Patho for Primary Care, Module 1A
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| Atrophy | decrease in cell size
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| Most significant adaptive changes in cells include... | atrophy, hyperplasia, metaplasia
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| hyperplasia | increase in number of cells
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| metaplasia | reversible replacementof one mature cell type by another less mature cell type
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| dysplasia (deranged cellular growth) is not ........... | considerred a true adaptation, but an atypical hyperplasia
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| Etiology of pathologic atrophy | decrease in workload
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| Etiology of Physiologic atrophy | Occurs in early development. e.g. thymus gland in childhood.
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| myofilaments | part of muscle fiber which causes muscle contraction
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| autophagy | self-eating process creating autophagic vacuoles
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| autophagic vacuoles | membrane bound vesicles within the cell that contain cellular debris - small fragments of mitochondria and endoplasmic reticulum-and hydrolytic enzymes.
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| Hypertrophy | Increase in the size of the cell
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| Hypertrophy is associated with.... | increase in accumulationj of protien in the cellular components, not cellular fluid.
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| WOuld hypertrophy in the heart secondary to HTN be pathologic of physiologic? | Pathologic
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| Where does hypertrophy appear as an adaptive response | Heart and striated muscles as they cannot react by mitotic division and production of new cells to share the work.
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| physiologic hypertrophy occurs where | skeletal muscle in relation to heavy work
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| Cardiac hypertrophy causes what peptide to be re-introduced? | ANP - atrial natriuretic peptide (causes salt secretion by kidney, decreasing blood volume and pressure, and reducing hemodynamic load.
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| COmpensatory hyperplasia | Allows certain organs to regenerate
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| Which cells do not regenerate? | nerve cells, lens cells of the eye, skeletal muscle cells, myocardial cells
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| Cellular injury is caused by | a lack of oxygen (hypoxia), free radicals, caustic or toxic chemicals, infectious agents, unintentional and intentional injury, inflammatory and immune responses, genetic factors, insufficient nutrients, or physical trauma from many causes.
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| List the manifestations of cellular injury. | General sense of fatigue and malaise
A loss of well being
Altered appetite
fever
increased heart rate
increase in leukocytes (because of infection)
pain
presence of cellular enzymes
lactate dehydrogenase
creatine kinase
aspartate aminotransfe
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| What are the 2 main types of cell death? | necrosis and apoptosis
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| Necrosis | Necrosis is the sum of the changes after local cell death and includes the processes of inflammation and cellular lysis.
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| The 4 major types of necrosis are: | coagulative, liquefactive, caseous, and fat. Different types of necrosis occur in different tissues
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| What are the structural signs that indicate irreversible injury and progression to necrosis? | the dense clumping and disruption of genetic material and the disruption of the plasma and organelle membranes.
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| Gangrene necrosis/gangrene | tissue necrosis caused by hypoxia and subsequent bacterial invasion.
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| Apoptosis | a different type of cellular death, is a process of selective cellular self-destruction called programmed cell death.
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| Describe the water distribution in the human body. x 6 | Body fluids are distributed among functional compartments and are classified as ICF or ECF
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| The sum of all fluids is... | The sum of all fluids is the TBW, which varies with age and amount of body fat.
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| Water moves b/w the ___ and ___ compartments principally by _________. | Water moves between the ICF and ECF compartments principally by osmosis.
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| How does water move b/w the plasma and interstitial fluid? | Water moves between the plasma and interstitial fluid by osmosis and hydrostatic pressure, which occur across the capillary membrane.
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| What is movement across the capillary wall called and how is it described? | Movement across the capillary wall is called net filtration and is described according to the Starling law.
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| What is edema? | Edema is a problem of fluid distribution that results in accumulation of fluid within the interstitial spaces.
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| What is edema caused by? | caused by arterial dilation, venous or lymphatic obstruction, loss of plasma proteins, increased capillary permeability, and increased vascular volume
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| The pathophysiologic process that leads to edema is related to... | related to an increase in forces favoring fluid filtration from the capillaries or lymphatic channels into the tissues
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| The pathophysiologic process that leads to edema may be | localized or generalized and usually is associated with weight gain, swelling and puffiness, tighter-fitting clothes and shoes, and limited movement of the affected area.
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| How are alterations in water balance classified? | Alterations in water balance may be classified as isotonic, hypertonic, or hypotonic.
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| When do isotonic alterations occur? | Isotonic alterations occur when changes in TBW are accompanied by proportional changes in electrolytes.
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| When do hypertonic alterations develop? | Hypertonic alterations develop when the osmolality of the ECF is elevated above normal, usually because of an increased concentration of ECF sodium or a deficit of ECF water.
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| What may be the cause of water deficit? | Water deficit, or hypertonic dehydration, is rare but can be caused by lack of access to water, pure water losses, hyperventilation, arid climates, or increased renal clearance.
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| Discuss the etiology and clinical manifestations of hyperchloremia | Hyperchloremia is caused by an excess of sodium or a deficit of bicarbonate.
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| Discuss the etiology and clinical manifestations of hypernatremia | (sodium levels >147 mEq/L) may be caused by an acute increase in sodium or a loss of water.
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| Discuss the etiology and clinical manifestations of Hyponatremia | (serum sodium concentration <135 mEq/L) usually causes movement of water into cells.
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| What is hyponatremia caused by? | caused by sodium loss, inadequate sodium intake, or dilution of the body’s sodium level.
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| Water excess | rare but can be caused by compulsive water drinking, decreased urine formation, or the syndrome of inappropriate secretion of ADH.
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| causes of metabolic acidosis | an increase in noncarbonic acids or loss of bicarbonate from the extracellular fluid.
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| clinical manifestations of metabolic acidosis | HA, lethargy, coma, Kussmaul respirations, anorexia, n/v, diarrhea, abd discomfort,
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| S/S of severe metabolic acidosis | disrythmias, hypotension, death
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| Causes of metabolic acidosis | an increase in bicarbonate usually caused by loss of metabolic acids from conditions such as vomiting, gastrointestinal suctioning, excessive bicarbonate intake, hyperaldosteronism, and diuretic therapy
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| Clinical manifestations of Metabolic alkalosis | muscle cramps, hyperactive reflexes r/t volume depletion, weakness, parasthesas, numbness/tingling of fingertips & perioral area, tetany, seizures; Slow, shallow respirations= + CO2 = confusion, convulsions
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| S/S of severe Metabolic alkalosis | atrial tachycardia, dysrhythmias
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| Causes of Respiratory Alkalosis | occurs with alveolar hyperventilation and excessive reduction of carbon dioxide, or hypocapnia
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| Clinical manifestations of respiratory alkalosis | dizziness, confusion, tingling of extremities, convulsions, coma, carpopedal spasm, tachypnea
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| Causes of respiratory acidosis | decrease of alveolar ventilation and an increase in levels of carbon dioxide, which in turn causes hypercapnia.
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| Initial s/s of respiratory acidosis | HA, restlessness, blurred vision, apprehension. Respiratory rate is initially rapid and gradually becomes depressed.
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| initial s/s of respiratory acidosis are followed by... | Lethargy, muscle twitching, tremors, convulsions, coma
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| List the human defense mechanisms | Innate immunity includes natural barriers and inflammation.
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| Natural barriers include... | physical, mechanical, and biochemical barriers at the body's surface
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| Name the physical and mechanical barriers as the first lines of defense | skin and mucous membranes
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| Name biochemical barriers as first lines of defense against invading pathogens | Antibacterial peptides in mucous secretions, perspiration, saliva, tears, and other secretions
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| What role do Cathelicidins and defensins play in the first line of defense? | two classes of antimicrobial peptides produced by epithelial cells.
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| How do normal bacterial flora fit into the first line of defense? | provide protection by inhibiting colonization by pathogens and by releasing chemicals that prevent infection.
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| Does inflammation have memory cells? | no
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| What does the vascular response in acute inflammation include? | vasodilation, increased capillary permeability, and white blood cell adherence to inner vessel walls and their migration through vessel walls.
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| What are the 3 plasma protien systems which provide a biochemical barrier against invading pathogens in the circulation? | complement system, clotting system, kinin system
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| What 3 pathways can the complement proteins be activated in? | the classical pathway, the alternative pathway, and the lectin pathway.
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| Activation of the complement pathways results in ..... | opsonization, activation of anaphylatoxins, cell lysis, and leukocyte chemotaxis.
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| The clotting cascade (coagulation) prevents... | spread of microorganisms, contains
microorganisms and foreign bodies at site of greatest inflammatory cell activity, and provides a framework for repair and healing.
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| What do the kinin system proteins promote? | vasodilation and increased capillary permeability and induce pain.
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| Plasmin and Hageman factor (factor XII) interact to.... | activate the clotting cascade, the complement system, and the kinin proteins.
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| What are some of the inhibitors in the plasma proteins? | carboxypeptidase, histaminases, kinases, and C1 esterase inhibitor.
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| What are the types of cells involved in the inflammatory process? | mast cells, neutrophils, monocytes/macrophages, eosinophils, NK cells, platelets, and nonleukocytic cells.
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| What are the names of the 5 biochemical mediators that are responsible for the vascular changes associated with inflammation and for modulating thelocalization and activities of other inflammatory cells? | histamine, chemotactic factors, leukotrienes, prostaglandins, and platelet-activating factor
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| Inflammatory response is intiated upon... | tissue injury or when PAMPs are recognized by PRRs on cells of the innate immune system.
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| What do the PRRs include? | TLRs, complement, scavenger, glycan, and mannose receptors
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| What do the TLRs recognize? | PAMPs, complement receptors recognize complement fragments, and scavenger receptors promote phagocytosis.
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| What do the central cells of inflammation release? | histamine, chemotactic factors, cytokines, leukotrienes, prostaglandins, growth factors, and other mediators
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| What do H1 histamine receptors promote? | inflammation
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| What do H2 histamine receptors do? | inhibit the inflammatory response
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| What is phagocytosis? | the destruction of microorganisms and cellular debris
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| What are the stages of phagocytosis? | recognition and adherence, engulfment, lysosomal fusion, and destruction.
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| phagocytic killing can be... | oxygen-dependent with the production of reactive oxygen intermediates or oxygen-independent with lysosomal enzymes.
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| Basophils | granulocytes that are very similar to mast cells
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| Cytokines | soluble factors that regulate the inflammatory response and include interleukins, interferons, and tumor necrosis factor.
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| What are ILs? | biochemical messengers primarily produced by macrophages and lymphocytes and significantly help regulate the inflammatory response.
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| What do INFs do? | provide protection from viral infection in uninfected cells
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| Tumor necrosis factor | is primarily produced by macrophages and promotes inflammation with both local and systemic effects.
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| Chemokines | synthesized by a number of different cells and induce leukocytes chemotaxis, and are classified as either CC or CXC, depending on their amino acid arrangement.
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| CC chemokines | affect monocytes, lymphocytes, and eosinophils.
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| CXCchemokines | generally affect neutrophils.
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| Complement proteins can be activated in what 3 pathways? | classical, alternative, lectin
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| Activation of the complement pathway results in: | opsonization, activation of anaphylatoxins, cell lysis, and leukocyte chemotaxis
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| The clotting cascade prevents... | spread of microorganisms, contains
f) microorganisms and foreign bodies at site of greatest inflammatory cell activity, and provides a framework for repair and healing.
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| Kinin system proteins promote... | vasodilation and incrased capillary permiability and induce pain.
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| Neutrophils | the predominant phagocyte of early inflammation. They are attracted to the inflammatory site by chemotactic factors.
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| Monocytes/Macrophages | arrive at the inflammatory site later than neutrophils and remain longer to clean up debris and promote wound healing
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| Eos | help control mast cell vascular mediators and defend against parasite infection
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| NK cells | Recognize and eliminate viruses, cancer cells, and other abnormal cells.
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| Platelets | interact with the coagulation cascade to stop bleeding and release a number of mediators that promote and control inflammation.
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| Cytokines | soluble factors that regulate the inflammatory response and include interleukins, interferons, and tumor necrosis factor
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| Local manifestations of acute inflammation are.... | the result of vascular changes associated with the inflammatory processk including vasodilation and increased cap permeability.
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| S/S of local manifestations of acute inflammation | redness, heat, swelling, pain
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| Fx of vascular changes r/t acute inflammation are: | to dilute toxins, carry plasma proteins and leukocyts tothe injury site, carry bacterial toxins and debris away from the site.
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| Sytemic manifestations of acute inflammation are: | fever, leukocytosis, and increase in levels of circulating plasma proteins.
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| Chronic inflammation is characterized by... | a dense infiltration of lymphocytes and macrophages. The body may wall off and isolate the inf to protect against tissue damage by formation of a granuloma
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| Resolutioin (regeneration) | return of tissue to nearly normal structure and fx
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| Repair | healing by scar tissue formation
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| Healing by Primary Intention | Inflammatory lesions proceed to resolution, meaning original tissue structure and fx have been restored if little tissue has been lost or injured tissue is capable of regeneration.
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| Mast cells are found in what parts of the body? | skin, GI system, lining of respiratory system
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| What are the causes of mast cell activation? | Physical injury,chemical agents, Immunologic means (anaphylatoxins), activation of TLRs by bacteria and viruses, allergic reaction
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| What is the mast cell's response to stimuli? | release of histamine, chemotactic factors, cytokines
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