal tissues
Reflects hypercalcemia **due to hyperparathyroidsim, vit D intoxication, destruction of bone, renal failure Occurs in interstitial CT of blood vessels, kidneys, lungs and gastric mucosa |
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71. What two mechanisms are involved in cellular aging?
During the aging process what type of atrophy do organs undergo? What is the brown lipofuscin pigment derived from? What is this caused by? |
1. Genetic program
2. Repeat environmental injury Brown atrophy Derived from lipid peroxidation Caused by repeated free radical injury induced by environmental factors |
