Week 5 Flashcards

(130 cards)

1
Q

What are the 3 main cancer treatment options?

A
  • Surgery
  • Radiation
  • Chemotherapy
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2
Q

What do most chemotherapy medication act to do of chemotherapy?

A

Most chemotherapy medications act to disrupt cellular replication (DNA/RNA synthesis). This mechanism will also disrupt “healthy cells” leading to chemo toxicity

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3
Q

What are the common side effects of chemotherapy?

A
  • Poor Nutrition: nausea, loss of appetite, weight loss
  • Hair loss
  • Constipation
  • Anemia/ Blood disorders*
  • Secondary illness (low WBC often)
  • Osteopenia*
  • Reduced lean tissue mass
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4
Q

What is a key thing to keep in mind when working with patients that are going through chemotherapy?

A

To time rehab optimally, so they can maintain their tissue mass as much as possible

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5
Q

What are the different mechanisms of chemotherapy drugs?

A
  • Target certain part of the cell cycle
  • Receptors on the cell to alter the cell cycle leading to cell death
  • Immunotherapy – “revs” up the immune system
  • Genetic targeted therapy: identifies genetic mutations in the cancer cells
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6
Q

What is an example of alkylating agents used to treat cancer?

A

Cytoxan

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7
Q

What is the mechanism of alkylating agents used to treat cancer?

A

Mimics alkyl group to bind to DNA to prevent replication

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8
Q

What are the adverse effects of alkylating agents used to treat cancer?

A
  • Cardio./pulmonary toxicity
  • GI
  • Blood disorders
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9
Q

What is an example of antimetabolites drug used to treat cancer?

A

Capecitabine (oral)

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10
Q

What is the mechanism of antimetabolites drug used to treat cancer?

A

Blocks DNA/RNA replication by interfering with metabolites used in replication

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11
Q

What are the adverse effects of antimetabolites drug used to treat cancer?

A
  • Blood disorders
  • GI
  • Dermatitis
  • Fatigue
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12
Q

What is an example of the genetic target drug used to treat cancer?

A

Zelboraf (oral)

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13
Q

What is the mechanism of genetic target drug used to treat cancer?

A

Inhibits activity of mutations in cells

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14
Q

What are the adverse effects of genetic target drug used to treat cancer?

A
  • Edema
  • Fatigue
  • Headache
  • Rash
  • Nausea
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15
Q

What is an example of the plant alkaloids drug used to treat cancer?

A

Taxol

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16
Q

What is the mechanism of plant alkaloids drug used to treat cancer?

A

Breaks down/interferes with cellular microtubules key for mitosis (mitotic spindles)

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17
Q

What are the adverse effects of plant alkaloids drug used to treat cancer?

A
  • Blood disorders
  • Skin rash
  • Peripheral neuropathy
  • GI
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18
Q

What is an example of the bio-response modifier drug used to treat cancer?

A

Interferons

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19
Q

What is the mechanism of bio-response modifier drug used to treat cancer?

A

Enhance body’s ability to respond to cancer, not cytotoxic

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20
Q

What are the adverse effects of bio-response modifier drug used to treat cancer?

A
  • Flu-like symptoms

* Depression

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21
Q

What is an example of the heavy metal drug used to treat cancer?

A

Carboplatin

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22
Q

What is the mechanism of heavy metal drug used to treat cancer?

A

Act similar to alkylating agents except use platinum to form cross links. Key for bladder, testicular, ovarian CA)

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23
Q

What are the adverse effects of heavy metal drug used to treat cancer?

A
  • Blood disorders
  • GI
  • Fatigue
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24
Q

What are some of the rehab concerns for patients on chemotherapy?

A
  • Bleeding Risk
  • Chemo may lead to non-specific blood disorders
  • May lead to low platelets, hemoglobin, hematocrit
  • Patients may be on bone modifying agents, so might not be able to stress the skeletal system as much
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25
What are the factors that are to be considered to select an antibiotic?
* Prediction of infecting organism (Spectrum) * Susceptibility data/local resistance patterns * Site of infection * Duration of hospitalization/prior antibiotics * Allergy history * Age * Renal/Hepatic status * Immunologic status * Pregnancy * Cost
26
What are some examples of a gram positive bacteria/infection?
• Staphylococcus aureus (MRSA or MSSA) • Streptococci
27
What are the antibiotics used to treat gram positive bacteria/infection?
* Penicillins * Cephalosporins * Vancomycin (I.V.)
28
What are some examples of a gram negative bacteria/infection?
* E coli | * Pseudomonas
29
What are the antibiotics used to treat gram negative bacteria/infection?
* Cephalosporins (varies) | * Zosyn
30
What goes on in the empiric therapy period used for a patient with an infection?
Choose an antibiotic before the labs come back (24- 72 hours)
31
What goes on in the directed therapy period used for a patient with an infection?
Narrow down the antibiotic spectrum based on the specific organism – MINIMIZE RESISTANCE!!
32
Why should a person finish all their antibiotics even after they feel better?
Resistant strain starts to multiply causing a new (harder to treat) infection
33
What is a way to maximize the effectiveness of an antibacterial medication?
To find out the concentration levels of which all the organisms will be killed over a period of time.
34
What is the test that is used to find out the concentration levels of which all the organisms will be killed over a period of time.?
Sensitivity Testing Minimum Inhibitory Concentration
35
What is minimum inhibitory concentration of an organism?
Concentration at which the growth of the organism is | inhibited
36
How is the breakpoint of an organism determined?
Based on serum/tissue levels of | respective agent
37
What types of antibiotic is a cell wall synthesis inhibitor?
* Penicillins * Cephalosporins * Carbapenems
38
What is the MOA of a cell wall synthesis inhibitor antibiotic?
* Binds to specific penicillin binding proteins | * Inhibits the final step for peptidoglycan synthesis in bacterial cell walls
39
What types of antibiotic is a cell cell membrane toxicity drug?
Daptomycin
40
What is the MOA of a cell membrane toxicity antibiotic?
* Punches holes in the cell membrane | * Causing fluid disruption causing the cell to burse
41
What types of antibiotic is a cell nucleic acid toxicity drug?
* Levaquin | * Cipro
42
What is the MOA of a nucleic acid toxicity antibiotic?
* Disrupt the activity of the enzymes responsible for DNA transcription * Inhibits replication
43
What types of antibiotic are protein synthesis inhibitors?
* Gentamycin * Azithromycin * Linezolid * Tetracycline
44
What is the MOA of a protein synthesis inhibitors antibiotic?
• Causes the production of membrane proteins that do not maintain cell membrane function • Leads to cell death
45
What are the side effects/ rehab considerations of antibiotics?
* Rashes * Risk for allergic reactions * Nausea, vomiting, diarrhea * “C.diff” (severe diarrhea secondary to the loss of good bacteria) * Heart arrhythmias * Many require renal dosing adjustments * Food interactions (calcium, magnesium, etc.)
46
How are skin/soft tissue infections spread?
* Disruption of natural host defenses * Damage to corneal layer allowing for bacterial penetration * Reduced blood supply to affected area
47
What are the bacteria that are commonly found in the skin?
* Staph. epidermis * Staph. aureus * Streptococcal species
48
What is a primary bacterial infection?
Typically single bacteria infections, involving undamaged skin and usually carried through the blood
49
What is a secondary bacterial infection?
A polymicrobic infection that typically involves damaged skin
50
What is the mechanism of osteomyelitis?
Spread of infection to bone from adjacent soft tissues and | joints usually from trauma of surgery
51
What is the empiric therapy treatment option for osteomyelitis?
Vancomycin + gram (-) medication. EX: cefepime
52
What is the targeted therapy method for treating osteomyelitis caused by MSSA?
Nafcillin/oxacillin/cefazolin
53
What is the targeted therapy method for treating osteomyelitis caused by MRSA, staph?
Vancomycin
54
What is the targeted therapy method for treating osteomyelitis caused by any gram (-) or pseudomonas?
Cipro, Levquin, ceftazidime, cefepime
55
What layers of tissue is affected by cellulitis?
* Epidermis * Dermis * Superficial fascia
56
How do people usually get cellulitis?
Generally involves history of | previous minor trauma, ulcer or surgery or blood supply issues like diabetes
57
What are the signs and symptoms of cellulitis?
* Inflammation, erythema and possible edema | * Less common crepitus and lymphatic involvement
58
What are other ways cellulitis can be diagnosed?
When blood cultures/needle aspiration show bacteria like: • Group A streptococcus • Staph aureus • Haemophilus influenzae
59
What are the empiric therapy treatment options for cellulitis?
* Severe – nafcillin/oxacillin * Mild - 1st generation cephalosporin (Keflex) In the case of a penicillin allergy, use clindamycin
60
What are the directed therapy treatment options for cellulitis?
Adjust antibiotic selection based on culture results
61
What are the key mechanisms of antiviral drugs?
* Able to enter the cells infected with virus * Interfere with viral nucleic acid synthesis and or regulation * Interfere with ability of virus to bind to cells * Stimulate the body's immune system: Vaccines * Best response to antiviral medications are in patients with competent immune systems * Healthy immune system works synergistically with the medication to eliminate or suppress viral activity
62
What are the viruses controlled by current antiviral therapy?
* Cytomegalovirus (CMV) * Hepatitis viruses * Herpes viruses * Human immunodeficiency virus (HIV) * Influenza viruses (the “flu”) * Respiratory Syncytial Virus (RSV)
63
What are antiviral medications used for?
Used to treat infections caused by viruses other than HIV
64
What are antiretroviral (ARV) medications used for?
Used to treat infections caused by HIV, the virus that causes AIDS
65
What are the catabolic reactions that insulin has on the liver?
Inhibits glycogenolysis - Inhibits gluconeogenesis - Inhibits conversion of fatty acids and amino acids to ketoacids
66
What are the anabolic actions that insulin has on the liver?
- Stimulates glycogen synthesis | - Increases triglyceride synthesis and very-low-density lipoprotein formation
67
How does insulin increase protein synthesis in the muscle?
- Increases amino acid transport | - Increases ribosomal protein synthesis
68
How does insulin increase glycogen synthesis in the muscle?
- Increases glucose transport | - Induces glycogen synthase and inhibits phosphorylase
69
How does insulin increase triglyceride storage in adipose tissue?
- Lipoprotein lipase is induced to release triglycerides from lipoproteins - Glucose transport into cell provides glycerol phosphate to permit esterification of fatty acids supplied by lipoprotein transport - Intracellular lipase is inhibited by insulin
70
What is Diabetes?
A heterogeneous group of syndromes characterized by an elevation of blood glucose and metabolic perturbation caused by a relative or absolute insulin deficiency
71
What are the main types of diabetes?
* Type I – insulin-dependent DM | * Type II – non-insulin-dependent DM
72
What are the other types of diabetes?
* Maturity-onset DM of the young (MODY) | * Gestational diabetes
73
What are the management methods for type 1 diabetes?
* Insulin | * Adjunctive therapies
74
What are the management methods for type 2 diabetes?
* Exogenous insulin * Anti-diabetic drugs * Adjunctive therapies
75
What are the indications for insulin?
* Type I diabetes mellitus * Type II diabetes mellitus * Hyperkalemia * DKA/diabetic coma
76
What is the MOA of insulin?
Stimulating peripheral glucose uptake and inhibiting hepatic | glucose production
77
What are the parameters for the administration of insulin?
* Subcutaneous injection * Rotate site * Check blood sugars regularly
78
How should insulin be stored?
* Refrigerate until use | * Once vial is punctured, it is good for 28 days and can be left at room temperature
79
What is the role of rapid- acting insulin in blood sugar management?
Rapid- acting insulin covers insulin needs for meals eaten at the same time as the injection. This type of insulin is used with longer- acting insulin
80
What is the role of short- acting insulin in blood sugar management?
Short-acting insulin covers insulin needs for meals eaten within 30-60 mins
81
What is the role of intermediate- acting insulin in blood sugar management?
Covers insulin needs for about half the day or overnight. This type of insulin is often combined with rapid or short acting insulin
82
What is the role of long- acting insulin in blood sugar management?
Covers insulin needs for about one full day. The type of insulin is often combined when needed, with rapid or short acting insulin
83
What is the role of pre-mixed insulin in blood sugar management?
Generally taken twice a day before mealtime
84
What is the insullin dosing for patients with type 1 diabetes?
• Starting daily dose: 0.5-1 unit/kg/day in divided doses • Adjust according to fasting (premeal) blood glucose of 80- 130 mg/dL and peak postprandial blood glucose < 180 mg/dL • Provide 50% as long acting insulin and 50% as prandial (near meals) insulin • 1 unit of can account for 30 grams of carbohydrate (14-50) • 1 unit can lower 50 mg/dL blood glucose (10-100)
85
What are the special considerations that impact insulin dosage and needs?
* Renal dysfunction * Exercise * Acute Stress
86
What are the S/S of hypoglycemia?
* Anxiety * Blurred vision * Palpitations * Shakiness * Slurred speech * Sweating
87
What is the non-pharmacological treatment for a patient exhibiting signs of hypoglycemia?
Glucose/simple sugars: 3-4 glucose tablets, ½ can of soda (NOT diet)
88
What is the pharmacological treatment for a patient exhibiting signs of hypoglycemia?
Glucagon injection | • Dose: 1 mg IM, IV, SQ; may repeat in 20 minutes if needed
89
What are the non-pharmacological management methods for insulin?
• Energy balance, diet, exercise: Low-carb, low-fat, calorie-restricted diet is recommended • Cardiovascular disease/HTN blood pressure goal < 140/90 mm Hg (Angiotensin Converting Enzyme II Inhibitor (ACE-I) OR Angiotensin Receptor Blockers (ARB) are first line)
90
What are the PT considerations for when treating a patient with diabetes?
• Exercise has an insulin-type effect, reducing BG • Be aware of the signs of hypoglycemia (confusion, fatigue, sweating, nausea) • Inquire about insulin regime, BS prior to session - Delay session start for snack or insulin treatment if needed - Have sources of glucose on-hand in clinic • Instruct patient about how exercise can alter BG - Adjust insulin by reducing dose 15-30% • Help ensure compliance through strong patient education throughout therapy
91
What are the ways to decrease blood lipid levels in patients with diabetes?
• Patients with type II diabetes should receive a moderate to high intensity statin (i.e. atorvastatin, simvastatin, rosuvastatin etc.) • Weight loss • Fiber, omega-3 fatty acids (fish oils), fibrates can be used as adjunct therapy
92
Why should antiplatelet agents be used in patients with diabetes?
To prevent ischemic events. EX: low dose aspirin (81 mg)
93
What are the things that needs to be monitored in patients with diabetes?
• Smoking cessation • Regular Screening for Cardiovascular Diseases and Coronary Artery Disease • Depression/Stress/Anxiety/Other psychosocial conditions need to be screen for regularly • Diabetic neuropathies especially in extremities need to be screened for on a regular basis - Fastidious foot care - Regular foot exams (annually) • Eye exams • Monitor kidney function
94
What is the mechanism of supplemental drug: St. John’s Wort in rats?
Inhibits metabolism and reuptake of serotonin, dopamine, and epinepherine.
95
What are the studies behind supplemental drug: St. John’s Wort?
No more effective than placebo for mild to moderate depression (similar to RX agents) with fewer side effects. Not effective for major depression
96
What are the limitations of supplemental drug: St. John’s Wort?
* Short duration * Did not use DSM criteria * Variable doses used * Comparative doses of antidepressants were typically subtherapeutic
97
What are the recommendations for supplemental drug: St. John’s Wort?
* More rigorous studies needed – they always say this * Associated with allergic reactions and photosensitization; no evidence for efficacy * Relatively inexpensive * Drug interactions do exist – strong inducer of CYP and p-glycoprotein * Patient should not self treat depression!
98
What is the mechanism of supplemental drug: echinacea?
* Enhances phagocytosis, stimulates certain cytokines * Bacteriostatic * Anti-inflammatory actions
99
What are the studies behind supplemental drug: echinacea?
May be beneficial for early treatment of URTI, though | larger, properly designed trials show no benefit over placebo
100
What are the limitations of of supplemental drug: echinacea?
Not great methodology of trials conducted
101
What are the recommendations for supplemental drug: echinacea?
• Limited evidence • May be effective in reducing the cold’s severity and duration if taken early, but more robust evidence refutes these claims • Probably safe for short term use, allergies and gastrointestinal pain are commonly reported • Long term use should possibly be avoided due to immunosuppression, though evidence for this is scarce
102
What is the mechanism of supplemental drug: ginkgo biloba?
* Free radical scavengers * Inhibits platelet activating factor * Increases GABA
103
What are the studies behind of supplemental drug: ginkgo biloba?
• Larger, better quality studies see no effect beyond placebo. • Potentially increases memory and attention • Improved behavioral performance and cognition of patients with Alzheimer’s and vascular dementia • No effect on mild to moderate dementia or age-associated memory impairment
104
What are the recommendations for supplemental drug: ginkgo biloba?
* May increase mental function in some patients with dementia, but the benefits are modest at best * Risk of complications is low, allergies have been observed, seeds are toxic * Preliminary data has linked long term gingko ingestion to the development of cancer in mice * Drug interactions may exist, must use carefully * May increase risk of bleeding * These patients should not self medicate and still need to be followed by a physician
105
What is the mechanism of supplemental drug: saw palmetto?
* Inhibit 5-alpha-reductase * Blocks testosterone and dihydrotestosterone uptake by the prostate * Anti-inflammatory activity
106
What are the studies behind supplemental drug: saw palmetto?
* Improved urologic symptoms and flow when compared to finasteride with fewer side effects * Higher quality, larger trials have found saw palmetto to be no better than placebo in the tested populations.
107
What are the limitations of of supplemental drug: saw palmetto?
* Mostly short duration studies | * Variability in study designs
108
What are the recommendations for supplemental drug: saw palmetto?
* May decrease prostate symptoms * Limited data available * Probably safe * Limited (known) drug interactions
109
What is the mechanism of supplemental drug: garlic?
Potentially inhibits cholesterol | synthesis. Also effects on plasma protein and cell membrane remodeling
110
What are the studies behind of supplemental drug: garlic?
* RCT’s show mixed results on lipid-lowering ability * Better quality, larger trials have shown no effect * Potentially has modest ability to lower LDL * Possible antihypertensive effect * Antiplatelet, antithrombotic and fibrinolytic activity seen
111
What are the recommendations for supplemental drug: garlic?
* Limited and mixed results showing a benefit in lowering cholesterol * Probably safe * Inexpensive * Well tolerated with few side effects * Drug interactions do exist, must use carefully * Must use high doses to see any effect
112
What is the mechanism of action of supplemental drug: ginger?
Potentially reduces GI motility and anything with an upset stomach
113
What are the studies behind of supplemental drug: ginger?
* Hyperemesis gravidarum (severe morning sickness) | * Results are mixed for treating motion sickness and nausea associated with surgery or chemotherapy
114
What are the recommendations for supplemental drug: ginger?
• Safe, Inexpensive • Readily available in multiple formulations • Some evidence for its use as an antiemetic • Drug interactions may exist, must use carefully
115
What is the mechanism of action of supplemental drug: ginseng?
Proposed: central cholinergic and dopaminergic effects and stimulation if the HPA axis
116
What are the studies behind of supplemental drug: ginseng?
* Claims to increase energy and improve mental abilities | * Multiple studies have show no effects on exercise performance, mood, memory or concentration
117
What are the recommendations for supplemental drug: ginseng?
* Very limited human studies with contradictory results * No good evidence to support use * Not cheap * Drug interactions do exist
118
What are the herbal agents that can be used for pain relief?
* Arnica montana * Black Cohosh * Chamomile * Boswellia Serrata - Frankincense * Evening Primrose Oil * Kava * Peppermint * Piscidia - Jamaican Dogwood * SAM-e * St. Johns Wort * Willow Bark * Wintergreen Oil
119
What are the characteristics of herbal agent: black cohosh?
Generally used to treat symptoms of menopause, though high quality trials show no effect
120
What are the characteristics of herbal agent: chamomile?
• Used for stomach and gastrointestinal pain, cramps, rheumatism, neuralgia, inflammation, ulcers • No robust evidence supporting its use for any medical condition
121
What are the effects of chondroprotective agents?
``` Reduce osteoarthritis by: • Increase proteoglycan synthesis • Decreased collagenolytic activity • Increase in hyaluronic acid production • Inhibit lysosomal enzyme release ```
122
What is the MOA of chondroprotective agents: glucosamine and chondroitin?
• Both glucosamine and chondroitin have in vitro antiinflammatory activity and are proposed to prevent breakdown of synovial structures • Exogenous glucosamine has been shown to distribute to joints (knees) and increase the synthesis of hyaluronic acid ** Unclear if this occurs at synovial concentrations that can be achieved through supplements (5 µM vs. 500 µM)**
123
What are the clinical trial effects of chondroprotective agents: glucosamine and chondroitin?
* No benefit was seen relative to placebo in short term (<5 months) treatment with glucosamine chondroitin sulfate, or a combination * Some evidence suggests a moderate benefit for short term treatment in patients with moderate to severe OA * Long term (2 years) trials show no benefit over placebo in any subgroup
124
What are the adverse effects of glucosamine?
* Heartburn * Moderate constipation * Diarrhea * Nausea/epigastric pain * Hypersensitivity
125
What are the adverse effects of chondroitin?
* Moderate constipation * Diarrhea * Nausea/epigastric pain * Hypersensitivity
126
What are the cautions/contraindications of glucosamine?
* Avoid in Pregnancy * Shellfish Allergy * Diabetics/Glucose * Intolerance * CHF/Renal Impairment
127
What are the cautions/contraindications of chondroitin?
Avoid in Pregnancy
128
What are the concerns with taking chondroprotective agents?
``` Not FDA regulated • No proven safety or efficacy • FDA can restrict sale only if problems occur with their use. Allergic reactions can still occur • Can be serious such as anaphylactic shock Toxicities • Direct • Unlisted poisonous ingredients • Excessive pharmacologic activity ```
129
What are the adulteration/contamination concerns seen with chondroprotective agents?
* May contain elements such as lead, mercury, arsenic, zinc, aluminum and tin * May contain conventional drugs such as Tylenol or aspirin
130
What are the misidentification/mislabeling concerns seen with chondroprotective agents?
• Many plants look alike and have similar botanical names -> may get “mixed up” • Unintentional or deliberate: trying to save money • Varying amounts of active ingredient among different manufacturers