NUR 631 Topic 8 Midterm Study Guide
NUR 631 Topic 8 Midterm Study Guide
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Cellular biology and Alterations
• Compensatory hyperplasia after partial resections (mod 1) (51-53)
o Ex: liver, hepatocyte growth
o Adaptive mechanism that enables certain organs to regenerate
o Even with removal of 70% of the liver, it will regenerate within about 2 weeks
o 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)
o 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.
o 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
BENIGN TUMORS MALIGNANT TUMORS
Grow slowly
Have a well-defined capsule
Are not invasive
Are well differentiated; look like the tissue from which they arose
Have a low miotic index; dividing cells are rare
Do not metastasize Grow rapidly
Are not encapsulated
Invade local structures and tissues
Are poorly differentiated; may not be able to determine the tissue of orgin
High miotic index; many dividing cells
Can spread distantly; often through blood vessels and lymphatics
Genetics
• Recurrence of autosomal diseases (152-154, 155-156)
o Autosomal dominant - Affected offspring are produced by the union of a normal parent with an effected heterozygous parent
Affected parent can pass either a disease gene or a normal gene to his or her children
Each event has a probability of 0.5, so on average half the children will be normal and half will express the disease.
o Autosomal recessive – individual must be homozygous for a recessive allele to express the disease – can survive the population one generation to the next
Characterized by delay of onset, incomplete penetrance, and variable expressivity – most common is cystic fibrosis
Recurrence risk for the offspring of carrier parents is 25%
• Klinefelter’s syndrome (mod 1) (148, 156, 914)
o Causes
Chromosomal disorder XXY – genotype
Genetically male – due to Y
• Male XY, female XX
Random, not inherited – nondisjunction in the X chromosomes in the mother
o Signs and Symptoms
Both male and female sexual characteristics
Decreased T more female hormones causing
• Less body and facial hair
• Gynecomastia (risk breast CA)
• Weak muscles and bones (osteoporosis), shy (tall, lanky, shy)
• Can result in decreased IQ
• Higher risk of AI disorders
Majority - Infertility
o Testing
Clinical Exam
Chromosomal testing
Hormones
Immunology
• Rickets disease (1599-1600)
o Disorder in which growing bones fails to become mineralized, resulting in “soft” bones and skeletal deformity.
o 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
o Most common form is x-linked hypophosphatemic rickets in industrialized nations
o In US it happens in children due to lack of dietary vitamin D – can lead to early fracture or slow bone healing after fracture
o 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
o Normalization of calcium, phosphorus, and vitamin D levels before surgical intervention, deformity often improves when bone metabolism improves
o Hypocalcemia
• Epstein-Barr Virus (318t, 1078-1079, 1011)
o Adenovirus, herpesviruses – transmitted via saliva, disease: mono, burkitt lymphoma
o Strongly associated with non-hodgkin lymphoma in children
o EBV and African Burkitt Lymphoma
o Etiologic agent for mono: EBV – ubiquitous, lymphotrophic, gamma-group herpesvirus accounting for approximately 85% of mono cases
o Early EBV infections are usually asymptomatic and provide immunity to EBV later in life
• Human Herpes Virus (HHV) 8 (382, 383, 1645)
o Kaposi’s Sarcoma
Commonly occurs in older men but now occurs in a markedly more virulent form in immunocompromised individuals (AIDS)
o Linked to several rare lymphomas
o Associated with cancer in humans
o Member of Herpesviridae family
• Complement Cascade (197, 198f, 287f)
o 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
o 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)
o Aka passive immunity
o Does not involve host’s response at all
o Occurs when preformed antibodies or T lymphocytes are transferred from a donor to the recipient.
o 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
o Temporary immunity
• IgM and IgG and IgA and IgE (229-230, 247, 254-255)
o IgA (p.229)- Fungal infection skin, GI tract, Mouth Vaginal
IGA in breast milk, works at GI system
o 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
o 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 H1
Protects from parasites/worms
o 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.
o Bronchial constriction (2) Edema (3) Vasodilation (4) H2 (5) Increase gastric secretions (6) Decreases the release of histamine from mast cells and basophils
o IgG, IgM, and IgA bind to the surface of parasites, activate complement, generate chemotactic factors for neutrophils and macrophages, and serve as opsonins for those phagocytic cells; unique to parasitic infections, the eosinophil is a primary cell in the granuloma
• IgE-mediated hypersensitivity (263-265)
o Type 1 reactions – most common allergies (i.e. pollen)
o IgE can contribute to a few autoimmune and alloimmune diseases, and many common allergies (poison ivy) are not mediated by IgE.
o Short life span in the blood
o Individual is usually sensitized when exposed to antigen in future.
o 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
o Mast cells are principal effector cells involved
• SLE (Lupus) (mod 2) (277-278)
o Antigen-antibody mediated
o Type III hypersensitivity
o Chronic, multisystem, inflammatory disease, most common, complex and serious of autoimmune disorders
o 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
o Occurs more often in women, age 20-40
o Clinical Manifestations: arthralgias or artiritis, vasculitis, rash, renal disease, hematologic abnormalities (anemia)
Develops slowly and has frequent remissions and exacerbations
o 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)
o 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+ > 5.5
o Renal Failure
o Spironolactone
o Hypoaldosteronism
Addison’s Disease
o Burns/Cell lysis
o Hemolytic Anemia's
o Rhabdomyolysis
o Acidosis
o Insulin Deficiency
o Signs and Symptoms
Tingling, cramps/diarrhea
Weakness Flaccid Paralysis
Arrhythmias Cardiac Arrest
o 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
o Treat contributing causes and correct imbalance
o Calcium gluconate – restores normal neuromuscular irritability
o Glucose – stimulates insulin secretion
o Glucose + insulin – facilitates cellular entry of potassium
o Buffered solutions – correct metabolic acidosis and lowers serum potassium level
o Oral/rectal – exchanges sodium for potassium in the intestine
o Dialysis – renal failure
• Calcium and phosphate balance (119-120)
o Calcium is a necessary ion for many fundamental metabolic processes
Normal serum levels: 9-10.5
Major cation associated with the structure of bones and teeth
Enzymatic cofactor for blood clotting and is required for hormone secretion and function of cell receptors
Helps with contraction of muscles, transmission of nerve impulses, plasma membrane stability and permeability
o Phosphate is found primarily in bone, and smaller amounts in ICF and ECF spaces
Normal serum levels: 2.5-4.5
Acts as IC and EC anion buffer in the regulation of acid-base balance
o Balance of both are rigidly controlled – if the concentration of one ion increases or decreases, the other will increase or decrease
o Regulated by 3 hormones – parathyroid hormone (PTH), vitamin D, calcitonin
• Metabolic acidosis with partial resp compensation (127f-128f, 125-128, 127t)
pH <7.35; CO2 >45; HCO3 <22
Shock
• Cardiogenic
• Hypovolemic
• Neurogenic
• Anaphylactic
• Septic
DKA
Seizures
Renal failure
Diarrhea
Aspirin OD
Methanol/Formaldehyde (formic acid)
Ethylene glycol (glycolic and acedic acid)
o Compensatory for respiratory alkalosis
o Hyperventilation – the respiratory system compensates for a metabolic acidosis as the reduced pH stimulates hyperventilation, lowering the Paco2 and the amount of bicarb circulating in the blood.
o HA and lethargy are early symptoms, deep, rapid respirations (Kussmaul) are indicative of respiratory compensation.
Endocrinology
• Obesity and Type 2 DM (177-178)
o Causes
Familial predisposition
Lifestyle
Metabolic Syndrome/Insulin Resistance (incr. risk with obesity)
o Abnormal insulin secretion/action
Beta cell dysfunction
Insulin resistance
o Increased free fatty acids and fat deposition – incr. inflammation (release of cytokines) and intracellular lipid deposits
o Incr. glucagon secretion
o Alteration in the production of adipokines by adipose tissue - Leptin resistance
o 2 most important factors are positive family hx and obesity
o 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)
o
• Antidiuretic Hormone (109, 696-699, 718-719)
o Directly regulates water balance
o Secreted when plasma osmolality increases or circulating blood volume decreases and blood pressure drops
o Action is to increase permeability of renal tubular cells to water, increasing water reabsorption and promoting the restoration of plasma volume and blood pressure
o Regulated by a feedback mechanism
o Synthesized in hypothalamic neurons but stored and secreted by posterior pituitary
o Major homeostatic function is the control of plasma osmolality as regulated by ADH
o Effects may be inhibited by hypercalcemia, prostaglandin E, hypokalemia
o Increase in ADH – stress, trauma, pain, exercise, nausea, nicotine, exposure to heat, drugs (morphine)
o Decrease in ADH – decrease in plasma osmolality; increase in intravascular volume; hypertension; increase in estrogen, progesterone, angiotension II levels, alcohol ingestion
o Causes disease of posterior pituitary – abnormal secretion of ADH
o SIADH, DI
• Diabetes Insipidus and associated labs (719-720)
o Insufficient ADH
Polyuria
Polydipsia
Hypernatremia
o Neurogenic DI
Tumors, aneurysms, thrombosis, infections, immunologic disorders
o Nephrogenic
Renal collecting tubules are insensitive to ADH
o Dipsogenic
Excessive fluid intake lowers plasma osmolality to the point it falls below the threshold for ADH secretion.
o Dx: Distinguish from other polyuric states
Urine Spec grav, Urine osmo, Na, Serum Osm, Serum ADH, water restriction
o Tx: Desmopressin aka DDVAP
o 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.
o Dehydration develops rapidly without ongoing fluid replacement.
o Serum hypernatremia and hyperosmolality occur.
o Clinical Manifestations: polyuria, nocturia, continuous thirst, polydipsia
• Hyperparathyroidism (731-733)
o Characterized by greater than normal secretion of parathyroid hormone and hypercalcemia
Primary, secondary, tertiary
o 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.
o 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
o 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
o 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)
o Juvenile and IDDM
o 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
o 1A – Multifactorial, AI (viral)
Lymphocyte and macrophage infiltrate islets - inflammation (insulinitis) and islet beta cell death
o 1B – Secondary to other disorders, exp. Pancreatitis
o Genetic
First-degree relative (parent or sibling)
o Environmental
Viral, H.pylori, Cow’s Milk, Lack of Vit. D
o Clinical manifestations
Abnormal alpha and beta cell function
Long preclinical period with gradual beta cell destruction, leading to insulin deficiency and hyperglycemia
An 80% to 90% loss of function of the insulin-secreting beta cells in the islet of Langerhans occurs before hyperglycemia develops
• Polydipsia, Polyphagia, Polyuria, Weight loss, Fatigue
Neurology
• Fight or Flight syndrome
o Heart increases pumping action during stress or fear
o Sympathetic nervous system
Activates and releases norepinephrine
o The adrenal medulla produces a hormonal cascade that results in the secretion of catecholamines, especially norepinephrine and epinephrine. The hormones estrogen, testosterone, and cortisol, as well as the neurotransmitters dopamine and serotonin, also affect how organisms react to stress.
• Arachnoid Villi (466)
o Function as one way valves directing CSF outflow into the blood but preventing blood flow into the subarachnoid space
o Villi protrude from the arachnoid space, through the dura mater, and lie within the blood flow of the venous sinuses
CSF is reabsorbed by means of a pressure gradient between the arachnoid villi and the cerebral venous sinuses
• Circle of Willis (467, 468f)
o Intracranial Aneurysm – bifurcations in or near Circle of Willis
o Also called arterial circle
o Has ability to compensate for reduced blood flow from any one of its major contributors (collateral blood flow)
o 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)
o Cranial nerves are part of the peripheral nervous system (PNS) – project through the brain and pass through foramina in the skull
o 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)
o 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
o Causes
AI – poss. Post viral, F (20-40)
Higher rates in lower temperature environments – poss. Less Vit D
Infections, trauma, pregnancy – can cause exacerbations
o 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
o Risk Factors
Genetic polymorphism
Environmental – vit D def, smoking, EBV
o Testing
MRI – brain and spinal cord
Lumbar puncture
• Myofascial pain syndrome (492-493, 1579t)
o Associated with injury to muscle, fascia, and tendons and includes myositis, fibrositis, myofibrositis, and myalgia and muscle strain
o Second most common pain syndrome
o Pain results from muscle spasm, tenderness, and stiffness
o Neuroaxonal degeneration with alterations in neuromuscular transmission may occur
o Compression of the trigger points causes referred pain, motor dysfunction, and autonomic responses
o 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)
o Most common cause of acute kidney injury
o Reduced effective blood volume causes renal hypoperfusion that occurs rapidly over a period of hours with elevation of BUN and plasma creatinine levels
o 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
o 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)
o 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)
o 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)
o 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.
o 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
o Patho: aneuploidy, chromosome translocation is responsible for development of myeloma; proto-oncogene mutation – inactivation of tumor-supressor genes
o 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
o See box 29-4 page 1035 for diagnostic criteria – must have 3 major criteria for diagnosis
• BRCA1 and BRCA2 mutations (174, 831)
o Associated with familial ovarian cancer
o BRCA1 – chromosome 17; BRCA2 – chromosome 13
o Women who inherit a mutation experience a 50-80% lifetime risk of developing breast CA
o BRCA1 mutations also increase risk for ovarian cancer (20-50%), also confer a modestly increased risk of prostate cancer and colon cancer
o BRCA2 mutations confer an increased risk of ovarian cancer (10-20%); 6% of males who inherit BRCA2 will develop breast cancer
o Most common cause of breast cancer
• Cancer treatment symptoms (392, 395)
o Box 12-2 page 396
o Fatigue is the most frequent reported symptom of cancer and cancer treatment r/t sleep disturbances, various biochemical changes
o Leukopenia and thrombocytopenia r/t toxic chemotherapy drugs
o Infection r/t being predisposed from advanced disease and chemotherapy causing immunosuppression
o GI – decreased cell turnover leading to oral ulcers (stomatitis), malabsorption, diarrhea, disruption of flora
o Hair and Skin – alopecia can result from chemo effects on hair follicles, skin breakdown and redness, and dryness
• Human papillomavirus and cancer (382, 423-424)
o Causes almost all cervical cancer, infects basal skin cells and commonly causes warts
o HPV 16,18,31, 45 are associated with highest risk of developing cervical, penile, and anogenital cancer
o Most HPV can be handled by the immune system and doesn’t cause cancer
o When it does causes cancer, typically people are infected with HPV for a decade or longer and the viral DNA becomes integrated into the genomic DNA of the infected basal cell of the cervix and directs the persistent production of viral oncogenes
o Detected by PAP
o Cofactors: smoking, oral contraceptives, decreased immunity, multiple children, poor oral hygiene use, chronic inflammation
o Once an HPV virus enters an epithelial cell, the virus begins to make proteins that can interfere with normal functions in the cell, enabling the cell to grow in an uncontrolled manner, and avoid apoptosis
o Most common sexually transmitted disease in US
o Can also cause oropharyngeal cancer, especially in men
• Hodgkin Lymphoma (1023-1027)
o Malignant lymphoma characterized by its progression from one group of lymph nodes to another, the development of systemic symptoms, and Reed Sternberg cells (hallmark of HL)
Necessary for the diagnosis of HL but not specific to HL
o Linked to EBV
o CM: adenopathy, mediastinal mass, splenomegaly, abdominal mass, fever, night sweats, weight loss, prutitus, thrombocytosis, leukocytosis, eosinophilia, elevated ESR, elevated alk phos, paraneoplastic syndromes
Hematology
• Know the different types of anemias and the CBC component (986t)
o Reduction in total number of erythrocytes or a decrease in the quality or quantity of hemoglobin
o Normocytic/Normochromic – normal
o Macrocytic – higher mean corpuscular volume (MCV)
o Microcytic – lower MCV
o Hyperchromic – higher mean corpuscular hemoglobin concentration (MCHC)
o Hypochromic – lower MCHC
o See table 28-3 on page 986
• Chronic myelogenous leukemia (CLL) (1020, mod 4)
o Is usually diagnosed in adults
o Philadelphia chromosome is often present and BCR-ABL1 causes initiation of CML.
o Advances slowly and insidiously
o Infections, fever, and weight loss
o Chronic phase
Lasts 2 to 5 years
Symptoms: May not be apparent
o Accelerated phase
Lasts 6 to 18 months
Primary symptoms develop: Splenomegaly
o Terminal blast phase
“Blast crisis” – increase in basophils/blast cells
Survival: Only 3 to 6 months
o Group of diseases called myeloproliferative disorders which include polycythemia vera, primary thrombocytosis, and idiopathic myelofibrosis (invasion of bone marrow by fibrous tissue)
o Clonal and thought to arise from a hematopoietic stem cell – cells observed are heterogeneous in differentiation
• Eosiniphil vs Neutrophils (209-210, 949 – 208-210, 212)
o Eosinophil
Serve as body’s primary defense against parasites, help regulate vascular mediators released from mast cells (critical)
• Eosinophil lysosomes contain several enzymes that degrade vasoactive molecules, thereby controlling the vascular effects of inflammation
o Includes histaminase which mediates the degradation of some of histamine
o Neutrophil
Predominant phagocytes in the early inflammatory site, arriving within 6-12 hours after the initial injury, where they ingest bacteria, dead cells, and cellular debris
• Mature cell incapable of division and sensitive to the acidic environment of inflammatory lesions, it is short lived at inflammatory site and becomes a component of pus
• Primary role is removal of debris in sterile lesions such as burns, and phagocytosis of bacteria in nonsterile lesions
• Erythropoietin use (959, 960f, 993, 1334)
o Figure 27-14 page 960
1. Decreased arterial oxygen levels result in 2. Decreased tissue oxygen (hypoxia) that 3. Stimulates the kidney to increase 4. Production of erythropoietin. Erythropoietin is carried to the bone marrow 5. And binds to erythropoietin receptors on proerythroblasts, resulting in increased red cell production and maturation and expansion of the erythron 6. The increased release of red cells into the circulation frequently corrects hypoxia in the tissues 7. 8. Perception of normal oxygen levels by the kidney causes 9. Diminished production of erythropoietin (negative feedback) and return to normal levels of erythrocyte production.
o Treatment with recombinant human erythropoietin improves anemia in 30% of those with myelodysplastic syndrome.
o Produced by the fetal liver and the adult kidney and is essential for normal erythropoiesis.
Stimulates the bone marrow to increase the rate of red blood cell production
Anemia of chronic renal failure and cancer chemotherapy is treated with recombinant human erythropoietin
Also effects the endothelium and promotes angiogenesis, mitogenesis, and anti-apoptosis and is neurotrophic.
• Anemia after subtotal gastrectomy for gastritis
o Pernicious anemia due to vitamin B12 deficiency
• Jaundice in hemolytic anemia (996-1001)
o Jaundice is present (icterus) when heme destruction exceeds the liver’s ability to conjugate and excrete bilirubin.
o Jaundice is first noticed in the neonatal period. Children and adults with congenital hemolytic anemia may not have icterus, or it may be mild enough that it remains unnoticed.
o In some individuals, faint scleral icterus may be the only indication of hemolytic disease.
• Hemophilia A is what kind of inherited disorder (1071)
o Factor 8 def
o X-linked recessive that affects men and transmitted by women
Infection
• Wet gangrene (mod 1) 91
o Liquefactive
o Develops when neutrophils invade the site causing liquefactive necrosis
o Occurs in internal organs, causing site to become cold, swollen, black
Foul odor is present, produced by pus, death can ensue [Show Less]