Exam II Flashcards

Question

Osteomyelitis

Answer 1

- Is usually caused by a Staphylococcus aureus infection - Is often outside the body (exogenous); can be from a bloodborne (endogenous) infection  Infection spreads under the periosteum and along the bone shaft or into the bone marrow  In adults: Affects the cortex  Sequestra: Sections of dead bone from periosteal separation  Involucrum: Periosteal new bone

Answer 2

Acute and chronic inflammation, fever, pain, necrotic bone

Answer 3

Antibiotics, debridement, surgery, hyperbaric oxygen therapy

Answer 4

Primary develop directly from disease process and secondary from primary lesions or from patient behavior such as picking/scratching

Answer 5

Benign tumor of the skin o Proliferation of cutaneous basal cells that produce smooth or warty elevated lesions o Treatment: Cryotherapy with liquid nitrogen or electrocautery

Answer 6

Benign tumor of the skin o Tumor of squamous cell differentiation arising from hair follicles o Treatment: Curettage or excision; intralesional fluorouracil (5-FU), bleomycin, interferon or methotrexate

Answer 7

Benign tumor of the skin o Premalignant lesion composed of aberrant proliferations of epidermal keratinocytes caused by prolonged exposure to UV radiation o Treatment: Ablative and topical therapies (5-FU and imiquimod), protection from the sun

Answer 8

o Tumor of the epidermis o Types: In situ (Bowen disease) and invasive o Mutation of the TP53 gene and other oncogenic signals o Treatment: Cryotherapy, 5-FU, photodynamic therapy

Answer 9

Is a tumor of the skin originating from melanocytes ABCDE rule is used as a guide  Asymmetry  Border irregularity  Color variation  Diameter larger than 6 mm  Elevation that includes a raised appearance or rapid enlargement Treatment

Answer 10

- Vascular malignancy - Presentations  Drug-induced immunosuppression: After kidney transplantation, for example  Endemic form in equatorial Africa  Classic form, exhibited on the lower legs of older men  Epidemic and nonepidemic forms related to acquired immunodeficiency syndrome (AIDS) - Kaposi-associated herpes virus 8 (HHV-8) found in all forms

Answer 11

- Incurable - Local lesions: Surgical excision - Multiple disseminated: Combination of immunomodulatory, cytotoxic, and antiviral drugs - Highly active antiretroviral therapy (HAART) for treating AIDS: Decreasing the incidence rate

Answer 12

o Infection of hair follicles o Staphylococcus aureus: Common cause o Treatment: Soap and water and topical application of antibiotics

Answer 13

o Boils: Inflammation of the hair follicles o Develop from preceding folliculitis; spread through follicular wall into the surrounding dermis o S. aureus: Common causative organism

Answer 14

- Collection of infected hair follicles - Erythematous, painful, swollen mass that drains through many openings - Development of abscesses - Clinical manifestations  Systemic symptoms that occur during early stages: Chills, fever, malaise

Answer 15

- Bacterial (acute or chronic) infection of the cuticle - Clinical manifestations: Painful; abscess may develop - Treatment  Hands: Kept dry  Abscesses: Incision and drainage  Severe bacterial cases: Systemic antibiotics

Answer 16

- Fungal or dermatophyte infection of the nail plate - Clinical manifestations: Turns yellow or white - Treatment  Débridement  Systemic antifungal therapy

Answer 17

- Transduction - Transmission - Perception - Modulation

Answer 18

o Heat loss through electromagnet waves (come from surfaces with temperatures higher than the surrounding air temperature)

Answer 19

o Direct molecule to molecule transfer from one surface to another (warmer surface loses heat to the cooler surface)

Answer 20

o Transfer of heat through currents of gases or liquids (exchanging warmer air at the surface of the body with cooler air in the surrounding space)

Answer 21

Diverting core-warmed blood to the surface of the body

Answer 22

o Loss of the ability to think rapidly and clearly; impaired judgment and decision making

Answer 23

Beginning loss of consciousness; disorientation to time, followed by disorientation to place and impaired memory; recognition of self is lost last

Answer 24

Limited spontaneous movement or speech; easy arousal with normal speech or touch; may not be oriented to time, place, or person

Answer 25

Mild-to-moderate reduction in arousal (awakeness) with limited response to the environment; falls asleep unless verbally or tactilely stimulated; answers questions with minimum responses

Answer 26

Condition of deep sleep or unresponsiveness; person may be aroused or caused to open eyes only by vigorous and repeated stimulation; response is often withdrawal or grabbing at stimulus

Answer 27

No verbal response to the external environment or to any stimuli; noxious stimuli such as deep pain or suctioning yields motor movement

Answer 28

Associated with purposeful movement on stimulation

Answer 29

Associated with unresponsiveness or no response to any stimulus

Answer 30

Brain has no potential for recovery and can no longer maintain the body’s internal homeostasis State laws  Entire brain, brainstem, and cerebellum stops functioning  Brain is autolyzing (self-digesting) or has already autolyzed on postmortem examination

Answer 31

o Death of the cerebral hemispheres is exclusive of the brainstem and cerebellum o Brainstem may continue to maintain internal homeostasis (normal respiratory and cardiovascular functions, temperature control, and gastrointestinal function)

Answer 32

Severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway

Answer 33

Onset after age 40 years old

Answer 34

* Caused by other neurodegenerative diseases and acquired disorders * Most common form is Drug-induced Parkinsonism

Answer 35

 Wide-eyed, unblinking, staring expression with immobile facial muscles  Slow gait  Short, shuffling steps

Answer 36

 Drug therapy: levodopa, anticholinergic drugs, antihistamines, amantadine  Occupational therapy, physical therapy, language, and swallowing therapy

Answer 37

o A way to assess the level of consciousness in a patient with acute brain injury

Answer 38

Scores range from 3 to 15  Mild: GCS score of 13–15; is associated with mild concussion  Moderate: GCS score of 9–12; is associated with structural injury such as hemorrhage or contusion  Severe: GCS score of 3–8; is associated with cognitive and/or physical disability or death

Answer 39

Is caused most commonly by motor vehicle accidents (MVAs) but also occasionally by falls and sporting accidents Temporal fossa: is the most common site  Is caused by injury to the middle meningeal artery or vein

Answer 40

 Include loss of consciousness at the time of injury, followed by a lucid period that lasts from a few hours to a few days, and increasingly severe headaches, vomiting, drowsiness, confusion, seizure, and hemiparesis

Answer 41

Is a medical emergency; surgical evacuation of the hematoma

Answer 42

 Develops within hours  Is often located at the top of the skull  Expanding clots directly compress the brain

Answer 43

 Develops after 48 hours to 2 weeks

Answer 44

 Develops over weeks to months  Subdural space gradually fills with blood

Answer 45

Begins with headache, drowsiness, restlessness or agitation, slowed cognition, and confusion

Answer 46

Burr hole to remove the clot

Answer 47

Approximately 80% complain of chronic headaches and have tenderness at the site of injury

Answer 48

Craniotomy to evacuate the gelatinous blood Percutaneous drainage

Answer 49

Hematoma acts as an expanding mass  Increased ICP and compression of brain tissues with resultant edema and ischemia Delayed: appears 3–10 days after injury

Answer 50

Decreasing level of consciousness

Answer 51

 Reducing ICP; allowing the hematoma to reabsorb slowly  Surgery

Answer 52

Mechanisms  Rotational and twisting movements  Acceleration-deceleration forces Axonal damage  Shearing or stretching of nerve fibers

Answer 53

- Mild concussion - classic concussion - mild TBI - moderate TBI - severe TBI

Answer 54

Transient Ischemic Attack Thrombotic stroke Embolic stroke Hemorrhagic stroke

Answer 55

Neurologic deficits are not permanent Clinical Manifestations  Weakness, numbness, sudden confusion, loss of balance, loss of vision, or sudden severe headache

Answer 56

o Arterial occlusions are caused by thrombi formed in the arteries that supply the brain or in intracranial vessels o Is attributed to atherosclerosis and inflammatory disease processes

Answer 57

o Fragments break from a thrombus that is formed outside of the brain o A second stroke usually occurs

Answer 58

o Is spontaneous bleeding into the brain o Is also called spontaneous intracranial hemorrhage o Systolic and diastolic pressures have significantly increased over several years

Answer 59

Focal neurologic deficits, altered consciousness, headache

Answer 60

 Needs to be initiated within 3–4 hours of symptom onset  Limit hematoma enlargement  Prevent or control seizures and cerebral edema

Answer 61

Chronic autoimmune disease o Immunoglobulin G (IgG) antibody produced against acetylcholine receptors on the postsynaptic membrane Defect in nerve impulse transmission at the neuromuscular junction o Autoantibodies, complement deposits, and membrane attack complexes destroy the acetylcholine receptor (AChR) sites, causing decreased transmission of the nerve impulse

Answer 62

o Exertional fatigue and weakness that worsens with activity, improves with rest, and recurs with resumption of activity o Weakness and fatigue of muscles of the eyes and the throat, causing diplopia, difficulty chewing, talking, and swallowing

Answer 63

severe muscle weakening, leading to respiratory distress

Answer 64

resembles myasthenic crisis but weakness occurs 30–60 minutes after taking anticholinergic medication

Answer 65

Plasmapheresis

Answer 66

 Withhold anticholinergic drugs until blood toxic levels fall  Provide ventilatory support  Prevent respiratory complications

Answer 67

 Anticholinesterase drugs, corticosteroids, immunosuppressant drugs (Rituximab, a chimeric monoclonal antibody against the protein CD20, primarily found on B cells), azathioprine, cyclosporine, mycophenolate mofetil  Immunotherapy

Answer 68

- Levels of antidiuretic hormone (ADH) are abnormally high - Ectopic secretion of ADH is the most common cause; is also common after surgery and some cancers - Water retention: action of ADH on renal collecting ducts increases their permeability to water, thus increasing water reabsorption by the kidneys - For diagnosis, normal renal, adrenal, and thyroid function must exist

Answer 69

o Hyponatremia: sodium <135 mEq/L o Hypoosmolality: <280 mOsm/kg o Urine hyperosmolality: higher than serum osmolality o Hypervolemia o Weight gain o Serum sodium levels below 110–115 mEq/L: can cause severe and sometimes irreversible neurologic damage

Answer 70

o Correction of underlying causal problems o Emergency correction of severe hyponatremia by the administration of hypertonic saline o Vaptans o Most important: fluid restriction between 800 and 1000 mL/day o Resistant or chronic SIADH: demeclocycline

Answer 71

Insufficient amounts of ADH o Polyuria and polydipsia o Partial or total inability to concentrate the urine

Answer 72

Insensitivity of the renal collecting tubules to ADH

Answer 73

Excessive fluid intake, lowering plasma osmolarity to the point that it falls below the threshold for ADH secretion

Answer 74

Is characterized by the inability of the kidney to increase permeability to water o Excretion of large volumes of dilute urine o Increase in plasma osmolality: 300 mOsm or more, depending on adequate water intake o Urine output: 8–12 L/day; normal output: 1–2 L/day

Answer 75

o Polyuria, nocturia, continual thirst o Low urine-specific gravity: <1.010 o Low urine osmolality (<200 mOsmL/kg) o Hypernatremia o Diuresis

Answer 76

administration of the synthetic vasopressin analog desmopressin acetate (DDAVP)

Answer 77

treatment of any reversible underlying disorders, discontinuation of etiologic medications, and correction of associated electrolyte disorders; administration of thiazide diuretic agents

Answer 78

effective management of water ingestion

Answer 79

Connective tissue proliferation o Enlarged tongue, interstitial edema, increase in size and function of sebaceous and sweat glands, coarse skin and body hair Bony proliferation o Large joint arthropathy, kyphosis, enlargement of facial bones and hands and feet, protrusion of the lower jaw and forehead, need for increasingly larger sized shoes, hats, rings, and gloves Symptoms of diabetes o Polyuria and polydipsia Central nervous system (CNS) symptoms o Headache, seizure activity, visual disturbances, papilledema

Answer 80

o Primary treatment: transsphenoidal surgery or endonasal endoscopic surgery for the removal of the GH-secreting adenoma o Radiation therapy o Octreotide, octreotide long-acting, and lanreotide (somatostatin analogs) to lower GH levels o Cabergoline (dopaminergic agonists) to lower prolactin levels o Pegvisomant to block GH receptor

Answer 81

o Hyperthyroid condition o Is an autoimmune disease; develops autoantibodies

Answer 82

 Ophthalmopathy * Exophthalmos: increased secretion of hyaluronic acid, orbital fat accumulation, inflammation, and edema of the orbital contents * Diplopia: double vision  Pretibial myxedema (Graves dermopathy): leg swelling

Answer 83

 Antithyroid drugs, radioactive iodine, or surgery  Does not reverse infiltrative ophthalmopathy or pretibial myxedema

Answer 84

 Iodine deficiency (endemic goiter): most common worldwide  Autoimmune thyroiditis (Hashimoto disease): most common hypothyroidism in the United States

Answer 85

 Thyroid hormone deficiency present at birth  If not treated, cretinism develops  Neonatal screening to reduce incidents  Administration of T4

Answer 86

 Most common endocrine malignancy from ionizing radiation  Changes in voice and swallowing and difficulty in breathing, related to a tumor growth impinging the trachea or esophagus  Some may have normal T3 and T4 levels

Answer 87

 Low basal metabolic rate, cold intolerance, lethargy, tiredness, and slightly lowered basal body temperature; also possible diastolic hypertension  Myxedema  Nonpitting, boggy edema, especially around the eyes, hands, and feet; thickening of the tongue  Myxedema coma  Medical emergency, diminished level of consciousness; hypothermia without shivering, hypoventilation, hypotension, hypoglycemia, lactic acidosis, and coma

Answer 88

 Levothyroxine (synthetic hormone)  Myxedema coma  Thyroid hormone, combined with circulatory and ventilatory support  Management of hyponatremia and hypothermia

Answer 89

 Excess secretion of PTH from one or more parathyroid glands and hypercalcemia  80%–85% caused by parathyroid adenomas

Answer 90

 Increase in PTH, secondary to a chronic disease * Chronic renal failure * Dietary deficiency of vitamin D, calcium  Hypercalcemia does not occur

Answer 91

 Excessive secretion of PTH and hypercalcemia from long-standing secondary hyperparathyroidism

Answer 92

inherited disorder that causes abnormally high levels of calcium in the blood (hypercalcemia) and low to moderate levels of calcium in urine (hypocalciuric)

Answer 93

 Most asymptomatic  Hypercalcemia and hypophosphatemia, possible kidney stones from hypercalciuria, alkaline urine, pathologic fractures  Secondary: low serum calcium but elevated PTH

Answer 94

Surgery, bisphosphonates, corticosteroids, and calcimimetics

Answer 95

o Abnormally low PTH levels  Depressed serum calcium level  Increased serum phosphate level o Usual causes: parathyroid damage in thyroid surgery, autoimmunity, or genetic mechanisms o Pseudohypoparathyroidism: inherited condition

Answer 96

 Hypocalcemia  Lowering of the threshold for nerve and muscle excitation  Muscle spasms; hyperreflexia; tonic-clonic convulsions; laryngeal spasms; death from asphyxiation  Chvostek and Trousseau signs  Phosphate retention

Answer 97

 Calcium and vitamin D  Phosphate binders, if needed

Answer 98

* Environmental and genetic factors are thought to trigger cell-mediated destruction of pancreatic beta cells (type 1A) * Autoantibody, T-cell, and macrophage destruction of pancreatic beta cells occur with a loss of insulin production and a relative excess of glucagon

Answer 99

Occurs secondary to other diseases, such as pancreatitis, or secondary to a more fulminant disorder termed idiopathic diabetes (type 1B)

Answer 100

 Long preclinical period with gradual beta-cell destruction, leading to insulin deficiency and hyperglycemia  Loss of function of the insulin-secreting beta cells in the islet of Langerhans occurs before hyperglycemia develops  Polydipsia, polyuria, polyphagia, weight loss, and fatigue

Answer 101

 Combination of insulin, meal planning, exercise, and self-monitoring of blood glucose  Transplant: islet cells and the whole pancreas

Answer 102

o Is more common than type 1 diabetes mellitus o Genetic, epigenetic, and environmental interactions: must be genetically predisposed o Insulin resistance and decreased insulin secretion by beta cells: are major mechanisms

Answer 103

 Response of insulin-sensitive tissues (especially liver, muscle, and adipose tissue) to insulin is suboptimal  Obesity makes one prone to insulin resistance

Answer 104

 Beta cell mass is decreased  Inflammation and changes occur in adipokines

Answer 105

 Pancreatic alpha cells are less responsive to glucose inhibition; hyperglycemia—abnormally high levels of glucagon increase hepatic production of glucose

Answer 106

 Fatigue, pruritus, recurrent infections, visual changes, or symptoms of neuropathy (paresthesia or weakness)

Answer 107

o Primary adrenal insufficiency, hypocortisolism o Rare, autoimmune mechanisms o Inadequate corticosteroid and mineralocorticoid synthesis; elevated ACTH

Answer 108

 Hypocortisolism and hypoaldosteronism  Weakness, hyperpigmentation, vitiligo

Answer 109

 Lifetime glucocorticoid and mineralocorticoid replacement therapy; 150 mEq sodium per day

Answer 110

 Overproduction of pituitary ACTH by a pituitary adenoma  Lose diurnal and circadian patterns of ACTH and cortisol secretion  Lack of ability to increase ACTH and cortisol in response to stressors

Answer 111

 Weight gain of adipose tissue in the trunk, facial, and cervical areas  Is described as “truncal [central] obesity,” “moon face,” and “buffalo hump”  Sodium and water retention, glucose intolerance, protein wasting  Renal stones  Purple striae  Bronze or brownish hyperpigmentation of the skin

Answer 112

Medication, radiation, surgery

Answer 113

o AKA white blood cell (WBC) o Defense mechanisms

Answer 114

Humoral and cell mediated immunity

Answer 115

Phagocytosis; mononuclear phagocyte system

Answer 116

Phagocytosis; particularly during early phase of inflammation, bactericidal

Answer 117

Inflammatory response, often present in allergic reactions

Answer 118

Anti-parasitic and antibacterial

Answer 119

Is the most common macrocytic anemia Is caused by a vitamin B12 deficiency Lacks intrinsic factor from the gastric parietal cells  Required for vitamin B12 absorption May be congenital or autoimmune disorder  Autoantibodies against intrinsic factor

Answer 120

 Genetics  Endocrine disorders  Gastrectomy, ileal resection, tapeworms, demand of vitamin B12

Answer 121

 Weakness, fatigue  Paresthesias of the feet and fingers, difficulty walking  Loss of appetite, abdominal pains, weight loss  Sore tongue that is smooth and beefy red, secondary to atrophic glossitis  “Lemon yellow” (sallow) skin as a result of a combination of pallor and icterus  Hepatomegaly, splenomegaly  Neurologic symptoms from nerve demyelination • Not reversible, even with treatment  Is often unrecognizable in older adults because of its subtle, slow onset and presentation

Answer 122

 Weekly/monthly injections or high oral doses of vitamin B12 are administered  If left untreated, death will result

Answer 123

o Most common type of anemia worldwide o Highest risk: toddlers, adolescent girls, women of childbearing age, those living in poverty, infants consuming cow’s milk, older adults on restrictive diets, teenagers on junk food diets

Answer 124

 Dietary lack and eating disorders  Impaired absorption  Increased requirement  Chronic blood loss  Medications (that cause GI bleeding)  Some surgeries

Answer 125

 Fatigue, weakness, shortness of breath  Pale earlobes, palms and conjunctivae  Brittle, thin, coarsely ridged, and spoon-shaped (concave or koilonychia) nails  Burning mouth  Angular stomatitis: dryness and soreness in the corners of the mouth  Become symptomatic: when hemoglobin (Hgb) 7–8 g/dL

Answer 126

 Identify and eliminate sources of blood loss  Iron replacement therapy: PO, IM, IV  Sodium ferric gluconate complex in sucrose (Ferrlecit) and iron sucrose injection (Venofer)  Duration of therapy: usually 6–12 months after the bleeding has stopped but may continue for as long as 24 months

Answer 127

Most aplastic anemias are autoimmune disorders; some are due to chemicals, drugs, physical agents, unpredictable exposures; inherited or idiosyncratic Pathophysiology  Hypocellular bone marrow that has been replaced with fat

Answer 128

Reduction or absence of all three types of blood cells

Answer 129

 Rare genetic anemia from defects in DNA repair

Answer 130

 Hypoxemia, pallor (occasionally with a brownish pigmentation of the skin)  Weakness along with fever and dyspnea with rapidly developing signs of hemorrhaging if platelets are affected

Answer 131

 Bone marrow transplantation Peripheral blood stem cell transplantation * May receive radiation or chemotherapy before procedure Immunosuppression * Antithymocyte globulin with cyclosporin * Corticosteroidal medications Identification of high-risk individuals If not treated or identified, death occurs

Answer 132

o Accelerated destruction of RBCs o Congenital versus acquired o Intravascular versus extravascular hemolysis o Paroxysmal nocturnal hemoglobinuria  Deficiency in CD55 and CD59: cause complement-mediated intravascular lysis and release of hemoglobin  Anemia, hemoglobinuria, severe fatigue, abdominal pain, and thrombosis

Answer 133

 Autoantibodies against antigens normally on the surface of erythrocytes  Warm reactive antibody type  Cold agglutinin type  Cold hemolysin type (paroxysmal cold hemoglobinuria)  Based on the optimal temperature at which the antibody binds to the erythrocytes

Answer 134

Uncommon but most common form of AIHA

Answer 135

IgM antibodies

Answer 136

 Form of immune hemolytic anemia that is usually the result of an allergic reaction against foreign antigens  Called the hapten model  Caused by penicillin, cephalosporins (more than 90%), hydrocortisone

Answer 137

 May be asymptomatic  Jaundice (icterus)  Aplastic crisis  Splenomegaly

Answer 138

 Acquired: removal of the cause or treatment of the underlying disorder  First line: corticosteroids  Second line: splenectomy and rituximab (monoclonal antibody)  Paroxysmal nocturnal hemoglobinuria: eculizumab

Answer 139

o Complex, acquired disorder: clotting and hemorrhage simultaneously occur o Cause: variety of clinical conditions that release tissue factor o Characterized by a cycle of intravascular clotting, followed by active bleeding

Answer 140

Wide variability  Bleeding from venipuncture sites  Bleeding from arterial lines  Bleeding from surgical wounds  Purpura, petechiae, and hematomas  Symmetric cyanosis of the fingers and toes

Answer 141

 Eliminate underlying pathology  Control thrombosis  Maintain organ function  Administer replacement therapy  Replace anticoagulants

Answer 142

o Greater than 30% lymphoblasts in bone marrow or blood o Genetic anomaly: Philadelphia chromosome

Answer 143

Most common adult leukemia (older than 50 years) Clinical manifestations  Fatigue caused by anemia  Bleeding resulting from thrombocytopenia (reduced numbers of circulating platelets)  Fever caused by infection  Anorexia, weight loss, diminished sensitivity to sour and sweet tastes, muscle atrophy, and difficulty swallowing  Central nervous system (CNS) involvement

Answer 144

Reed-Sternberg cells in the lymph nodes o Are necessary for the diagnosis but not specific to Hodgkin lymphoma o Are derived from malignant B cells that usually become binucleate o Release cytokines

Answer 145

derived from B cell in the germinal center that has not undergone successful immunoglobulin gene rearrangement and would normally be induced to undergo apoptosis

Answer 146

presents with earlier stage disease, longer survival, and fewer treatment failures [10% have a tendency to histologically transform into diffuse large B-cell lymphoma]

Answer 147

o Enlarged painless neck lymph nodes o Lymphadenopathy, causing pressure or obstruction o Mediastinal mass o Fever, weight loss, night sweats, pruritus, fatigue

Answer 148

o Approximate cure rate: 75% o Combined treatment with radiation therapy and chemotherapy o High-dose chemotherapy with bone marrow or stem cell transplantation o Monoclonal antibodies o Nonmyeloablative allogeneic stem cell transplantation

Answer 149

- WHO/REAL scheme now calls this "B cell neoplasms" and includes T-cell and natural killer (NK) neoplasms - Is linked to chromosome translocations - Clonal expansion of B cells (85%–90%), T cells, and/or NK cells occurs - Changes in proto-oncogenes and tumor-suppressor genes contribute to cell immortality and thus an increase in malignant cells

Answer 150

o Localized or generalized painless lymphadenopathy o Nodal enlargement and transformation over months or years o Retroperitoneal and abdominal masses with symptoms of abdominal fullness and back pain o Ascites (fluid in the peritoneal cavity) and leg swelling

Answer 151

o Survival: extended periods but less than the survival rate for Hodgkin lymphoma o Dependent on the type (B cell or T cell), tumor stage, histologic status (low, intermediate, high grade), symptoms, age, and any comorbidities o Chemotherapy or radiation o Combination of chemotherapy and radiation o Monoclonal antibody: rituximab o Radioimmunotherapy: combination of radiation therapy with monoclonal antibody therapy

Exam II Flashcards

(175 cards)