Therapeutics Hematology/oncology Exam 1

Front 1

1. usually caused by an acute injury
2. musculoskeletal, soft tissue, skin
3. dull, aching, sharp, constant, "ouch" pain
4. localized and readily identifiable
5. mediated by prostaglandins, acute phase reactants

Back 1

nociceptive or somatic pain

Front 2

1. cause may be unknown
2. usually involves internal organs (liver, pancreas, GI, GU tracts)
3. difficult to localize
4. may describe as "nausea" or "gnawing" feeling
5. mediated by enteric and sympathetic nervous systems

Back 2

visceral pain

Front 3

1. caused by nerve injury, irritation or damage
2. central (spinal cord injury, stroke)
3. peripheral (diabetic neuropathy, post-herpetic neuralgia_
4. burning, shooting tingling, numbness
5. associated with: hyperalgesia, allodynia

Back 3

neuropathic pain

Front 4

indications for NSAIDs (6)

Back 4

1. rheumatoid and osteoarthritis
2. chronic inflammatory conditions
3. musculoskeletal
4. bony pain (tumor, etc.)
5. lower back pain (?)
6. post-operative pain (celebrex--doesn't affect platelets)

Front 5

contraindications for NSAIDs (6)

Back 5

1. peptic ulcer disease (PUD)
2. renal insufficiency
3. platelet dysfunction
4. uncontrolled CHF/ HTN (Na and fluid retention)
5. ASA-sensitive asthma
6. pregnancy (esp. in last 3-6 months)

Front 6

risk factors for GI toxicity (7)

Back 6

1. history of complicated ulcer
2. multiple NSAIDs (including ASA)
3. high doses of NSAIDs
4. use of anticoagulant
5. age >70
6. use of corticosteroids
7. SSRI?--affect platelet function

Front 7

pain indications for pregabalin (3)

Back 7

1. post-herpetic neuropathy
2. diabetic peripheral neuropathy
3. fibromyalgia

Front 8

pain indications for gabapentin (1)

Back 8

1. post-herpetic neuropathy

Front 9

state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist

Back 9

physical dependence

Front 10

state of adaptation in which exposure to a drug induces changes that result in diminution of one or more the the drug's effects over time

Back 10

tolerance

Front 11

primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manisfestations. it is characterized by behaviors that include one or more of the following: imparied control over drug use, compulsive use, continued use despite harm and craving

Back 11

addiction

Front 12

presentation of acute pain (7)

Back 12

1. tachycardic
2. tachypneic
3. increase in BP
4. increase in temperature
5. diaphoretic
6. agitated/delirious
7. restlessness

Front 13

presentation of chronic pain (4)

Back 13

1. vitals normal
2. uncomfortable
3. no CNS changes
4. no autonomic changes

Front 14

side effects of opioids (6)

Back 14

1. nausea
2. vomiting
3. rash
4. pruritis
5. sedation
6. hallucinations

Front 15

1. natural opioid (IR, ER)
2. used first line in acute pain
3. dose: 1-2 mg IV q 4h; 15 mg PO q 4h; 1 mg IV q 10 min for PCA
4. SE: nausea, itching, constipation
5. active metabolites are cleared renally (reduce dose if renal impairment)

Back 15

morphine

Front 16

1. semi-synthetic opioid (IR, ER)
2. 10 mg IV morphine = 1.5 mg IV of this medication
3. less itching than morphine
4. dose: 0.2 mg IV q 4h; 2-4 mg PO q 4h; 0.2 mg q 10 min PCA
5. active metabolites renally cleared (reduce dose if renal impairment)

Back 16

hydromorphone

Front 17

1. synthetic (fewer histamine-related effects)
2. used for anesthesia in higher doses
3. no active metabolites (may be used in renal impairment)
4. dosing is in MCG (PCA 10 mcg IV q 10 min)
5. fast onset of action (IV) and very short half life
6. continuous infusion may lead to accumulation in fatty tissues
7. no standard oral dosage forms
8. transmucosal products: for breakthrough pain in cancer patients; only in patients who are already taking opioids

Back 17

fentanyl

Front 18

oral semi-synthetic opioids (3)

Back 18

1. oxycodone (IR/ER) with or without APAP--5 mg q 4-6h
2. hydrocodone (IR only) with APAP--5 mg q 4-6h
3. oxymorphone (IR/ER)--10 mg q 4-6h

**all oral formulations

Front 19

1. not a good choice
2. lots of nausea, histamine release
3. converted to morphine in the liver by CYP 2D6
4. pharmacogenetic differences: rapid metabolizers = morphine toxicity; slow metabolizers = very little or no morphine

Back 19

codeine

Front 20

agents in phase 1 of metabolism that go through cyp 2D6 activity (4)

Back 20

1. codeine
2. tramadol
3. hydrocodone
4. oxycodone

Front 21

agents in phase 1 of metabolism that go through CY3A4 activity (5)

Back 21

1. methadone
2. buprenorphine
3. fentanyl
4. tramadol
5. oxycodone

Front 22

which glucuronate of morphine is 10x more effective?

Back 22

M-6-glucuronide

Front 23

which agents are ok to use in renal insufficiency (4)

Back 23

1. fentanyl
2. methadone
3. oxycodone
4. hydrocodone

Front 24

what to do if persistant sedation from opioid? (3 steps)

Back 24

1. hold 1-2 doses of opioid
2. restart with 25% reduction of dose
3. dose more frequently

Front 25

at risk populations for respiratory depression (4)

Back 25

1. extremes of age
2. concurrent CNS depression
3. severe lung disease
4. sleep apnea

Front 26

treatment for nausea/vomiting in patients using opioid (3)

Back 26

1. promethazine/prochlorperazine
2. 5-HT3 antagonist (ondansetron)
3. consider changing opioid

Front 27

treatment for itching in patients using opioids (5)

Back 27

1. antihistamine (not always effective)
2. nalbuphine
3. naloxone
4. ondansetron (?)
5. consider switching opioid (morphine>hydromorphone>fentanyl, methadone)

Front 28

mediators of the immune system involved in RA (5)

Back 28

1. immunoglobulins
2. rheumatoid factors (antibodies)
3. the complement system
4. interleukins (interleukin 1)
5. T cells and B cells (cellular components)

Front 29

main targets for newer treatment options for RA because these two agents cause inflammation and cartilage/ bone destruction (2)

Back 29

1. tumor necrosis factor (TNF)
2. interleukin-1

Front 30

diagnosis of RA depends on what factors (3)

Back 30

1. characteristic symptoms
2. lab tests
3. radiographic findings

Front 31

first sites involved in RA (2)

Back 31

1. metacarpolphalangeal joints (MCP)
2. proximal interphalangeal (PIP) joints

**within the hands

Front 32

key features in diagnosing RA (5)

Back 32

1. evidence of clinical synovitis
2. morning stiffness or stiffness after prolonged period of inactivity (key feature: morning stiffness lasting longer than 1 hour)
3. generalized complaints of fever and fatigue
4. examination of hands--tells if patient is having early, late, or progressive disease
5. other joints involved

Front 33

other joints involved in RA (7)

Back 33

1. wrists (almost always)
2. elbows (frequently)
3. shoulder (late in disease)
4. feet (common)
5. hip
6. spine (especially cervical)
7. knees

Front 34

non-pharmacological treatment options for RA (3)

Back 34

1. joint protection
2. conservation of energy
3. motion and strengthening exercises

Front 35

role of corticosteroids in RA (3)

Back 35

1. bridge therapy to control symptoms during the initial phases of disease modifying antirheumatic drugs or during flare-ups
2. intra-articular injections of acutely inflamed joints
3. pregnancy

Front 36

cautions with corticosteroids in RA (4)

Back 36

1. avoid using without DMARDs
2. try to taper to lowest effective dose and limit therapy to <6 months
3. supplement with calcium and vitamin D
4. consider use of bisphosphonates

Front 37

how long does it take to see the efficacy of hydroxychloroquine?

Back 37

3-6 months; not considered failure until after 6 months

Front 38

1. dose: 200 mg BID
2. MOA: categorized as anti-malaria agent whose mechanism is unknown; deemed moderately effective for RA
3. onset of action: efficacy may not be apparent for 3-6 months
4. AE: relatively benign with nausea and epigastric pain being most common; serious AE are rare; hemolysis may occur in those with glucose-6-phosphate dehydrogenase deficiency; retinal damage may occur
5. monitoring: visual field checks at baseline and ever 6-12 months
6. misc: likely the least effective of DMARDs and is more useful in mild disease or in combo with other DMARDs; one of the largest advantages is the safety profile

Back 38

hydroxychloroquine

Front 39

dosing for MTX

Back 39

initiate with 7.5 mg q weekly then increase by 5 mg every 1-2 months up to weekly dose of 20-30 mg

Front 40

MOA of MTX

Back 40

folate antagonist--interferes with synthesis of DNA and cell reproduction

mechanism inRA is unclear but believed to have anti-inflammatory and immunosuppressive effects

Front 41

onset of action for MTX in RA

Back 41

4-6 weeks but could be as early as 2-3 weeks

Front 42

GI adverse effects of MTX (4)

Back 42

1. nausea
2. vomiting
3. diarrhea
4. stomatitis

Front 43

hematologic adverse effects of MTX (2)

Back 43

1. thrombocytopenia
2. leukopenia (less likely)

Front 44

pulmonary adverse effects of MTX (2)

Back 44

1. hypersensitivity pneumonitis
2. pulmonary fibrosis

Front 45

hepatic adverse effects of MTX (1)

Back 45

1. elevations in liver enzymes

Front 46

monitoring parameters for MTX (3)

Back 46

1. LFTs
2. CBC with platelets
3. renal function q 4-8 weeks

Front 47

what is considered the DMARD of choice for initial treatment in moderate to severe RA

Back 47

MTX

**also forms basis or anchor drug for combination therapy with other DMARDs

Front 48

MTX is best to avoid in? (3)

Back 48

1. underlying hepatic disease
2. significant alcohol use
3. severe renal disease

Front 49

1. dose: load with 100 mg QD x 3 days then 20 mg QD
2. MOA: prodrug whose metabolite inhibits pyrimidine synthesis and decreases proliferation of lymphocytes
3. indication: approved as monotherapy for RA or in combination with NSAIDs/ corticosteroids
4. onset of action: usually within 1 month
5. AE: diarrhea, alopecia (reversible), rash, increase in LFT
6. monitoring: LFTs, CBC, creatinine q 4-8 weeks
7. as effective as MTX in established and recent RA
8. loading dose required due to the half life of the drug
9. d/c and ingest cholestyramine 8 grams TID x 11 days before considering child conception
10. has been combined with MTX but need to watch liver function!

Back 49

leflunomide (Arava)

Front 50

what do patients need to be screened for before starting biologic DMARDs or biologic response modifiers ? (2)--these two are of primary concern also important to screen for other infections/diseases before starting

Back 50

1. tuberculosis--patients with dormant disease can have their TB reactivated
2. fungal infections

Front 51

TNF-alpha inhibitor selection based on (3)

Back 51

1. willingness to self-inject
2. willingness to make frequent office visits
3. willingness of insurance to pay/insurance preferance

Front 52

when will patients notice improvement with TNF-alpha inhibitors?

Back 52

1-4 weeks after initiation but may take up to 3 months to see full effect

Front 53

TNF-alpha inhibitors

recent FDA warning added to include risk of infection from ____ and ___

Back 53

1. legionella
2. listeria

Front 54

which biologic agent is approved only for use with MTX and not as a monotherapy

Back 54

inflixamab

Front 55

which biological DMARD is reserved for patients who have failed other biologics because of its ability of variation dosing

Back 55

inflixamab

Front 56

1. anti-TNF alpha monoclonal antibody which is cloned 100% from human segments; it is indistinguishable from human IgG1
2. approved for the treatment of moderately to severely active RA in adult patients who have displayed inadequate response to 1 or more DMARDs

Back 56

adalimumab (Humira)

Front 57

which TNF alpha inhibitor is given only once monthly?

Back 57

golimumab (Symponi)

Front 58

1. humanized antibody Fab fragment conjugated to polyethylene glycol (pegylation process)
2. more rapid onset of action and fewer injection site reactions

Back 58

certolizumab pegol (cimzia)

Front 59

TNF alpha inhibitor agents (5)

Back 59

1. etanercept (Enbrel)
2. infliximab (Remicade)
3. adalimumab (Humira)
4. golimumab (Symponi)
5. certolizumab pegol (Cimzia)

Front 60

1. MOA: co-stimulation modulator; prevents one of two stimulation mechanism for t-cell activation and results in reduction in the release of cytokines (IL-1, TNF, IL-6)
2. indication: moderate to severe RA in patients who have had an inadequate response to MTX and TNF antagonists
3. onset: within 2 weeks; full effect noted within 3 months
4. caution in those with underlying COPD--may have increased development of adverse effects
5. should not be administered with other BRMs due to lack of added benefit (fine to give with MTX)

Back 60

abatacept (Orencia)--T-lymphocyte therapy

Front 61

1. two 1000 mg IV infusions separated by 2 weeks; methylprednisolone 10 mg (or equivalent) given 30 min before infusion to minimize infusion related reaction; suggested premedication before infusion with APAP and antihistamine
2. MOA: monoclonal IgG kappa antibody which selectively targets CD-20 inflammatory process
3. combination with MTX in those with moderate to severe disease and who have had an inadequate response to one or more TNF antagonist therapies
5. onset: with in 16 weeks
6. CARDIAC monitoring throughout infusion

Back 61

retuximab (Rituxin)
B-lymphocyte therapy

Front 62

1. initiate with 4 mg/kg by IV infusion over 60 minutes every 4 weeks then increase to 8 mg/kg based on clinical response
2. MOA: interleukin-6 receptor inhibitor which blocks the IL-6 induced t-cell activation; will also block local joint production of IL-6
3. need to monitor for myelosuppression and negative effects on lipids

Back 62

tocilizumab (Actemra)

Front 63

indication for use of what biologic?

1. in combo with MTX for those with early RA who have never received DMARDs and have high disease activity
2. those with intermediate and longer duration of RA in those who have had prior MTX therapy with an inadequate response

Back 63

anti-TNF agent (interchangeably)

Front 64

indication for use of what biologic?

used in patients for whome MTX in combination with DMARDs or sequential administration of other nonbiological DMARDs led to an inadequate response and at least moderate disease activity and features of a poor prognosis

Back 64

abatacept

Front 65

indication for use of what biologic?

used in patient for whome MTX in combination with DMARDs or sequential administration of non-biologic DMARDs led to an inadequate response and high disease activity and features of a poor prognosis

Back 65

rituximab

Front 66

___ invariably are the center of SLE pathogenesis

Back 66

B-lympocytes

Front 67

which co-morbidities have been associated with lupus? (5)

Back 67

1. infection
2. cardiovascular disease
3. osteoporosis
4. avascular necrosis
5. malignancies

Front 68

drugs most commonly associated with lupus (2)

Back 68

1. procainamide
2. hydralazine

Front 69

other drugs associated with lupus that have good evidence linking them to lupus (5)

Back 69

1. chlorpromazine
2. isoniazid
3. methyldopa
4. minocycline
5. quinidine

Front 70

1. considered first-line therapy for those with mild symptoms of lupus
2. particularly useful for fever, arthritis, and other musculoskeletal symptoms
3. choice of agent in class is empiric; dosing typically higher

Back 70

NSAIDs

Front 71

1. mainstay of treatment in patients with lupus especially during flares
2. these will inhibit b-cell and t-cell responses

Back 71

corticosteroids

mild disease: prednisone 10-20 mg QD
severe disease: prednisone 1-2 mg/kg/day
patients may also receive IV pulse therapy with methylprednisolone (30 mg/kg max 1 g/day)

Front 72

1. considered first line treatment (along with NSAIDs) for treatment of mild lupus
2. agent will cause a down-regulation of interferon-alpha and decrease the antigen processing for autoantigen presentation
3. dosing is 200-400 mg QD and the medication is fairly benign
4. max effect not present for 3-6 months

Back 72

hydroxychloroquine

Front 73

1. inactive until metaoblized into mercaptopurine after which it inhibits DNA synthesis thus preventing cell proliferation in the immune system
2. considered to be a steroid-sparing agent
3. dosing 1-3 mg/kg/day
4. AE: typical toxicity is GI--oral ulcers, NVD, epigastric pain
5. dose related toxicities myelosuppression may occur including leukopenia and less commonly thrombocytopenia

Back 73

azathioprine (imuran)

Front 74

1. often considered an induction agent for lupus flares (other immunosuppressive agents are preferred for maintenance)
2. optimal dosing has not been defined however IV pulse therapy based on body surface area is employed
3. toxicities often limit use--myelosuppression, malignancy, immunosuppression, hemorrhagic cystitis

Back 74

cyclophosphamide

Front 75

1. pro-drug of mycophonolic acid which inhibits inosine monophosphate dehydrogenase; causes disruption of an essential step for DNA synthesis in lymphocytes with the end result of blocking proliferation of activated T and B lymphocytes
2. useful for both induction and remission of SLE
3. dosing is 500-3000 mg QD (typical dose of 2000 mg)
4. adverse effects are mainly GI (NVD; rarely will cause leukopenia)

Back 75

mycophenolate mofetil

Front 76

LUPUS

1. agent will deplete B cells from the peripheral blood but has a sparing effect on the T cell sthus less immnuosuppressive than other agents
2. dosing is 500-1000 mg q 2 weeks x 2 doses; then 375 mg/mm2 q weekly for 2-4 doses
3. requires pretreatment with corticosteroid, antihistamine,and APAP to reduce infusion related reactions (fever, chills, hypertension, arthralgias, pruritis)

Back 76

rituximab

Front 77

1. this is a monoclonal antibody which binds to and inhibits the action of the soluble form of the b-lymphocyte stimulator (BLyS)--it is known that levels of BLyS are increased in many patients with lupus and some have proposed the levels can be correlated to disease severity
2. indicated for those with active, auto-antibody positive, SLE who are receiving standard therapy (not recommended in combo with other bioligcs or IV cyclophosphamide)
3. dosing 10 mg/kg IV over an hour at 2 week intervals for first 3 doses; then 4 week intervals thereafter
4. serious infections, depression, avoidance of live vaccines are a few warnings
5. common ADR: N/D, fever, infection, depression, and migraines however d/c rates are similar to placebo

Back 77

belimumab (Benlysta)

Front 78

agents use for lupus therapy (8)

Back 78

1. NSAIDs
2. corticosteroids
3. hydroxychloroquine
4. azathioprine
5. cyclophosphamide
6. mycophenolate mofetil
7. rituximab
8. belimumab (Benlysta)

Front 79

how would you treat mild/moderate nephritis?

Back 79

pulse corticosteroids and long term suppression with azathioprine with or without coritcosteroids

Front 80

how would you treate severe/unresponseive lupus nephritis?

Back 80

1. pulse IV corticosteroids and/or oral cyclophosphamide or azathioprine (IV pulse cyclophosphamide has been preferred)
2. mycophenolate mofetil considered a viable option and often preferred in place of IV cyclophosphamide; also shown to be option in those who are refractory to pulse IV cyclophosphamide)

Front 81

1. need agressive therapy to reduce the potential for mortality
2. best managed by agressive IV pulse cyclophophamide and corticosteroids

which form of lupus?

Back 81

neuropsychiatric lupus

Front 82

1. typically start with NSAIDs
2. corticosteroids may also be used especially for refractory cases

which complication of lupus?

Back 82

pericarditis and pleuritis

Front 83

leading causes of death in 1905 (5)

Back 83

1. infection
2. diseases of early infancy (diarrhea, enteritis)
3. diseases of circulatory system
4. diseases of nervous system
5. violence

Front 84

leading causes of death in 2005 (8)

Back 84

1. cardiac
2. cancer
3. CVA (cerebrovascular accident)
4. chronic respiratory
5. accidents
6. diabetes related
7. alzheimer's disease
8. influenza/pneumonia

Front 85

Proof that medicare requires that deems patient still eligible for hospice benefit (4)

Back 85

1. losing weight
2. sleeping more than awake
3. active symptoms requiring intervention
4. tissue documented disease

Front 86

acute effects of radiation therapy (7)

may be seen during and may persist for several weeks

Back 86

1. erythema
2. nausea
3. vomiting
4. anorexia
5. mucositis
6. dry mouth
7. local edema

Front 87

indications for radiation therapy (4)

Back 87

1. pain (bone mets, visceral pain from soft tissue mets, neuropathic pain secondary to tumor in nerve tissue)
2. local pressure (spinal canal compression, cranial nerve palsies)
3. obstruction (bowel/Gi, superior vena cava, limb swelling)
4. bleeding (hematuria, vaginal, rectal)

Front 88

ways to prevent constipation (5)

Back 88

1. encourage activity (if tolerated)
2. maintain adequate hydration
3. dietary modification
4. anticipate constipating effects of drugs and alter if possible
5. create favorable environment

Front 89

1. binds ions and water in the colonic lumen thereby increasing the bulk and water content of the stool

2. aids to stimulate reflex peristalsis

3. increase intestinal gas/bloating/fecal impaction

4. requires adequate water intake otherwise will get the opposite effect

Back 89

bulk forming agents

1. psyllium (metamucil)

2. methylcellulose (citrucil)

3. polycarbophil (fibercon)

Front 90

1. claimed to be non-absorbed, pharmcologically inert

2. useful in combinate

Back 90

emollient agents (stool softeners)

1. docusate sodium (colace)

2. docusate calcium (Surfak)

Front 91

1. non-absorbable sugars that are metabolized by colonic bacteria to low molecular weight acids

2. create an osmotic effect whereby the pH of the stool is lowered and there is an increase in intraluminal fluid

Back 91

osmotic agents

1. sorbitol

2. lactulose

3. polyethyleneglycol (PEG) (Miralax)

4. glycerin suppositories

Front 92

1. poorly absorbed anions and cations create an osmotic effect resulting in retention of fluid in the lumen

2. magnesium containing products are the most commonly used and in addition to the above mechanism, this cation also stimulates the release of cholecystokinin which is a hormone that stimulates bowel motility and fluid retention

Back 92

saline laxative

1. milk of magnesia (PRN use)

2. magnesium citrate (usually bowel preps?)

Front 93

1. selective for GI tract

2. intended for outpatients who have failed other regimens

Back 93

opioid antagonists

1. methylnaltrexone (relistor)

Front 94

1. directly stimulate myenteric plexus to cause stimulation of colonic activity

2. _____ will stimulate mucosal nerve plexus of the colon

Back 94

stimulant laxatives

1. sennosides (senakot)

2. bisacodyl (dulcolax)---answer to point 2

Front 95

1. usually reserved (patient preference) however very effective in evacuating colon

2. _____ are not preferred due to irritating effects and risk of colitis and/ proctitis

Back 95

enemas

1. tap water

2. saline

3. soap suds (answer to point 2)

Front 96

pharmacological options that are used to help palliative care patients increase appetite (5)

Back 96

1. corticosteroids (easiest)
2. medroxyprogesterone (at hight doses)
3. mirtazepine/ tricyclic antidepressants
4. methylphenidate
5. dronabinol (marinol)

Front 97

pharmacological options that are used to help reduce oral secretion in palliative care patients (3)

Back 97

1. scopolamine patch

2. atropine (subQ/IV OR eye drops used orally)

3. glycopyrrolate (SubQ/IV or oral tab)

Front 98

what is mirtazepine useful for in palliative care patients (4)

Back 98

1. stimulation of appetite

2. sleep

3. anxiety

4. depression

Front 99

what is nortriptyline useful for in palliative care patients (4)

Back 99

1. pain

2. depression

3. sleep

4. appetite

Front 100

what are SSRIs useful for in palliative care patients (2)

Back 100

1. depression

2. anxiety

citalopram generally used

Front 101

what is in a ABH suppository?

Back 101

1. ativan 1 mg

2. benadryl 12.5 mg

3. haloperidol 2 mg

Front 102

what is in a DBR suppository?

Back 102

1. decadron (aka dexamethasone) 4 mg

2. benadryl 25 mg

3. reglan (aka metoclopramide) 10 mg