NUR 631 Midterm Study Guide: Cell Biology, Genetics, Immunology, Fluids, Exams of Nursing

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This study guide provides a content outline that can be used to prepare for the topic quiz. This outline may not be inclusive of all quiz content. Cellular biology and Alterations  Compensatory hyperplasia after partial resections (mod 1) (51-53)  Ex: liver, hepatocyte growth  Adaptive mechanism that enables certain organs to regenerate  Even with removal of 70% of the liver, it will regenerate within about 2 weeks  Compensatory hyperplasia occurs in epidermal, intestinal epithelia, hepatocytes, bone marrow and fibroblasts. Some type off hyperplasia is noted in bone, cartilage and smooth muscles – Example- callus, wound healing as part of inflammation process  Tumor progress from benign to malignant (364-366)  Benign tumors are usually encapsulated and well differentiated. They retain some normal tissue structure and do not invade the capsules surrounding them or spread to regional lymph nodes or distant locations. ▪ Generally named according to the tissues from which they arise, and include the suffix –oma.  Some benign tumors can progress to cancer and are then referred to as malignant. They have more rapid growth rates and specific microscopic alterations, including loss of differentiation and absence of normal tissue organization. ▪ One hallmark is anaplasia – loss of cellular differentiation, irregularities of the size and shape of the nucleus, and the loss of normal tissue structure. ▪ May present with different degrees of encapsulation; some lack a capsule, and even if one is apparent, it’s integrity has been compromised so that tumor cells can grow to invade nearby blood vessels, lymph and surrounding structures. ▪ Most deadly characteristic is their ability to spread far beyond the tissue of origin – metastasis

 Testing ▪ Clinical Exam ▪ Chromosomal testing ▪ Hormones Immunology  Rickets disease (1599-1600)  Disorder in which growing bones fails to become mineralized, resulting in “soft” bones and skeletal deformity.  Results from insufficient vitamin D, insensitivity to vitamin D, wasting of Vitamin D by the kidney, or inability to absorb Vitamin D and calcium in the gut  Most common form is x-linked hypophosphatemic rickets in industrialized nations  In US it happens in children due to lack of dietary vitamin D – can lead to early fracture or slow bone healing after fracture  Can lead to short stature, bowing of the limbs with broad, irregular growth plates, often listless and irritable with hypotonia and muscle weakness may be unable to walk without support; abnormal parietal flattening and frontal bossing occur in the skull  Normalization of calcium, phosphorus, and vitamin D levels before surgical intervention, deformity often improves when bone metabolism improves  Hypocalcemia  Epstein-Barr Virus (318t, 1078-1079, 1011)  Adenovirus, herpesviruses – transmitted via saliva, disease: mono, burkitt lymphoma  Strongly associated with non-hodgkin lymphoma in children  EBV and African Burkitt Lymphoma  Etiologic agent for mono: EBV – ubiquitous, lymphotrophic, gamma- group herpesvirus accounting for approximately 85% of mono cases  Early EBV infections are usually asymptomatic and provide immunity to EBV later in life  Human Herpes Virus (HHV) 8 (382, 383, 1645)  Kaposi’s Sarcoma ▪ Commonly occurs in older men but now occurs in a markedly more virulent form in immunocompromised individuals (AIDS)  Linked to several rare lymphomas  Associated with cancer in humans  Member of Herpesviridae family

 Complement Cascade (197, 198f, 287f)  Activated by 3 pathways ▪ Classical pathway – activated by proteins of the adaptive immune system (antibodies) bound to their specific targets (antigens)

• Forms antigen-antibody complex (immune complex) ▪ Lectin pathway – activated by mannose-containing bacterial carbohydrates ▪ Alternative pathway – activated by gram-negative bacterial and fungal cell wall polysaccharides  C3 deficiency blocks all three pathways ▪ People with this deficiency are at risk for recurrent life-threatening infections with encapsulated bacteria at an early age, as well as a SLE-like syndrome that may be complicated by kidney disease (glomerulonephritis)  Passive-acquired immunity (227)  Aka passive immunity  Does not involve host’s response at all  Occurs when preformed antibodies or T lymphocytes are transferred from a donor to the recipient.  Can occur naturally as in the passage of maternal antibodies across the placenta to the fetus, or artificially, as in a clinic using immunotherapy for a specific disease  Temporary immunity  IgM and IgG and IgA and IgE (229-230, 247, 254-255)  IgA (p.229)- Fungal infection skin, GI tract, Mouth Vaginal ▪ IGA in breast milk, works at GI system  IgM (p. 229) - First antibody that produced during primary response to antigen. It synthesize early in neonatal life and may be increased as response to infection in utero  IgE (p.229) primary cause of common allergies (hay fever, dust, bee stings). Complement T helper cells and immune responses ▪ IgE bind to receptors on the surface of mast cells causing release of histamine H ▪ Protects from parasites/worms  IgG (p. 229) most abundant, 80-85%, most of protective activity against infections – selective transport across the placenta, maternal IgG is also the major class of antibody found in the blood of the fetus and newborn.  Bronchial constriction (2) Edema (3) Vasodilation (4) H2 (5) Increase gastric secretions (6) Decreases the release of histamine from mast cells and basophils  IgG, IgM, and IgA bind to the surface of parasites, activate complement, generate chemotactic factors for neutrophils and macrophages, and serve as

those phagocytic cells; unique to parasitic infections, the eosinophil is a primary cell in the granuloma  IgE-mediated hypersensitivity (263-265)  Type 1 reactions – most common allergies (i.e. pollen)  IgE can contribute to a few autoimmune and alloimmune diseases, and many common allergies (poison ivy) are not mediated by IgE.  Short life span in the blood  Individual is usually sensitized when exposed to antigen in future.  Histamine is the most potent mediator which affects several key target cells – contracts bronchial smooth muscles, causing bronchial constriction; increases vascular permeability, causing edema, and causes vasodilation, increasing blood flow into the affected area ▪ Interaction of histamine with H2 receptors results in increased gastric acid secretion and a decrease of histamine released from mast cells and basophils – action of histamine through H2 receptors suggests an important negative-feedback mechanism that stops degranulation  Mast cells are principal effector cells involved  SLE (Lupus) (mod 2) (277-278)  Antigen-antibody mediated  Type III hypersensitivity  Chronic, multisystem, inflammatory disease, most common, complex and serious of autoimmune disorders  Characterized by the production of a large variety of autoantibodies against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and many other self-components ▪ Most characteristic autoantibodies produced are against nucleic acids, histones, ribonucleoproteins, and other nuclear material  Occurs more often in women, age 20-  Clinical Manifestations: arthralgias or artiritis, vasculitis, rash, renal disease, hematologic abnormalities (anemia) ▪ Develops slowly and has frequent remissions and exacerbations  11 common clinical findings (dx based on serial or simultaneous presence of 4) ▪ Facial rash confined to cheeks (malar rash) ▪ Discoid rash (raised patches, scaling) ▪ Photosensitivity ▪ Oral or nasopharyngeal ulcers ▪ Nonerosive arthritis of at least two peripheral joints ▪ Serositis (pleurisy, pericarditis) ▪ Renal disorder (proteinuria) ▪ Neurologic disorder (seizure, psychosis)

▪ Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia) ▪ Immunologic disorders ▪ Presence of antinuclear antibody (ANA)  No cure, treat symptoms, and minimize autoimmune response – NSAIDS, Steroids, immunosuppressive drugs, IVIg ▪ Protect from sunlight Fluid and Electrolytes and Acid-base  Treatment of Hyperkalemia (mod 3) 119 o K+ > 5.  Renal Failure  Spironolactone  Hypoaldosteronism ▪ Addison’s Disease  Burns/Cell lysis  Hemolytic Anemia's  Rhabdomyolysis  Acidosis  Insulin Deficiency  Signs and Symptoms ▪ Tingling, cramps/diarrhea ▪ Weakness  Flaccid Paralysis ▪ Arrhythmias  Cardiac Arrest  Should be investigated when there is a history of renal disease, massive trauma, insulin deficiency, Addison disease, use of potassium salt substitutes, or metabolic acidosis  Treat contributing causes and correct imbalance  Calcium gluconate – restores normal neuromuscular irritability  Glucose – stimulates insulin secretion  Glucose + insulin – facilitates cellular entry of potassium  Buffered solutions – correct metabolic acidosis and lowers serum potassium level  Oral/rectal – exchanges sodium for potassium in the intestine  Dialysis – renal failure  Calcium and phosphate balance (119-120)  Calcium is a necessary ion for many fundamental metabolic processes ▪ Normal serum levels: 9-10. ▪ Major cation associated with the structure of bones and teeth

▪ Metabolic Syndrome/Insulin Resistance (incr. risk with obesity)

 Abnormal insulin secretion/action ▪ Beta cell dysfunction ▪ Insulin resistance  Increased free fatty acids and fat deposition – incr. inflammation (release of cytokines) and intracellular lipid deposits  Incr. glucagon secretion  Alteration in the production of adipokines by adipose tissue - Leptin resistance  2 most important factors are positive family hx and obesity  See figure 22-15 page 740  Know Autoimmune disorders (262-263, 264t-265t, 277-281, 275-276) o SEE TABLE 9-2 PAGE 264 o Hashimoto’s Thyroiditis ▪ Causes

• AI, FHX ▪ Signs and Symptoms
• Hypothyroidism, Painless unilateral or bilateral enlargement of the thyroid ▪ Testing
• TSH, T3/4, Antibodies o Graves Disease ▪ AI Hyperthyroid ▪ Causes
• Incr. F > 20, FHX, Tobacco ▪ Signs and Symptoms
• Sxs of hyperthyroid  exophthalmia, thyroid bruit, periorbital/ pretibial myxedema, diplopia
• Goiter
• Thyrotoxicosis  tachycardia, HTN, delirium, N/V,D -- risk for? ▪ Testing
• TSH, T3/4, Antibodies  Hormones that cause hyperglycemia (717-767, 804-834)

 Antidiuretic Hormone (109, 696-699, 718-719)  Directly regulates water balance  Secreted when plasma osmolality increases or circulating blood volume decreases and blood pressure drops  Action is to increase permeability of renal tubular cells to water, increasing water reabsorption and promoting the restoration of plasma volume and blood pressure  Regulated by a feedback mechanism  Synthesized in hypothalamic neurons but stored and secreted by posterior pituitary  Major homeostatic function is the control of plasma osmolality as regulated by ADH  Effects may be inhibited by hypercalcemia, prostaglandin E, hypokalemia  Increase in ADH – stress, trauma, pain, exercise, nausea, nicotine, exposure to heat, drugs (morphine)  Decrease in ADH – decrease in plasma osmolality; increase in intravascular volume; hypertension; increase in estrogen, progesterone, angiotension II levels, alcohol ingestion  Causes disease of posterior pituitary – abnormal secretion of ADH  SIADH, DI  Diabetes Insipidus and associated labs (719-720)  Insufficient ADH ▪ Polyuria ▪ Polydipsia ▪ Hypernatremia  Neurogenic DI ▪ Tumors, aneurysms, thrombosis, infections, immunologic disorders  Nephrogenic ▪ Renal collecting tubules are insensitive to ADH  Dipsogenic ▪ Excessive fluid intake lowers plasma osmolality to the point it falls below the threshold for ADH secretion.  Dx: Distinguish from other polyuric states ▪ Urine Spec grav, Urine osmo, Na, Serum Osm, Serum ADH, water restriction  Tx: Desmopressin aka DDVAP  All forms are characterized by the inability of the kidney to decrease permeability to water. Causes excretion of large volumes of dilute urine and an increase in plasma osmolality.  Dehydration develops rapidly without ongoing fluid replacement.  Serum hypernatremia and hyperosmolality occur.

 Clinical Manifestations: polyuria, nocturia, continuous thirst, polydipsia  Hyperparathyroidism (731-733)  Characterized by greater than normal secretion of parathyroid hormone and hypercalcemia ▪ Primary, secondary, tertiary  Sporadic disease characterized by inappropriate excess secretion of PTH by one of more of the parathyroid glands ▪ PTH secretion is increased and not under the usual feedback control mechanisms ▪ Calcium level in the blood increases because of increased bone resorption and GI absorption of calcium, but fails to inhibit PTH secretion.  Primary ▪ Cause unknown – one of the most common endocrine disorders ▪ 80-85% of cases caused by parathyroid adenomas ▪ Normal feedback mechanisms, such as elevated serum levels of ionized calcium, fail to normally inhibit PTH secretion by the parathyroid gland ▪ Hypercalcemia and hypophosphatemia are hallmarks ▪ See table 22-4 page 732  Secondary ▪ Caused by an increase in PTH secondary to a chronic disease state, such as chronic kidney disease or intestinal malabsorption, which causes hypocalcemia or chronic Vit D deficiency  Tertiary ▪ Excessive secretion of PTH and hypercalcemia that occurs after long- standing secondary hyperparathyroidism ▪ Develops in individuals with chronic secondary hyperparathyroidism and after renal transplantation  Type 1 Diabetes (734-739, 740f)  Juvenile and IDDM  Beta cell destruction, usually leading to absolute insulin deficiency, immune mediated diabetes is most common form ▪ Cellular-mediated autoimmune destruction of pancreatic beta cells ▪ Individual prone to ketoacidosis ▪ Little or no insulin secretion, insulin dependent ▪ Usually not obese  1A – Multifactorial, AI (viral) ▪ Lymphocyte and macrophage infiltrate islets - inflammation (insulinitis) and islet beta cell death  1B – Secondary to other disorders, exp. Pancreatitis

 Formed by the posterior cerebral arteries, posterior communicating arteries, internal carotid arteries, anterior cerebral arteries, and anterior communicating artery  Cranial nerves functions and abnormalities associated with them (447-448, 469, 471f, 472t)  Cranial nerves are part of the peripheral nervous system (PNS) – project through the brain and pass through foramina in the skull  Cranial nerves + Function  1. Olfactory –purely sensory, carries impulses for sense of smell  2. Optic – purely sensory, carries impulses for vision  3. Oculomotor – Contains motor fibers to inferior oblique and to super, inferior, and medial rectus extraocular muscles that direct eyeballs; levator muscles of eyelid; smooth muscles of iris and ciliary body; and proprioception (sensory) to brain from extraocular muscles  4. Trochlear – Proprioceptor and motor fibers for superior oblique muscle of eye (extraocular)  5. Trigeminal – Both motor and sensory for face; conducts sensory impulses from mouth, nose, surface of eye, and dura mater; also contains motor fibers that stimulate chewing muscles  6. Abducens – contains motor fibers to lateral rectus muscle and proprioceptor fibers from the same muscle to brain  7. Facial – a) supplies motor fibers to muscles of facial expression and to lacrimal and salivary glands; b) carries sensory fibers from taste buds of anterior part of tongue  8. Vestibulocochlear (acoustic) – purely sensory; vestibular branch transmits impulses for sense of equilibrium; cochlear branch transmits impulses for sense of hearing  9. Glossopharyngeal – a) motor fibers serve pharynx (throat) and salivary glands; b) sensory fibers carry impulses from pharynx, posterior tongue (taste buds), and pressure receptors of carotid artery  10. Vagus – Fibers carry sensory and motor impulses for pharynx; a large part of this nerve is parasympathetic motor fibers, which supply smooth muscles of abdominal organs; receives sensory impulses from viscera  11. Spinal accessory – provides sensory and motor fibers for sternocleidomastoid and trapezius muscles and muscles of soft palate, pharynx, and larynx  12. Hypoglossal – carries motor fibers to muscles of tongue and sensory impulses from tongue to brain o Trigeminal Neuralgia ▪ Inflammation and demyelination of CN 5 - trigeminal ▪ Causes

• MS, tumor, Structural, superior cerebellar artery

▪ Signs and Symptoms

• Paroxysmal intense searing pain (secs to mins)
• Pain can be triggered by – chewing, brushing teeth, talking ▪ Testing
• Clinical, MRI ▪ R/O Post herpetic neuralgia, Migraine, Dental cause o Bell’s Palsy ▪ Weakness and paralysis of one side of the face
• Especially orbicularis oculi and frontalis ▪ Causes
• Cranial Nerve – 7 - facial
• Viral URI, herpes simplex, EBV ▪ Signs and Symptoms
• Sudden onset, paralysis (may be preceded by pain behind ear), pain, HA ▪ Testing ▪ CT R/O stroke, MRI  Multiple Sclerosis (618-621)  Chronic demyelination (loss of oligodendrocytes) of CNS (brain, spinal cord, optic nerve)  scarring  Affects white and gray matter  4 different types
• Remitting and Relapsing
• Relapsing – Progressive
• Progressive – Primary, Secondary  Causes  AI – poss. Post viral, F (20-40)  Higher rates in lower temperature environments – poss. Less Vit D  Infections, trauma, pregnancy – can cause exacerbations  Signs and Symptoms (often unilateral)  Visual changes, optic neuritis  Balance, memory, weakness, parasthesias – increased DTR’s  Charcots triad- intention tremor, scanning speech, nystagmus  Lhermitte’s sign – electric shock like pain into back or legs with flexed neck  Exacerbated by heat  Risk Factors  Genetic polymorphism

 Testing  MRI – brain and spinal cord  Lumbar puncture  Myofascial pain syndrome (492-493, 1579t)  Associated with injury to muscle, fascia, and tendons and includes myositis, fibrositis, myofibrositis, and myalgia and muscle strain  Second most common pain syndrome  Pain results from muscle spasm, tenderness, and stiffness  Neuroaxonal degeneration with alterations in neuromuscular transmission may occur  Compression of the trigger points causes referred pain, motor dysfunction, and autonomic responses  During early stages pain is localized then becomes more deep and generalized  Begins as a result of poor muscle tone, inactivity, muscle or tendon strain, or sudden vigorous exercise that can evolve into chronic pain state Nephrology  Prerenal injury (1360, 1385)  Most common cause of acute kidney injury  Reduced effective blood volume causes renal hypoperfusion that occurs rapidly over a period of hours with elevation of BUN and plasma creatinine levels  GFR ultimately declines because of the decrease in filtration pressure  Poor perfusion can result from renal artery thrombosis, hypotension related to hypovolemia or hemorrhage, renal vasoconstriction and alterations in renal regional blood flow, microthrombi, or kidney edema that restricts arterial blood flow  Possible causes: hypovolemia, hemorrhagic blood loss (trauma, GI bleed, complications of childbirth), loss of plasma volume (burns, peritonitis), water and electrolyte loss (severe vomiting or diarrhea, intestinal obstruction, uncontrolled DM, inappropriate use of diuretics), systemic hypotension or hypoperfusion, septic shock systemic inflammation, cardiac failure or shock, massive PE, stenosis or clamping of renal artery, increased intra-abdominal pressure (abdominal compartment syndrome) --- most common: dehydration, hemorrhage, sepsis  IgG nephropathies (glomerulonephritis) (1352-1358)  Associated with Nephritic Syndrome  Rapidly progressive or crescentic glomerulonephritis

• Type 1: Formation of IgG antibodies against pulmonary capillary and glomerular basement membrane (Goodpasture syndrome);

activation of complement and neutrophils; more common in young men; causes pulmonary hemorrhage and renal failure o Histopathology: Accumulation of fibrin, macrophages, and epithelial cell prolifteration into the Bowman space forms crescents and occludes glomerular capillary blood flow decreasing glomerular filtration; antiglomerular basement membrane antibodies lead to necrotizing, proliferative glomerulonephritis, and renal failure; diffuse lesions  Major symptoms: hematuria with red blood cell casts, proteinuria exceeding 3-5g/day with albumin as the major protein

• Nephritic sediment: blood in urine with red cell casts, white cell casts, varying degrees of protein Oncology  Punched out lesions on a chest x-ray (1030-1035)  Multiple Myeloma  Bone lesions result from infiltrations of the bone by malignant plasma cells and stimulation of osteoclasts to reabsorb bone  Process results in release of calcium (hypercalcemia) and the development of “lytic lesions” (round, punched out, regions of bone)  Multiple Myeloma (1030-1035)  Multiple myeloma is the most common primary malignant bone neoplasm in adults. It arises from red marrow due to monoclonal proliferation of plasma cells and manifests in a wide range of radiographic abnormalities. Multiple myeloma remains incurable.  Clonal plasma cell cancer characterized by the slow proliferation of malignant cells as tumor masses in the bone marrow that usually results in destruction of bone  Patho: aneuploidy, chromosome translocation is responsible for development of myeloma; proto-oncogene mutation – inactivation of tumor-supressor genes  Clinical Manifestations: elevated levels of calcium, renal failure, anemia, bone lesions; weakness, fatigue, weight loss, anorexia – often misdiagnosed with a slipped disc  Destruction of bone tissue causes pain and pathologic fractures. Bones most commonly involved are vertebrae, ribs, skull, pelvis, femur, clavicle, scapula  Proteinuria – renal failure secondary to hypercalcemia  Anemia – normocytic, normochromic – results from inhibited erythropoiesis caused by tumor cell infiltration of bone marrow  See box 29-4 page 1035 for diagnostic criteria – must have 3 major criteria for