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Nurs5315 Exam_1_Study_Guide_Objective
Altered Cellular Biology - Class Objectives Explain adaptive responses of cells in terms of cellular structure and function. (including atrophy, hypertrophy, hyperplasia, metaplasia)-
- Cell adaptation: o Adaptation is a process and on a continuum. o Reversible process. Cell structure may change or functionality changes. o o Intent is to be temporary. If permanent, it becomes pathophysiologic. o Example: In heart failure, initial stress causes hypertrophy; CHF, stress is continuous and ongoing, structural functions changes and the condition becomes pathophysiologic. o When the cell is overwhelmed (unable to reverse cellular change), it changes, gets injured and dies.
- Atrophy: decrease in cell size d/t lack of use or reduced oxygen (muscle wasting d/t atrophy). Think small ER>less mitochondrion>less proteins. E.g. casted limb.
- Hypertrophy : increase in cell size d/t overwork or growth factors. Stress signals growth factors.
- Hyperplasia: increase in number of cells d/t either more cell division or cellular injury. May be compensatory (wound healing) or hormonal (prolactin in pregnancy), or pathologic (cancer cell). E.g. cervical hyperplasia,
- Metaplasia: reversible replacement. Replacement of one cell by another. Metaplastic cells can be cancerous. Imposter cells don’t do anything (doesn’t do what the original cell did) e.g. in the epithelium. Can be cancerous.
- Dysplasia: is not normal. Change in cell size,
shape and differentiation. Can be cancerous.
- Oxidative Stress: overwhelm the antioxidant enzymes.
- Free Radicals: reactive free radicals damage the mitochondria/cell membrane Describe how cells manifest injury.
- Cellular manifestations ; o Accumulation/infiltration: normal cellular substance (water, protein, lipid & carbohydrate excess) or abnormal substance (endogenous-abnormal metabolism, exogenous-infectious agents or a mineral). o Calcium-calcification. o Urate-cellular crystal calcification.
- Systemic manifestations: o Fatigue, malaise, loss of well-being, alteration in appetite. Fever. o Table 2.12 p. 88 Huether & McCance. Compare/contrast cell death "mechanisms" - cell necrosis, infarction, apoptosis, autophagy.
- Necrosis : pathological death. o Steps: Intracellular contents breakdown the cell à cell membrane breaks down à cell swells à intracellular contents spill out à affect cells around it with non-detox contents. o May be result of irreversible injury or programmed cell death.
- Apoptosis: Physiologic cell death, no swelling, hence they don’t release their cellular contents until they are detoxed and metabolized properly by the lysosomes. Not toxic! Cells die when they are supposed to die. Active process of self- destruction.
- Autophagy: Survival strategy. “Cell eating”. o May become destructive if this process continues (priority cells would then start breaking down). o IDEA : Cells wants to “recycle” non-priority cells before they undergo apoptosis.
➢ Cellular destruction, dissolution ➢ Result of irreversible injury or programmed. ✓ Cell infarction: area of coagulative necrosis ✓ Apoptosis: programmed cell death (physiologic, not toxic environment). Active process of self- destruction. ✓ Autophagy: survival strategy or may be destructive. Priority cells might be eaten as well. ❖ Discuss how action potentials support cellular function.
✓ Allows cell communication
✓ Movement of cations between ICF & ECF.
✓ Cell-cell communications = transmission & conduction of
nerve and cardiac impulses, muscle contraction.
✓ Resting potential, action potential, threshold
potential, depolarization, repolarization.
✓ Na and K pump (requires ATP) functions to move ions
across the cell membrane, regain resting potential following polarizing changes. ❖ Determine how potassium and calcium disorders alter action potential physiology. ✓ K-deficiency, cells are less excitable and vice versa (less K+, less Excitability (weakness). Influences resting membrane potential. ✓ Less Ca++, increased excitability and vice versa. Influences threshold potential. ✓ Low K+, increased C++> takes a bigger stimulus. Inflammation Chapter 7 Class Objectives:
❖ Describe the physiology of vascular, plasma protein, and cell mediator responses contribution to the inflammatory response. ✓ Vascular Response: S/S, redness, heat, swelling & pain d/t changes in small vascular structures. ➢ Vasodilation, increased permeability, WBCs move to & through vessel walls. ➢ Vascular response delivers other response materials & removes wastes from area. ➢ Important role in adaptive immunity (B & T lymphocytes); use of lymphatics to clear are of debris. ✓ Plasma Protein: complement- can cause direct destruction or activate other components. ➢ Classical pathway: antigen-antibody-complement complex. C3 and C5 covertase Enzyme. C3 and C covertase Enzyme. ➢ Activate one, subsequent activation of the rest; leads to cell lysis. ➢ Clotting factors- prevent spread to nearby tissues, trap ‘invaders’, hemostasis, repair/healing. ➢ Kinins (bradykinin)- vasodilation, vascular permeability, smooth muscle contraction, nerve cell stimulation, leukocyte chemotaxis. Cell travels to the injury site. ✓ Cell mediator Responses: activated by plasma protein systems & during cell destruction. ➢ Ligand binds to cell receptors, activates IC signals and cell activation. ➢ Cell receptors may recognize patterns, products of cell damage, complement. ❖ Explain the importance of cytokines – physiologically and pathophysiologically – in the inflammatory response. Include
❖ Explicate the importance and role of mast cells and histamine in the inflammatory response.
✓ Mast cells: Can participate in both acute & chronic
inflammatory responses. ➢ Activated by large stimuli. ➢ Released in response to heat, chemical agents, via immunologic activations, bacteria and virus acting on receptors. ➢ Released by degranulation or via synthesis of new mediators. ➢ Release chemotactic factors (neutrophil & eosinophil factors). ➢ Synthesize new mediators (leukotrienes, prostaglandins, platelet-activating factor.
✓ Histamine: H1 (pro), & H2 (anti) receptors.
➢ Vasoconstricting (large vessels) & vasodilating (small venule) effects- increase microcirculation. ➢ Increase vascular permeability. ➢ Histamine release is dependent upon the location of the need. ❖ Identify the role of specific phagocytes – neutrophils, eosinophils, basophils, monocytes, natural killer cells.
✓ Neutrophils: early inflammation, engulf bacteria, dead cells,
debris; ➢ Look for in bacteria responses.
✓ Eosinophils: Engulf parasites, regulate mast cell
vascular mediators; ➢ Look for in allergic reactions.
✓ Basophils: source IL- 4
➢ Seen w/ allergic responses.
✓ Monocytes: initiate cellular inflammatory response.
➢ arrive later for long haul defense and for wound healing.
✓ Natural Killer cells: recognize & eliminate virus, some
cancer cells. ❖ Describe the physiologic process of phagocytosis.
✓ Phagocytosis: recognition & attachment of the particle
to the ingesting leukocyte. ➢ Engulfment w/ subsequent formation of a phagocytic vacuole. ➢ Killing & degradation of ingested material. ➢ Recognize & adhere > engulf (ingest) > fuse (‘connect’ w/ lysosome granules) > destroy target. ❖ Describe how acute inflammation manifests.
✓ Fever: IL-1 released by neutrophils, macrophages
➢ Pyrogens act on hypothalamus to control temperature. ➢ Less sensitive, responsive in elders.
✓ Leukocytosis:
➢ ‘Left shift’- represents immature cells (especially bands) in circulation.
✓ Synthesis of plasma proteins:
➢ Most produced by liver – acute phase reactants. ➢ C reactive protein, fibrinogen, ferritin. Immunity and Immune System Chapter 8 &Chapter 9. Class Objectives: Immunity & Immune system Differentiate between active and passive immune responses; innate and adaptive or acquired immunity. ❖ Innate immunity – non specific – immediate – no memory o 1 st^ line (Physical, mechanical, biochemical barriers) o 2 nd^ line (Inflammatory response)
➔ Passive Immunity – no hose immune system response; provided. Only temporary
- Mom to fetus ➔ Acquired – produced after exposure to antigen or immunization; long term. Identify the key concepts of adaptive immunity – including antigen recognition, antibody production , and antigen presenting cells , lymphocyte production, and major histocompatibility complex.
- Antigen recognition (done through the following molecules)
- Antibody / Immonoglobulin (IgA, IgM, IgE, IgD) – Can initiate the adaptive immune response.
- Antibody production: ✓ IgG – most abundant. Maternal IgG protects baby for the 1 st^ 6mo of life. ✓ IgA2 – most abundant in body secretions ✓ IgM – produced early in neonatal life, may be increased in response to utero infection. Largest ✓ IgE – allergy and against parasitic infection. 2) Antigen receptors on the surface of B & T lymphocytes ✓ BCR and TCR bind with antigen to produce lymphocyte activation.
- Antigen processing – refers to the process in which each antigen is linked with the appropriate MCH class. ✓ Phagocytic cells process antigens by putting them on the phagocyte’s surface where lymphocytes initiate immune response. ✓ Most antigens are processed by APCs and presented on the surface of highly specialized molecules of the MCH. (
o Dendritic cells: antigen-presenting cell on the surface of T cells o Macrophages: good at presenting antigen to memory T helper cells for rapid response. o B lymphocytes. ✓
- Lymphocyte production –Colonal diversity
- Major histocompatibility complex ✓ Glycoproteins found on the surface of all human cells except RBCs
- Antigen presenting – most antigens must be processed by ACPs and presented on the surface of MCH ✓ MCH 1 – endogeneous antigens ✓ MCH 2 – exogeneous antigens ✓ CD1 - Lipid antigens Differentiate between the role, maturation, and activation of T cells and B cells in adaptive immunity. Humoral response (plasma + antibodies) B cell activation. Differentiated B cell goes into lymph nodes (secondary lymphoid organ) and comes out as a plasma cell. Each plasma cell is antigen specific. Primary immune response:
- 1 st^ exposure, production of IgM (in about 7 days) and IgG (shortly after). Levels gradually decrease. Secondary (anamnestic) immune response:
- 2 nd^ exposure, antibody produced quickly (bc of memory cells, larger amounts—Specially IgG. Levels remain
- B cells less responsive to new antigens; poor recall of previously recognized antigens
- Concept of “inflammaging” – link between chronic illness and chronic inflammation. Explain the difference between the processes and purpose of the primary and secondary immune responses. Congenital (primary) VS. Acquired (secondary).
- Primary deficiencies –from a genetic defect that disrupts lymphocyte development. o Generally present as repeated infections early in life. o May be B cell (decreased immonoglubulins) o T cell (fail to differentiate) o Complement (reccurent bacterial infections), failure of phagocytosis combined.
- Secondary deficiencies – those that are due to a secondary disease or other physiologic alterations. o Often due to therapy or illness i.e. HIV. Explain the mechanisms of immune system function/dysfunction in allergic responses, organ transplant rejection, and systemic lupus erythematous. Hypersensitivity
- Allergy: exaggerated response
- Autoimmunity: against the host
- Alloimmunity: against beneficial foreign tissues (transplant, transfusion). Deficiencies
- Congenital (Primary) – from genetic anomaly
- Acquired (Secondary) – caused by another illness, most common type of deficiency.
Summarize the effects of stress, nutrition, malignancy and health care therapies on the immune system. ❖ Stress – decreases adhesion molecules and decreased neutrophils chemotaxis ❖ Nutrition – Malnutrition is the predominant cause for secondary immune deficiencies. Protein synthesis trace minerals (zinc) needed for enzyme production. Vit A, C, E, B12 needed for T and B cell function. ❖ Malignancy – produce cytokines and vascular endothelial growth factors. ❖ Therapy induced – treatments (especially cancer therapies) target health and abnormal cells; opportunist infections, steroid therapy. Hematopoietic System - Class Objectives Differentiate among microcytic, normocytic, and macrocytic anemias (including examples of each) Microcytic Anemia (MCV <80) → characterized by abnormally small erythrocytes that contain abnormally reduced amounts of hemoglobin. Iron Deficiency Anemia → most common anemia that typically results from blood loss (ex. gastric ulcers, menorrhagia) or malabsorption (ex. Crohns, Gastric Bypass or poor dietary iron intake). It is often seen in children during growth periods, such as infancy and adolescence. Manifestations include cognitive impairment (if developed as an infant and left untreated), concave fingernails, and glossitis. Serum ferritin is completed to determine diagnosis. Thalassemia → inherited autosomal recessive disorder in which there is an overproduction of abnormal hemoglobin. The fundamental defect in beta- thalassemia is the uncoupling of alpha and beta chain synthesis of Hemoglobin A (primary polypeptide chain). This is most commonly seen in people of Eastern European descent. It causes mild hemolytic anemia,
Manifestations include pallor, mouth ulcerations, as well as high risk of infection, bleeding, and death
Sickle Cell Anemia → genetic autosomal recessive (get the gene from both parent) anemia that is characterized by the presence of an abnormal form of hemoglobin. If there is only one gene present, then the patient will only be a carrier for the disorder and have no manifestations of the disease. It is most common in African American. It is characterized by exacerbations, called sickle cell crisis, in which the body is triggered by infection, dehydration, hypoxia, or stress. It often presents as a vaso-occlusive crisis with acute pain (typically in large joints such as the knees), potentially pulmonary infiltrate, and acute pulmonary injury. There is an increased risk for CVA or MI if the abnormal cell blocks blood flow to the brain or heart. (Normocytic- normochromic). Anemia of Chronic Illness (Normocytic-Normochromic) → anemia that is seen secondary to chronic infection or inflammation. This anemia can occur at any age group and can present as microcytic or normocytic. Iron deficiency can be a complication so need to monitor serum ferritin. Goal is to treat the primary disorder_. Microcytic only when iron-deficiency occurs._
- Look for decreased Iron, less or more ferritin. Macrocytic Anemia (MCV >100) → characterized by unusually large stem cells (megaloblasts) in the marrow that mature into erythrocytes that are large in size. Folate Deficiency Anemia → anemia that is caused by a malabsorption or dietary deficiency. Folate is the essential vitamin for RNA and DNA synthesis within the maturing erythrocyte. It is typically seen in the elderly and in those that abuse alcohol. Folate is found in fruits and vegetables. There is a risk associated during pregnancy as it can lead to neural tube defects in the fetus. Another complication is seen with aspirin (often utilized in geriatric population), because it competes with folate and can cause a deficiency. Specific manifestations include cheilosis and mouth ulcers. Testing to determine is done by measuring the serum folate level.
