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278 Cards in this Set
- Front
- Back
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Atrophy
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A decrease in cellular size cause by again, disuse or lack of blood supply, hormonal stimulation or neural stimulation.
Amounts of ER, mitochondria and microfilaments decrease |
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Metastatic Calcification
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Occurs in normal tissue as the result of elevated serum calcum levels
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Dystrophic Calcification
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Occurs in dead or dying tissue
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Pathological Calcifications
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Involves the abnormal tissue deposition of calcim salts, together with smaller amount of iron, magnesium and other minerals
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Intracellular Accumulations
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represents the buildup of substances that cells cannot immediately use or eliminate
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Dysplasia
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An abnormal change in the size, shape and organization of mature tissue cells
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Metaplasia
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The reversible replacement of one mature cell type by another less mature cell type
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Hyperplasia
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An increase in the number of cells caused by an increased rate of cellular division.
Normal hyperplasia is stimulated by hormones or the need to replace lost tissues. |
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Hypertrophy
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An increase in cell size caused by increased work demand or hormonal stimulation.
Amounts of protein in the plasma membrane, endoplasmic reticulum, microfilaments and mitochondria increase. |
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Cellular Injury
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Occurs if the cell is unable to maintain homeostasis.
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Six biochemical themes important to cell injury are:
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1. Adenosine triphosphate deplation
2. Mitochondrial damage 3. Oxygen & oxygen0derived free radicals 4. Membrane damage 5. Protein folding defects 6. increased intracellular calcium and loss of calcium steady state |
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Ischemia
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The cessation of blood flow into vessels that supply the cell with oxygen and nutrients
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What are the three layers of human defense?
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Barriers, innate immunity (which includes the inflammatory response), and adaptive immunity.
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What are the first lines of defense that prevent damage to the individual and prevent invasion by pathogens?
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Physical and Mechanical barriers. These include the skin and mucous membranes.
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Inflammation
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Rapid and nonspecific protective response to cellular injury from any cause. It can occur only in vascularized tissue.
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Macroscopic hallmarks of inflammation
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Redness, swelling, heat, pain, and loss of function of inflamed tissues.
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Biochemical Barriers
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Antibacterial peptides in mucous secretions, perspiration, saliva, tears, and other secretions provide a biochemical barrier against pathogenic microorganisms. The normal bacterial flora provides protection by releasing chemicals that prevent colonization by pathogens.
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Free Radicals
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cause cellular injury because they have an unpaired electron that meks the molecule unstable.
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Oxidative Stress
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is a condition that occus when the generation of ROS exceeds the ability of the body to neutralize and eliminate ROS
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Antioxidants
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natural and synthetic molecules that inhibit the reactions of ROS with biologic structures or prevent the uncontrolled formation of ROS
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Contusion
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is bleeding into the skino r underlying tissues as a consequence of a blow
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Abrasion
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results from removal of the superficial layers of the skin caused by friction between the skin and injuring objects
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Laceration
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is the tear or rip resulting when the tensile strength of teh skin or tissue is exceeded.
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Incised wound
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is a cut that is longer than it is deep
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Asphxial injury
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is caused by failure of cells to recieve or utilze oxygen.
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Genetic disorders injure cells by:
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alternating the nucleus and the plasma membrane's structure, shape, receptios or transport mechanisms
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Injurious physical agents include:
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temperature extremes, changes in atmopheric pressue, ionizing radation, illumination,mechanical stresses and noise
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Microscopic Hallmark of Inflammation
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An accumulation of fluid and cells at the inflammatory site.
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Inflammation is mediated by what three key plasma protein systems?
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The complement system, the clotting system, and the kinin system. The components of all three systems are a series of inactive proteins that ate activated sequentially.
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Complement System
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Can be activated by antigen-antibody reactions or by other products, especially bacterial polysaccharides, resulting in the production of biologically active fragments and destruction of cells.
The most biologically potent of the complement system are C3b, C3a, and C5a. |
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Clotting System
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Stops bleeding, localizes microorganisms, and provides a meshwork for repair and healing.
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Kinin System
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Bradykinin is most important product of the kinin system, and causes vascular permeability, smooth muscle contraction, and pain.
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What is the leading cause of injury or death in the US?
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Errors in health care
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Cellular Swelling
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is the accumulation of excessive water in the cell and is caused by the failure of transport mechanisms. It is a sign of many types of cellular injury
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Dystrophic calcification
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always a sign of pathologic change because it occurs only in injured or dead cells.
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Metastatic calcification
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can occur in uninjured cells in individuals with hypercalcemia
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Systemic manifestations of cellular injury includes:
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fever, leukocytosis, increased heart rate, pain, and serum elevations of enzymes in the plasma
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Cellular death has historically been classified as what two things?
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Necrosis or apoptosis
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Necrosis
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is characterized by rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction, and lack of features of apoptosis.
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Apoptosis
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is known as regulated or programmed cell death, charactized by "dropping off" of cellular fragments called apoptosis bodies
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What are the four types of necroses?
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Coagulative, liquefactive, caseous, and fat necroses
Each occur in different tissues |
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What are the structural signs that indicate irreverible injury and progression to nectrosis?
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dense clumping and distruption of genetic material and the distription of the plasma and organelle membranes
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Cell types in the inflammatory process
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Many types including Mast cells, endothelial cells, platelets, phagocytes, natural killer cells, and lymphocytes.
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Pathogen-Associated Molecular Patterns / Damage-Associated Molecular Patterns
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Most cells express plasma membrane pattern recognition receptors that recognize molecules produced by infectious microorganisms called pathogen-associated molecular patterns, or products of cellular damage called damage-associated molecular patterns.
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Cytokines
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The cells of the innate immune system secrete many biochemical mediators that are responsible for activating other cells these cytokines include interleukins, chemokines, interferons, and other molecules
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Pro-inflammatory cytokines
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Most important are interleukin-1, interleukin-6, and tumor necrosis factor-alpha
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Interferons
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Produced by cells that are infected by viruses. Once released from infected cells, interferons can stimulate neighboring healthy cells to produce substances that prevent viral infection.
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Apoptosis
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is a distinct type of sublethal injury and is a process of selective cellular self-destruction that occurs in both normal and pathologic tissue changes
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Death by apoptosis causes loss of cells in many pathologic states, including what?
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Severe cell injury, accumulation of misfolded proteins, infections and obstruction in tissue ducts
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Endoplasmic Reticulum Stress
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excessive accumulation of misfolded proteins in the ER
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Excessive or not, apoptosis is known as what?
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dysregulated apoptosis
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Autophagy
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means "eating of self" and as a recycling factor it is a self-destructive process and a survival mechanism
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Gangrenous Necrosis
(gangrene) |
is tissue necrosis caused by hypoxia and the subsequent bacterial invasion
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Physiologic mechanisms of aging are associated with:
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cellular changes produced by genetic and environmental-lifestyle factors, chagnes in cellular regulatory or control mechanisms, degenerative extracellular and vascular alterations
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Frailty
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wasting syndrome of aging leaving a person vuleranle to falls, functional decline, disease and death
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Somatic death
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death of an entire organism
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Postmortem change
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diffuse and does not involve the inflammatory response
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Manifestation of somatic death includes:
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Cessation of respiration and circulation, gradual lowering of body temperature, pupil dilation, loss of elasticity and transparency of the skin, muscle stiffening and skin discoloration.
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Chemokines
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Synthesized by a number of different cells and induce leukocytes through chemotaxis.
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Mast Cell
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Most important activator of the inflammatory response, which initiates inflammation by releasing biochemical mediators from performed cytoplasmic granules and synthesizing other mediators in response to a stimulus.
Histamine is the major vasoactive amine released from mast cells. Causes dilation of capillaries and retraction of endothelial cells lining the capillaries, which increases vascular permeability. |
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Endothelial Cells
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They line the circulatory system and normally regulate circulating components of the inflammatory system and maintain normal blood flow by preventing spontaneous activation of platelets and members of the clotting systems.
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Endothelium during inflammation
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expresses receptors that help leukocytes leave the vessel and react to allow fluid to pass into the tissues.
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Platelets
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Interact with the coagulation cascade to stop bleeding and release a number of mediators that promote and control inflammation.
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Polymorphonuclear Neutrophil
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the predominant phagocytic cell in the early inflammatory response, exits the circulation by diapedesis through the retracted endothelial cell junctions and moves to the inflammatory site by chemotaxis.
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Eosinophils
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Release products that control the inflammatory response and are the principal cell that kills parasitic organisms.
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Macrophage
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Predominant phagocytic cell in the late inflammatory response, highly phagocytic, responsive to cytokines, and promotes wound healing.
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Dendritic cells
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Connnect the innate and acquired immune systems by collecting antigens at the site of inflammation and transporting them to sites, such as the lymph nodes, where immunocompetent B and T cells reside.
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Phagocytosis
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Multistep cellular process for the elimination of pathogens and foreign debris.
The steps include recognition and attachment, engulfment, formation of a phagosome and phagolysosome, and destruction of pathogens or foreign debris. Phagocytic cells engulf microorganisms and enclose them in phagocytic vacuoles, w/in which toxic products and degradative lysomal enzymes kill and digest the microorganisms. |
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Opsonins
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coat microorganisms and make them more susceptible to phagocytosis by binding them more tightly to the phagocyte. Ex: antibody and complement component C3b.
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Local Manifestations of Acute Inflammation
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Result of the vascular changes associated w/ the inflammatory process, including vasodilation and increased capillary permeability.
Symptoms include redness, heat, swelling, and pain. |
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Systemic Manifestations of Acute Inflammation
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Principal systemic effects of inflammation are fever and increases in levels of circulating leukocytes and plasma proteins.
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Chronic Inflammation
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Can be a continuation of acute inflammation that lasts 2 weeks or longer. It also can occur as distinct process w/out much preceding acute inflammation.
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Chronic Inflammation is characterized by?
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dense infiltration of lymphocytes and macrophages. The body may wall off and isolate the infection to protect against tissue damage by formation of granuloma.
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Resolution / Regeneration
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Return of tissue to nearly normal structure and function.
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Repair
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healing by scar tissue formation
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Healing by Primary Intention
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process where damaged tissue proceeds to resolution if little tissue has been lost or injured tissue is capable of regeneration
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Healing by Secondary Intention
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process where tissue that sustained extensive damage or those incapable of regeneration heal by the process of repair resulting in the formation of a scar.
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Resolution and Repair
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Occur in 2 separate phases, the reconstructive phase, in which the wound begins to heal, and the maturation phase, in which the healed wound is remodeled.
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Dysfunctional wound healing
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can occur as a result of abnormalities in either the inflammatory resonse or the reconstructive phase of resolution and repair.
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Pediatrics & Factors affecting Innate Immunity in Newborn Child
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Neonates often have transiently depressed inflammatory function, particulary neutrophil chemotaxis and alternative complement pathway activity.
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T Cell - independent
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immune response is adequate in the fetus and neonate
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T Cell - dependent
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immune response develops slowly during the first 6 months of life.
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Maternal Immunoglobulin Antibodies
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transported across the placenta into the fetal blood and protect the neonate for the first 6 months, after which they are replaced by the child's own antibodies.
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Age-Related Factors affecting Innate Immunity in Elderly
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Elderly persons are at risk for impaired wound healing, usually because of chronic illnesses.
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T Cell - elderly
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function and antibody production are somewhat deficient in elderly persons. Elderly individuals also tend to have increased levels of circulating autoantibodies. (antibodies against self-antigens)
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Adaptive immunity
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is a state of protection, primarily against infectious agents, that differs inflammation by being slower to develop, being more specific and having memory, that makes it much longer-lived
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B cells
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are responsible for humoral immunity that is mediated by circulating antibodies.
Are lymphocytes |
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T cells
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are responsible for cell-mediated immunity, in which they kill targets directly or stimulate the activity of other leukocytes. They are lymphocytes
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Adaptive immunity
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can either be active or passive depending on whether immune response components orginated in the host or came from a donor
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Antigens
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molecules that bind and react with components of the immune response
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Immunogens
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can induce an immune response
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All immunogens are antigens
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but not all antigens are immunogens
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Haptens
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antigens too small to be immunogens by themselves but become immunogenic after combining with larger molecules
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Antigenic-determinant
(epitope) |
is trhe precise chemical structure with which an antibody or B cell/T cell receptor reacts
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Self-antigens
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antigens on an individual's own cell.
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A condition known as tolerance
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Is an individual's immune system does not normally recognize self-antigens as immunogenic
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The response to antigens can be divided into what two phases?
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The primary and secondary responses.
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Primary response of humoral immunity
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is usually dominated by IgM, with lesser amounts of IgG
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Secondary response
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has more rapid production of largers amounts of antibody, predominantly IgG
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What is a typical antibody molecule constructed of?
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Two identical heavy chains and two identical light chains and has twp-fragment, antigen-binding portions that bind antigen and one-fragment, crystalline-binding portion that interacts with complement or receptors on cells
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Direct effects
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result from the binding of antibody directly to a harmful antigen or infectious agent
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Indirect effects
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result from activation of inflammation by antibodies through the fragment, crystalline binding portion of the molecule
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IgE is a special class of antibody that helps to what?
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Defend against parasitic infections
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Systemic immune system
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Antibodies function internally in the bloodstream and tissues
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Secretory or mucosal immune system
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Antibodies function externally in the secretion of muscous membranes
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There are several types of mature T cells including:
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T-cytotoxic cells, T-helper cells, T-regulatory cells, and memory cells
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Infection
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Bacteria injures cells by producing exotoxins or endotoxins
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Bacteria has what two types?
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Two forms - exotoxins and endotoxins
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Exotoxins
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Enzymes that can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis.
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Endotoxins
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Activate the inflammatory response and produce fever
Endotoxins released by blood-orne bacteria cause the release of vasoactive enzymes that increase the permeability ofblood vessels. Leakage from vessels causes hypotension that can result in septic shock |
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Septicemia
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The proliferation of bacteria in the blood.
Endotoxins released by blood-orne bacteria cause the release of vasoactive enzymes that increase the permeability ofblood vessels. Leakage from vessels causes hypotension that can result in septic shock |
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Viruses
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Enter host cells and use the metabolic processes of host cells to proliferate.
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Viruses that have invaded host cells may do what?
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Decrease protein synthesis, disrupt lysomal membranes, form inclusion bodies where synthesis of viral nucleic acids is occurring, fuse with host cells to produce giant cells, alter antigenic properties of the host cell, and transform host cells into cancerous cells.
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Mycoses
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Diseases caused by fungi and occur in two forms: yeasts and molds.
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Dermatophytes
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Fungi that infect skin, hair, and nails with diseases such as ringworm and athlete's foot.
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Fungi
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Release toxins and enzymes that are damaging to tissue
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Parasitic Microorganisms
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range from unicellular protozoa to large worms. Although less common in the United States, parasites and protozoa are common causes of infection worldwide.
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Parasites and Protozoa
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Common causes of infection worldwide.
Parasitic and protozoal infections are rarely transmitted from human to human. Infection mainly spreads through vectors or through contaminated water or food. |
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Immunodeficiency
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The failure of mechanisms of self-defense to function in their normal capacity.
Either congenital or acquired Clinical hallmark is a propensity to unusual or recurrent sever infections. The type of infection usually reflects the immune system defect |
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Congenital Immunodeficiencies
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Caused by genetic defects that disrupt lymphocyte development.
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Acquired Immunodeficiencies
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secondary to disease or other physiologic alterations.
Caused by superimposed conditions, such as malnutrition, medical therapies, physical or psychologic trauma, or infections. |
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Defects of Cell-mediated immune response
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The most common infections in individuals with this are fungal and viral
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Defects of Humoral Immune Response or Complement function
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The most common infections in individuals with this are primarily bacterial.
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Sever Combined Immunodeficiency
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A total lack of T cell function and a sever lack of B cell function
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DiGeorge Syndrome
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characterize by complete or partial lack of the thymus, the parathyroid glands, and cardiac anomalies.
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B Cell defects
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defects are diverse, ranging from a complete lack of the human bursal equivalent, the lymphoid organs required for B cell maturation, to deficiencies in a single class of immunoglibulins
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Immunodeficiency syndromes
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Usually are treated by replacement therapy. Deficient antibody production is treated by replacement of missing ummunoglobulins with commercial gamma-globulin preparations. Lymphcyte deficiencies are treated with the replacement of host lymphocytes with transplants of bone marrow, fetal liver, or fetal thymus from a donor.
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AIDS
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An acquired dysfunction of the immune system caused by a retrovirus that infects and destroys CD4 lymphocytes.
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Hypersensitivity
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Inappropriate immune response misdirected against the host's own tissues or directed against beneficial foreign tissues, such as transfusions or transplants; or it can be exaggerated responses against environmental antigens.
Can bee immediate. Most rapid immediate is Anaphylaxis |
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Mechanisms of Hypersensitivity
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Classified as IgE-mediated reactions, tissue-specific reactions, immune-complex-mediated reactions, and cell-mediated reactions.
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Anaphylaxis
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The most rapid immediate hypersensitivity reaction, is an explosive reaction that occurs within minutes of reexposure to the antigen and can lead to cardiovascular shock.
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Allergens
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Antigens that cause allergic responses.
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Type I Hypersensitivity
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IgE-mediated reactions occur after antigen reacts with IgE on mast cells, leading to mast cell degranulation and the release of histamine and other inflammatory substances.
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Type II Hypersensitivity
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Tissue-specific reactions are cause by four possible mechanisms: complement-mediated lysis, opsonization and phagocytosis, antibody-dependent cell-mediated cytotoxicity, and modulation of cellular function.
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Type III Hypersensitivity
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Immune complex-mediated reactions are caused by the formation of immune complexes that are deposited in target tissues, where they activate the complement cascade, generating chemotractic fragments that attract neutrophils into the inflammatory site.
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Type IV Hypersensitivity
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Cell-mediated reactions are caused by specifically sensitized T cells, whcih either kill target cells directly or release lymphokines that activate other cells, such as macrophages.
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Imune-Complex Disease
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can be asystemic reaction, such as serum sickness, or localized, such as the Arthus reaction.
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Alleriges
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can be midated by any of the four mechanisms of hypersensitivity.
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Allergic Reaction manifestations
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Clinical manifestations of allergic reactions are usually confined to the areas of initial intake or contact with the allergen
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Ingested Allergens
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induce gastrointestinal symptoms
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Airborne Allergens
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induce respiratory or skin manifestations
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Contact Allergens
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induce allergic responses at the site of contact.
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Atopic Individuals
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genetically predisposed to the development of allergies
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Alloimmunity
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The immune system's reaction against antigens on the tissues of other members of the same species.
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Alloimmune disorders
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Include transient neonatal disease, in which the maternal immune system becomes sensitized against antigens expressed by the fetus, and transplant rejection and transfusion reactins, in which the immune system of the recipient of an organ transplant or blood transfusion reacts against foreign antigens on the donor's cells
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Anemia
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Defined as a reduction in the number or volume of circulating red cells or an alteration in hemoglobin.
Most common classification is based on changes in the cell size--represented by the suffix cytic--and changes in the cell's hemoglobin content--represented by the suffix chromic. |
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Anemia Clinical Manifestations
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can be found in all organs and tissues throughout the body. Decreased oxygen delivery to tissue causes fatigue, dyspnea, syncope, angina, compensatory tachycardia, and organ dysfunction.
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Macrocytic Anemias
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Or megaloblastic, caused mostcommonly by deficiency of vitamin B12.
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Pernicious Anemia
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can be fatal unless vitamin B12 replacement is given
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Microcytic-hypochromic anemia
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characterized by abnormally small red cells with insufficient hemoglobin content. Most common cause is iron deficiency.
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Iron Deficiency Anemia
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Usually develops slowly, with a gradual insidious onset of symptoms, including fatigue, weakness, dyspnea, alteration of various epithelial tissues, and vague neuromuscular complaints.
Usually a result of a chronic blood loss or decreased iron intake. Once the source of blood loss is identified and corrected, iron replacement therapy can be initiated. |
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Sideroblastic Anemia
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results from impaired iron metabolism and abnormal sequestration of iron w/in the red cell. Treatment varies depending on the cause.
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Normocytic-normochromic anemia
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characterized by insufficient numbers of normal erythrocytes. Included in this category are aplastic, posthermorrhagic, and hemolytic anemia and anemia of chronic inflammation.
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Aplastic Anemia
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erythocyte stem cells are underdeveloped, defective, or absent. Unless cause is determined, bone marrow aplasia results in death
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Posthermorrhagic Anemia Cause
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Results from a sudden blood loss. Restoration of blood volume by plasma expanders or transfusions may diminish subjective symptoms of anemia. Hemoglobin restoration may take six to eight weeks.
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Hemolytic Anemia Cause
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Reults from premature destruction of red cells and make be acquired or hereditary. Of the acquired forms, autoimmune reaction and drug-induced hemolysis are the most common causes
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Anemia of Chronic Inflammation
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Associated with chronic infections, chronic inflammatory diseases, and malignancies.
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Polycythermia Vera
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characterized by excessive proliferation of erythrocyte precursors in teh bone marrow. Signs and symptoms result directly form increased blood volume and viscosity. Therapeutic phlebotomy to remove excessive blood volume and use of radioactive phosphorus have been helpful in decreasing the excessive red cell pool.
May spontaneously convert to acute myelogenous leukemia. |
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Quantitative Alterations of Leukocytes
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(sucha as too many or too few) can be caused by bone marrow dysfunction or premature destruction of cells in the circulation. Many quantitative changes in leukocytes occur in response to invasion by microorganisms.
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Leukocytosis
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Condition in which the leukocyte count is higher than normal and is usually a response to stress and invasion of microorganisms.
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Leukopenia
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Condition in which the leukocyte count is lower than normal and is caused by pathologic conditions, such as malignancies and hematologic disorders.
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Granulocytosis
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(particularly as a result of an increase in neutrophils) occurs in response to infection. The marrow releases immature cells, causing a shift to the left, when responding to an infection that has created a demand for neutrophils that exceeds the supply in the circulation.
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Eosinophilia
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results most commonly from parasitic invasion and ingestion or inhalation of toxic foreign particles.
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Basophilia
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seen in hypersensitivity reactions because o f the high content of histamine and subsequent release.
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Monocytosis
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occurs during the late or recuperative phase of infection when macrophages (which are mature monocytes) phagocytose surviving microorganisms and debris.
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Granulocytopenia
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a significant decrease in neutrophils, can be a life-threatening condition if sepsis occurs; it is often caused by chemotherapeutic agents, sever infection, and radiation.
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Infectious Mononucleosis
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an acute infection of B lymphocytes most commonly associated with the Epstein-Barr virus (abbreviated EBV), a type of herpes virus.
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Epstein-Barr Virus
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(EBV) a type of herpes virus infecting the B lymphocytes.
Transferred through close personal contact, commonly through saliva, thus its nick name, the kissing disease. |
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Mononucleosis Earliest Manifestations
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sore throat and fever caused by inflammation at the primary site of viral entry.
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Epstein-Barr-Virus-related infectious mononucleosis Causes
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Include fever lasting seven to ten days, sore throat, and enlargement and tenderness of the cervical lymph nodes. It is self-limiting and treatment consists of rest and symptomatic treatment
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Leukemia Pathologic Feature
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Uncontrolled proliferation of leukocytes, overcrowding the bone marrow and resulting in decreased production and function of the other blood cell lines.
All leukemias are classifed by the cell type involved, either lympocytic or myelogenous and are differentiated by onset, acute or chronic. Thus there are four major types of leukemia: acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (CML). |
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Leukemia Cause
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No exact cause is known, it is considered a clonal disorder. A high incidence of acute leukemias and chronic lymphocytic leukemia is reported in certain families, suggesting a genetic predisposition.
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Leukemia Clinical Manifestations
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Fatigue caused by anemia, bleeding caused by thrombocytopenia, fever secondary to infection, anorexia, and weight loss.
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Chemotherapy
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Treatment of choice for leukemia.
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Acute leukemia
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are associated with an increasing survival rate of 80% to 90%, with long-term survival of 30 to 40%.
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Chronic Leukemia
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are associated w/ a longer life expectancy than are acute leukemias. They progress differently than acute leukemias, advancing slowly and without warning. The presence of the Philadelphia chromosome is a diagnostic marker for chronic myelogenous leukemia.
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Iron Deficiency Anemia
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is the most common blood disorder of infancy and childhood; the highest incidence occurs between 6 month and 2 years
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Hemolytic disease of the newborn (HDN)
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results from incompatibility between the maternal and the fetal blood, which may involve differences in rhesus(Rh) factors or blood type(ABO)
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Kernicterus
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causes increased breakdown of red blood cells or decreased liver output of enzymes
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Lymphocytopenia
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The number of lymphocytes is decreased in most acute infections and in some immunodeficiency syndromes.
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Lymphocytosis
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occurs in viral infections (such as infections mononucleosis and infections hepatitis, in particular), leukemia, lymphomas, and some chronic infections
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Lymphomas
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Are tumors of primary lymphoid tissue (such as thymus or bone marrow) or secondary lymphoid tissue (such as lymph nodes, spleen, tonsils, and intestinal lymphoid tissue.
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Malignant Lymphomas
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two major types are Hodgkin lymphoma and non-Hodgkin lymphoma
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Reed-Sternberg Cell
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Distinctive abnormal chromosomes are present in multiple cells of the lymph nodes of an individual with Hodgkin lymphoma. The abnormal cell is called the Reed-Stenberg cell.
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Hodgkin Lymphoma
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A virus might be involved in the pathogenesis of Hodgkin lymphoma. Some familial clustering suggests an unknown genetic mechanism.
An enlarged, painless mass or swelling, most commonly in the neck, is an initial sign of Hodgkin lymphoma. Local symptoms are produced by lymphadenopathy, usually caused by pressure or obstruction. |
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Hodgkin Lymphoma Treatment
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Includes radiation therapy and chemotherapy. A cure is possible regardless of the stage of Hodgkin lymphoma; however, individuals treated with chemotherapy who relapse in less than two years have a poorer prognosis.
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non-Hodgkin Lymphoma
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The cause of lymph node enlargement and cancerous transformation in non-Hodgkin lymphoma is unknown. Immunosupressed persons have a higher incidence of non-Hodgkin lymphoma, suggesting an immune mechanism.
Generally, the swelling of lymph nodes is painless, and the nodes enlarge and transform over a period of months or years. Individuals with this can survive for long periods. The treatment used is chemotherapy |
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Burkitt Lymphoma
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involoves the jaw and facial bones and occurs in children from east-central Africa and New Guinea.
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Multiple Myeloma
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A neoplasm of B cells (which are immature plasma cells) and mature plasma cells. It is characterized by multiple malignant tumor masses of plasma cells scattered throughout the skeletal system and sometimes found in soft tissue.
Exact cause is unknown, but genetic factors and chronic stimulation of the mononclear phagocyte system by bacteria, viral agents, and chemicals have been suggested. |
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Multiple Myeloma manifestations
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major clinical manifestations include recurrent infections caused by suppression of the humoral immune response and renal disease as a result of Bence Jones proteinuria.
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Multiple Myeloma treatments
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Chemotherapy is the treatment of choice for multiple myeloma. Survival is still only two to three years with chemotherapy, however. Treatment with thalidomide is showing promise as an effective therapeutic agent in producing long-term remissions.
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Splenomegaly
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Enlargement of the spleen, may be considered normal in certain individuals, but its presence should not be ignored.
Results from acute inflammatory or infectious processes, congestive disorders, infiltrative processes, and tumors or cysts. |
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Hypersplenism
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overactivity of the spleen, results from splenomegaly. Results in sequestering of blood cells, causing increased destruction of red blood cells, which leads to the development of anemia.
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Thrombocytopenia
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characterized by a platelet count below 100,000 per square millimeter of blood; a count below 50,000 per square millimeter increases the potential for hemorrhage associated with minor trauma.
Exists in primary or secondary forms and is commonly associated with autoimmune diseases and viral infections; bacterial sepsis with dissemiated intravascular coagulation also results in thrombocytopenia |
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Thrombocythemia
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characterized by a platelet count more than 400,000 platelets per square millimeter of blood and is symptomatic when the count exceeds 1,000,000 per square millimeter, at which time the risk for intravascular clotting (known as thrombosis) is high.
Caused by accelerated platelet production in the bone marrow. |
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Thrombosis
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risk for intravascular clotting from high platelet count.
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Prolonged bleeding times are caused by what
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qualitative alterations in normal platelet adherence or aggregation prevent platelet plug formation and may result in prolonged bleeding times.
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Platelet dysfunction
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results from changes in the cellular contents and integrity.
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Coagulation Disorders
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usually caused by defects or deficiencies of one or more clotting factors.
Coagulation is imparied when there is a deficiency of vitamin K because of insufficient production of prothrombin and synthesis of clotting factors two, seven, nine, and ten, often associated with liver diseases. |
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Disseminated intravascular coagulation (DIC)
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is a complex syndrome resulting from a variety of clinical conditions that release tissue factor, causing an increase in fibrin and thrombin activity in the blood producing augmented clot formation and accelerated fibrinolysis.
Sepsis often associated w/ it. Characterized by a cycle of intravascular clotting followed by active bleeding caused by the initial consuption of coagulation factors and platelets and diffuse fibrinolysis. |
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Sepsis
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a condition that is often associated with disseminated intravascular coagulation
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Disseminated intravascular (DIC) diagnosis
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based on measurement in the blood of end products characteristic of dysfunctional coagulation activity.
Treatment is complex and nonstandardized and focused on removing the primary cause, restoring hemostasis, and preventing further organ damage. |
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Thromboembolic disease
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results from a fixed clot (known as thrombus) or moving clot (known as embolus) that blocks flow within a vessel, denying nutrients to tissues distal to the occlusion. Death can result when clots obstruct blood flow to the heart, brain, or lungs
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Embolus
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moving Clot
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Thrombus
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Fixed clot
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Hypercoagulability
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Result of deficient anticoagulation proteins. Secondary causes are conditions that promote venous stasis.
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Virchow Triad
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refers to three factors that can cause thrombus formation: loss of integrity of the vessel wall, abnormalities of blood flow, and alterations in the blood constituents.
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Endocrine function abnormalities are caused by?
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may be caused by elevated or depressed hormone levels that result from faulty feedback systems, dysfunction of the gland, altered metabolism of hormones, or production of hormones from nonendocrine tissues.
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Target Cells may fail to respond to hormones because of ?
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Cell surface receptor-associated disorders, intracellular disorders, or circulating inhibitors.
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Dysfunction in the action of hypothalamic hormones is related to what?
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Most commonly related to interruption of the connection between the hypothalamus and pituitary, the pituitary stalk.
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Disorders of the posterior pituitary include?
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syndrome of inappropriate antidiuretic hormone secretion and diabetes insipidus. This secretion is characterized by anormally high anti-diuretic hormone secretion; diabetes insipidus is characterized by abnormally low anti-diuretic hormone secretion.
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SIADH
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high anti-diuretic hormone levels interfere with renal free water clearance, leading to hyponatremia and hypoosmolality, and is associated with brain injury and with certain forms of cancer, apparently because of ectopic secretion of antidiurectic hormone by tumor cells.
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Diabetes Insipidus
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may be neurogenic or nephrogenic. Its principal clinical features are polyuria and polydipsia.
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Hypopituitarism
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can be primary or secondary. can affect any or all of the pituitary hormones and symptoms may range from mild to life-threatening.
Caused by pituitary adenomas. These are usually benign, slow-growing tumors that arise from cells of the anterior pituitary. |
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Primary Hypopituitarism
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can result from a primary tumor, trauma, infections, stroke, or surgical removal.
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Pituitary Adenoma Expansion causes what
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Causes both neurologic and secretory effects. Pressure from the expanding tumor causes hyposecretion of cells, dysfunction of the optic chiasma, and dysfunction of the hypothalamus and some cranial nerves.
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Hypersecretion of growth hormone in adults causes?
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acromegaly, in which growth hormone secretion becomes high and unpredictable. Pituitary adenoma is the most common cause of acromegaly.
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Growth Hormone high levels leads to what
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prolonged, abnormally high levels of growth hormone lead to proliferation of body and connective tissue and slowly developing renal, thyroid, and reproductive dysfunction.
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Prolactinomas results in?
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galactorrhea, hirsutism, amenorrhea, hypogonadism, and osteopenia.
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Thyrotoxicosis
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is a general condition in which elevated thyroid hormone levels cause greater than normal physiologic responses. The condition can be caused by a variety of specific diseases, each of which has its own pathophysiology and course of treatment.
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Hyperthyroidism
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has a range of endocrine, reproductive, gastrointestinal, integumentary, and ocular manifestations. These are caused by increased circulating levels of thyroid hormone and by stimulation of the sympathetic division of the autonomic nervous system.
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Graves Disease
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the most common form of hyperthyroidism, is caused by an autoimmune mechanism that overrides normal mechanisms for control of thyroid hormone secretion and is characterized by thyrotoxicosis, ophthalmopathy, and circulating thyroid-stimulating immunoglobulins.
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Toxic Nodular Goiter and Toxic Multinodular Goiter
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occur when thyroid hormone-regulating mechanisms and abnormal hypertrophy of the thyroid gland cause hyperthyroidism.
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Toxic multinodular goiter
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caused by independently functioning follicular cell adenomas.
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Thyrotoxic crisis
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a sever form of hyperthyroidism that is often associated with physiologic or psychologic stress. Without treatment, death occurs quickly.
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Primary Hypothyroidism
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caused by deficient production of thyroid hormone by the thyroid gland.
characterized by an increased thyroid-stimulating hormone, which stimulates goiter formation. |
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Secondary Hypothyroidism
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caused by hypothalamic or pituitary dysfunction. Symptoms depend on the degree of thyroid hormone deficiency.
Common manifestations include decreased energy metabolism, decreased heat production, and myxedema. |
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Autoimmune thyroiditis
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known as Hashimoto disease, is associated with humoral and cellular autoimmune destruction of the thyroid and gradual loss of thyroid function. occurs in those individuals with genetic susceptibility to an autoimmune mechanism that causes thyroid damage and eventual hypothyroidism.
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Subacute Thyroiditis
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self-limiting nonbacterial inflammation of the thyroid gland. The inflammatory process damages follicular cells, causing leakage of T3 and T4. Hyperthyroidism is then followed by transient hypothyroidism
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Transient Hypothyroidism
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corrected by cellular repair and a return to normal levels in the thyroid.
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Myxedema
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sign of hypothyroidism caused by alterations in connective tissue with water-binding proteins that leads to edema and thickened mucous membranes.
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Myxedema Coma
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sever form of hypothyroidism that may be life-threatening without emergency medical treatment.
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Congenital Hypothyroidism
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absence of thyroid tissue during fetal development or defects in hormone synthesis
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Thyroid carcinoma
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is a relatively rare cancer. Most consistent causal risk factor associated with thyroid carcinoma is exposure to ionizing radiation, especially in childhood.
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Hemolytic Anemia
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Infections of the newborn, often acquired by the mother and transmitted to the infant
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Sickle Cell Disease
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is a genetically determined defect of hemoglobin synthesis inherited by an autosomal recessive transmissionl it causes a change in shape of a red blood cell that results in decreased oxygen or hydration.
Most common among African or Mediterranean descent |
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Thalassemias
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Heterogeneous gruop of hereditary hypochromic anemias of varying severity.
Basic genetic defects include abnormalities of messenger-ribonucleic acid processing or deletion of genetic materials, resulting in a decrease in the chains for hemoglobin |
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Hemophilia
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is a condition characterized by impairment of the coagulation of blood and a subsequent tendency to bleed. The classic disease is hereditary and limited to males, being transmitted through the female to the second generation.
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Acquired Antibody-Mediated Hemorrhagic Diseases
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Idiopathic Thrombocytopenic purpura(ITP), transient neonatal thrombocytopenia, and autoimmune vascular purpura
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Idiopathic thrombnocytopenic purpura
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The most common of the childhood thrombocytopenic purpura. Is a disorder of platelet consumption in which antiplatelet antibodies bind to the plasma membranes of platelets.
Results in platelet sequestration and destruction by mononuclear phagocytes at a rate that exceeds the ability of the bone marrow to produce them |
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Childhood leukemias include
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Acute lymphoblasic, acute myeloblastic, and the very rare chronic myelocytic leukemia
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Acute lymphoblasic leukemia
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potentially curable disease, with about 80 percent of cases cured.
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Lymphomas of childhood are
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Hodgkin lymphoma and non-Hodgkin lymphoma
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non-Hodgkin lymphoma
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origin is unknown. Factors that ahve been implicated include defective host immunity, a viral agent, chronic immunostimulation, and genetic predisposition
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Hodgkin lymphoma
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Is thought to be caused by a yet unidentified etiologic agent.
In children is a readily curable disease with a 90 percent survival rate in children wtih limited disease and a 70 to 90 percent survival rate in those with advanced disease |
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Hyperparathyroidism
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May be primary or secdonary,is characterized by greater than normal secretion of parathyroid hormone.
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Primary hyperparathyroidism
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is caused by an interruption of the normal mechanisms that regulate calcium and parathyroid hormone levels.
Manifestations include chronic hypercalcemia, increased bone resorption, and hypercalciuria |
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Secondary hyperparathyroidism
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is a compensatory response to hypocalcemia and often occurs with chronic renal failure and vitamin D deficiency
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Hypoparathyroidism
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defined as abnormally low parathyroid hormone levels, is caused by thyroid surgery, autoimmunity or genetic mechanisms.
the lack of circulating parathyroid hormone causes depressed serum calcium levels, increased serum phosphate levels, decreased bone resorption and hypocalciuria |
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Diabetes Mellitus
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a group of disorders characterized by glucose intolerance, chronic hyperglycemia, and disurbances of carhoydrate, protein and fat metabolism.
A diagnosis is based on elevated plasma glucose concentrations and measurement of glycosylated hemoglobin. |
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Type 1 Diabetes Mellitus
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characterized by loss of beta cells, islet cell antibody, a lack of insulin and excess of glucagon, which causes improper metabolism of fat, protein and carbohydrates.
Seems to be caused by a gradual process of autoimmune destruction of beta cells in genetically susceptible individuals. Hyperglycemia causes polyuria and polydipsia resulting from osmotic diuresis |
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Ketoacidosis
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is caused by increased levels of circulating ketons without the inhibiting effects of insulin.
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Type 2 diabetes mellitus
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is caused by genetic susceptibility that is triggered by environmental factors. Most compelling environmental risk is obesity
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Gestational diabetes
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is glucose intolerance during pregnancy.
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Acute comlications of diabetes mellitus include
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hypoglycemia, diabetic ketoacidosis, and hyperosmolar hyperglycemic nonketotic syndrome
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hypoglycemia in diabetes
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is a comlication related to insulin treatment
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Diabetic ketoacidosis
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develops when there is an absolute or relative deficiency of insulin and an increase in the insulin counterregulatory hormones of catecholamines, cortisol, glucagon, and growth hormones
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Hyperosmolar hyperglycemic nonketotic syndrome
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is a pathophysiologically similar to disbetic ketoacidosis, although levels of free fatty acids are lower in hyperosmolar nonacidotic disbetes and lack of ketosis indicates that some level of insulin is present.
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Somogyi Effect
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is a combination of hypoglycemia with rebound hyperglycemia
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Dawn phenomenon
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is an early morning rise in glucose levels caused by nocturnal elevations in growth hormone
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Chronic complications of diabetes mellitus include
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microvascular disease, macrovascular disease and infections
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Microvascular disease
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characterized by thickening of the capillary basement membrane and eventual decreased tissue perfustion affecting the microcirculation
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Macrovascular disease
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associated with diabetes mellitus is most often related to the proliferation of atherosclerotic plaques in the arterial wall
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Cortical hyperfunction, or hypercotisolism
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causes Cushing disease, which does not involve the pituitary gland and Cushing disease, which is hypercortisolism with pituitary involvement
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Hypercortisolism
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is usually caused by Cushing disease and very rarely can be caused by ectopic production of adrenocorticotropic hormone. Complications include obesity, diabetes, protein wasting, immune suppression, and mental status changes
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Excessive aldosterone secretion
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causes hyperaldosteronism, which may be primary or secondary.
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Primary hyperaldosteronism
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is caused by an abnormality of the adrenal cortex.
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Secondary hyperaldosteronism
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involves an extra-adrenal stimulus, often angiotensin
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Hyperaldosteronism
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promotes increased sodium reabsorption, corresponding hypervolemia, increased extracelluar volume, hypokalemia related to renal reabsorption of sodium and excretion of potassium
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Hypersecretion of adrenal androgens and estrogens
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can be a result of adrenal tumors, either adenomas or carcinomas.
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Hypersecretion of estrogens
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causes feminizatio, the development of female sex characteristics.
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Hypersecretion of androgens
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causes virilization, the development of male sex characteristics
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Hypofunction of the adrenal cortex
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can affect glucocorticoid or mineralocorticoid secretion or both.
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Hypofunction
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can be caused by a deficiency of adrenocorticotropic hormone or by a primary deficiency in the gland itself
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Hypocortisolism
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or low levels of cortisol, is caused by inadequate adrenal stimulation by adrenocorticotropic hormone or by primary cortisol hyposecretion.
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Primary adrenal insufficiency
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is termed Addison disease
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Addison disease
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is characterized by elevated adrenocorticotropic hormone levels with inadequate corticosteroid synthesis and output.
Manifestations are related to hypocortisolism and hypoaldosteronism. Symptoms include weakness, fatigability, hypoglycemia and related metabolic problems, lowered response to stressors, hyperpigmentation, vitiligo, and manifestations of hypovolemia and hyperkalemia. |
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Hyperfunctions of the adrenal medulla
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is usually caused by a pheochromocytoma, a carecholamine-producing tumor. Symptoms of catecholamine excess are related to the sympathetic nervous system effects and include hypertension, palpitations, tachycardia, glucose intolerance, excessive sweating and constipation
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