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Clinical medicine A > Intro to onc part 2 (Billie) > Flashcards

Intro to onc part 2 (Billie) Flashcards

1
Q

what is the goal of cancer treatment

A

to first eradicate the cancer

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2
Q

if eradication cannot be accomplished, the goal of cancer treatment shifts to what

A
  1. palliation
  2. treatment of symptoms
  3. preservation of QoL while possibly extending life
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3
Q

what are the four main types of cancer treatment

A

surgery
radiation therapy (including photodynamic therapy)
chemotherapy
biologic therapy (icluding immunotherapy and gene therapy)

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4
Q

what are the local cancer treatments

A

surgery and radiation therapy

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5
Q

what are the systemic cancer treatments

A

chemotherapy and biologic therapy

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6
Q

what is the most effective means of treating cancer?

A

surgery

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7
Q

what are the 5 reasons surgery is used in relation to cancer

A

cancer prevention (prophylactic mastectomy/colonectomy)
diagnosis
staging
treatment
palliation

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8
Q

How much of cancer patients are cured by surgery

A

40%

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9
Q

what % of tumors are irremovable and why?

A

60% of solid tumors are irremovable because they have metastasized

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10
Q

what are the benefits of surgery in cancer even if it is not to cure the cancer.

A

Local control of tumor
Preservation of organ function
Debulking for subsequent treatments
Palliative/Supportive care
Placement of lines
Control of effusions and ascites
Removal of adhesions/strictures
Reconstructive surgery

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11
Q

what is radiation

A

a physical agent that destroys cancer cells

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12
Q

what is the main goal of radiation therapy in cancer

A

deprive cancer cells of their cell division potential

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13
Q

how does radiation work?

A

Radiation causes breaks in DNA that prevent replication and generates hydroxyl radicals from cell water that damages cell membranes, proteins, and organelles

Cancer cells are not as efficient as normal cells in repairing the damage caused by radiation resulting in differential cancer cell killing

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14
Q

us radiation local or systemic

A

local, but systemic effects can develop

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15
Q

systemic effects from radiation may develop depending on what factors?

A

volume of tissue irradiated,
dose fractionation,
radiation fields
individual susceptibility

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16
Q

what features of a particular cell make it more sensitive or resistant to the biologic effects of radiation

A

total absorbed dose
number of fractions (delivering radiation in repeated doses to maximize exposure during cell division)
time of treatment

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17
Q

what are the three ways that radiation therapy is delivered

A

Teletherapy
Brachytherapy
Systemic Therapy

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18
Q

what is radiation teletherapy

A

focused beams of radiation in the form of X-rays or gama rays are generated at a distance and aimed at the tumor within the patient

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19
Q

what is radiation brachytherapy

A

encapsulated/sealed sources of radiation implanted directly into or adjacent to tumor tissues

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20
Q

what is systemic radiation therapy

A

radionuclides targeted in some fashion to a site of tumor……radioactive iodine for thyroid cancer

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21
Q

what is the most commonly used form of radiation therapy

A

teletherapy

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22
Q

how can radiation therapy be used for palliation?

A

Relief of bone pain from metastatic disease, control of brain metastases, reversal of spinal cord compression and superior vena caval obstruction, shrinkage of painful masses, and opening of threatened airways.

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23
Q

what are the systemic effects of radiation therapy

A

fatigue, anorexia, nausea, and vomiting

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24
Q

what acute toxicities can result from radiation therapy

A

mucositis, skin erythema (ulceration in severe cases), and bone marrow toxicity.

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25
Q

how are acute toxicities from radiation therapies alleviated

A

interruption of radiation treatment

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26
Q

what are the chronic toxicities of radiation therapies

A

Radiation carcinogenesis with secondary malignancy; pericarditis; myocardial infarction; thyroid failure; cataracts; lung fibrosis; arteritis; spinal cord transection

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27
Q

what is radiofrequency ablation?

A

focused microwave radiation to induce thermal injury within a volume of tissue

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28
Q

what is cryosurgery?

A

use of extreme cold to sterilize lesions in certain sites

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29
Q

what is chemoembolization?

A

Infusion of chemotherapeutic agents directly into the target area via vascular catheters

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30
Q

what is chemotherapy used for

A

the treatment of active, clinically apparent cancer

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31
Q

what are the four broad types of cancer drug treatments

A

conventional cytotoxic chemotherapy agents
targeted agents
hormonal therapies
biologic therapies

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32
Q

what do conventional cytotoxic chemotherapy agents do?

A

mainly target DNA structure or segregation of DNA as chromosomes in mitosis.

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33
Q

what do targeted agents do?

A

designed and developed to interact with a defined molecular target important in either maintaining the malignant state or selectively expressed by the tumor cells.

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34
Q

what do hormonal therapies do?

A

work on the biochemical pathways underlying estrogen and androgen function

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35
Q

what do biological therapies do?

A

Have a particular target or may have the capacity to regulate growth of tumor cells or induce a host immune response to kill tumor cells.

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36
Q

what is the therapeutic index

A

the degree of separation between toxic and therapeutic doses.

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37
Q

what type of therapeutic index do chemotherapy agents have?

A

Narrow

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38
Q

what are the two valuable outcomes that can result as a use of chemotherapy agents, targeted agents, hormonal treatments, or biologicals

A

induced cancer cell death
induced cancer cell differentiation or dormancy

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39
Q

what is induced cancer cell death

A

esulting in tumor shrinkage with corresponding improvement in patient survival, or increase the time until the disease progresses.

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40
Q

what is cancer cell differentiation or dormancy

A

loss of tumor cell replicative potential and reacquisition of phenotypic properties resembling normal cells.

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41
Q

what are the two antimetabolites that can be used as a form of chemotherapy

A

methotrexate
5-flourouracil (5-FU)

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42
Q

what do antimetabolites do in cancer treatment?

A

Cause DNA damage indirectly, through misincorporation into DNA, abnormal timing or progression through DNA synthesis, or altered function of pyrimidine and purine biosynthetic enzymes

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43
Q

How does 5-FU work?

A

prevents thymidine formation (required for DNA replication)

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44
Q

how does methotrexate work?

A

competes and counteracts folic acid, causing folic acid deficiency in cancer cell and cell death

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45
Q

what are the common toxic manifestations when using antimetabolites in cancer treatment?

A

stomatitis, diarrhea and myelosuppression

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46
Q

What are the Mitotic Spindle Inhibitors used as a form of chemotherapy

A

vincristine
vinblastine
paclitaxel

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47
Q

What do mitotic spindle inhibitors do?

A

work on the interphase portion of cell division

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48
Q

what are common toxic manifestations of mitotic spindle inhibitors

A

alopecia
neuropathy
myelosuppression

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49
Q

what are the alkylating agents that are used as a form of chemoherapy

A

cyclophosphamide
Chlorambucil
cisplatin

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50
Q

How do alkylating agents work?

A

They break down, either spontaneously or after normal organ or tumor cell metabolism, to reactive intermediates that covalently modify bases in DNA

This leads to cross-linkage of DNA strands or the appearance of breaks in DNA as a result of repair efforts

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51
Q

which alkylating agent has toxic manifestations and what are they

A

cisplatin - neuro-toxicity (stocking-glove), hearing loss, renal failure

52
Q

what are the antitumor antibiotics used as chemotherapy

A

Doxorubicin

53
Q

what is the toxic manifestation associated with antitumor antibiotics

A

cardiotoxicity (arrhythmias acutely, chronically leads to cardiomyopathy)

54
Q

what is the MOA of antitumor antibiotics

A

As a class they bind to DNA directly and can frequently undergo electron transfer reactions to generate free radicals in close proximity to DNA, leading to DNA damage in the form of single-strand breaks or cross-links.

55
Q

where do antitumor antibiotics come from?

A

Produced by bacteria that in nature appear to provide a chemical defense against other hostile microorganisms.

56
Q

what are the topoisomerase inhibitors

A

etoposide

57
Q

what is stalking glove neuropathy

A

a neuropathy with distal to proximal pattern

58
Q

what is the MOA of topoisomerase inhibitors

A

inhibits DNA synthesis by forming a complex with topoisomerase II and DNA, causing breaks in DNA, which prevents the mitotic phase of cell division, causing cell death

59
Q

what are the toxic manifestations of topoisomerase inhibitors

A

secondary leukemia with high doses

60
Q

How do you treate neutropenia from bone marrow toicity secondary to chemo

A

Colony stimulating factors such as Filgastram, pegfilgrastim and sargramostim

Stimulate the production of neutrophils, monocytes, and eosinophils.

61
Q

how do you treat anemia from bone marrow toicity secondary to chemo

A

transfusions or epogen. (EPO stimulating agent

62
Q

how do you treate thrombocytopenia from bone marrow toicity secondary to chemo

A

conservative monitering
if sevrer enough, give platelets

63
Q

how do you treat nausea secondary to chemo?

A

ondansetron (anti-emetic)

64
Q

what is mucositis

A

oral soreness and ulcerations

65
Q

how do you treat mucositis due to chemo

A

magic mouth wash
diphenhydramine, lidocaine, Maalox

66
Q

how do you treat diarrhea due to chemo

A

Loperamide (antimotility drug) (Imodium)

or could use
Octerotide (somatostatin analogue) or opiate-based preparations if no response to Loperamide

67
Q

how do you treat skin toxicity due to chemo

A

Supportive care; cold packs; sun protection

68
Q

what does skin toxicity consist of

A

Hyperpigmentation, alopecia, photosensitivity, nail changes, acral erythema, and generalized rashes.

Acral erythema manifests as painful palms or soles accompanied by erythema, progressing to blistering desquamation and ulceration in its worst forms.

69
Q

how do you treat alopecia due to chemo

A

Psychological support
- “chemo caps”
- reduce scalp temp - very controversial

70
Q

what is the routine blood work during chemo

A

weekly
CBC
CMP
PT/aPTT

71
Q

what are paraneoplastic syndromes

A

the disorders that accompany benign or malignant tumors but are not directly related to mass effect or invasion.

72
Q

Neoplastic cells can produce a variety of products that stimulate ___________, _________, _____________, __________ and ____________ responses

A

Neoplastic cells can produce a variety of products that stimulate hormonal, hematologic, dermatologic, renal and neurologic responses

73
Q

what are the primary systems that paraneoplastic syndromes present as clinically

A

Endocrine
Metabolic
Hematologic
Neuromuscular

74
Q

what are the three mechanisms used to classify paraneoplastic syndromes

A

(1) effects initiated by a tumor product (eg, carcinoid syndrome, ectopic hormone production)
(2) effects of destruction of normal tissues by tumor (eg, hypercalcemia with osteolytic skeletal metastases)
(3) effects due to unknown mechanisms.

75
Q

why are paraneoplastic syndromes clinically important

A

(1) They sometimes accompany relatively limited neoplastic growth and may provide the clinician with an early clue to the presence of certain types of cancer.
(2) The metabolic or toxic effects of the syndrome may constitute a more urgent hazard to the patient’s life than the underlying cancer (eg, hypercalcemia, hyponatremia).
(3) Effective treatment of the tumor should be accompanied by resolution of the paraneoplastic syndrome and, conversely, recurrence of the cancer may be heralded by return of the systemic symptoms.

76
Q

what are the endocrine manifestations of paraneoplastic syndromes

A

hypercalcemia
hypoglycemia
gonadotropin secretion
cushings syndrome
SIADH

77
Q

what are the hematologic manifestations of paraneoplastic syndrome

A

coagulopathy
erythrocytosis (due to ectopic production of erythropoietin)

78
Q

what are the neurologic manifestations of paraneoplastic syndrome

A

lambert-eaton syndrome
subacute cerebellar syndrome

79
Q

what is lambert-eaton syndrome

A

immune mediated neurologic sndrome characterized by muscles weakness of the limbs

80
Q

what is subacute cerebellar syndrome

A

immune mediated cerebellar degeneration
characterized by dizziness, nauea, vertigo, tremors and sometimes dysphagia and blurry vision

81
Q

what are the dermatologic manifestations of paraneoplatic syndromes

A

Dermatomyositis
acanthosis nigricans

82
Q

what is dermatomyositis

A

a system disorder causing inflammation of the muscles and skin, as well as joints, lungs, esophagus and heart

83
Q

what is acanthosis nigricans

A

thickening of skin/brownish discoloration
Can occur with diabetes/obesity, typically in fold of neck, under breast
More likely to also involve the mucous membranes with cancer

84
Q

what is neutropenic fever

A

Defined as recurrent temperatures above 38’C or a single temperature above 38.3’C in the presence of neutropenia, defined as an absolute neutrophil count (ANC) less than 500 cells/mL (normal is above 1500)

85
Q

how does neutrophil cont correlate with death in neutropenic fever

A

The lower the ANC, the higher the risk for death

86
Q

what are the symptoms of neutropenic fever

A

vague and mild initially, but may rapidly progress to sepsis and death
Symptoms also vary based on site of infection and source of infection

87
Q

what is the etiology of neutropenic fever

A

Infectious agents may be viral, fungal or bacterial
Viral – CMV, HSV, VZV
Bacterial – Staph, Strep. Enterococcus, H. flu, E. coli, Klebsiella, Pseudomonas
Fungal – Candida or Aspergillosis

88
Q

when should you not give a rectal exam or obtain a rectal temp

A

It is an ABSOLUTE CI to perform a rectal exam on an immunocompromised pt!!

89
Q

how should you diagnose a neutropenic fever

A

Cultures should be taken from all lumens, skin and line sites, blood, urine, sputum and stool
Should be sent for bacterial, fungal and viral studies

Chest x-ray – however, may appear normal in patient with PNA, as it takes neutrophils to create an infiltrate

Labs should include – CBC with differential, CMP, coagulation panel and UA

90
Q

how do you treat neutropenic fever

A

IV empiric antibiotic therapy should be initiated - AFTER CULTURE IS TAKEN
Ceftazidime, Cefipime or Imipenem for antipseudomonal coverage
Aminoglycoside to cover gram – bacteria
Vancomycin to cover MRSA

91
Q

what is the clinical presentation of spinal cord compression

A

Back pain at the level of the tumor mass, which may be aggravated by lying down, weight bearing, sneezing, or coughing

Mix of nerve root and spinal cord symptoms

92
Q

what is the progression of spinal cord progression

A

lower extremity weakness
hyperreflexia
motor/sensory loss
loss of reflexes
loss of bowel/bladder function
paraplegia

93
Q

how do you diagnose a spinal cord compression

A

MRI is the diagnostic study of choice

94
Q

How do you treat spinal cord compression

A

High dose IV corticosteroids
Surgical decompression
Radiation

95
Q

what possible mechanisms could hypercalcemia be caused by in cancer

A
  1. Systemic effects of tumor-released proteins
  2. Direct osteolysis of bone by tumor
  3. Increased absorption of calcium due to increased active metabolite of Vitamin D
96
Q

what is the most common cause of hypercalcemia

A

a parathyroid hormone-related peptide secreted by the cancer cells

This activates the parathyroid hormone receptor, stimulating osteoclastic activity and promoting renal reabsorption of calcium

Usually a marker of advanced cancer, with median survival ranging from 1 to 3 months

97
Q

how many cancer patients have hypercalcemia at some point

A

20-30%

98
Q

what are the most common cancers causing hypercalcemia

A

myeloma, breast carcinoma, and non-small cell lung carcinoma (NSCLC)

99
Q

what are the symptoms of hypercalcemia

A

may include polydipsia, polyuria, generalized weakness, lethargy, anorexia, N/V, constipation, abdominal pain, AMS and psychosis
-rare with calcium < 12 mg/dL

100
Q

how do you diagnose hypercalcemia

A

Labs: Total serum calcium level and ionized calcium levels are elevated
EKG: may show shortened QT, ST depression and AV blocks

101
Q

what are the treatment options for hypercalcemia

A

Hydration and forced diuresis

Bisphosphonates, such as zoledronic acid or pamidronate IV can also be initiated

Calcitonin, which blocks bone resorption and also increases urinary calcium excretion by inhibiting renal calcium reabsorption, is second-line therapy

Hemodialysis may be necessary to provide a definitive treatment

102
Q

what is tumor lysis syndrome

A

A clinical syndrome that occurs 1 to 3 days following radiochemotherapy of most commonly hematologic malignancies
Especially Burkitt lymphoma

103
Q

what causes tumor lysis syndrome

A

massive release of cellular material including nucleic acids, proteins, phosphorus, and potassium.

104
Q

what can occur with tumor lysis syndrome

A

Acute kidney injury may then develop from the crystallization and deposition of uric acid and calcium phosphate within the renal tubules further exacerbating the hyperphosphatemia and hyperkalemia.
AND
Due to combination of hyperkalemia and hypocalcemia, development of fatal cardiac arrhythmias may occur

105
Q

what are the s/s of tumor lysis syndrome

A

Patient may present with lethargy, N/V, cloudy urine, and neuromuscular irritability, muscular spasm, seizure and altered mentation associated with hypocalcemia

106
Q

how will an ekg present in a patient with tumor lysis syndrome

A

may show peaked T waves of hyperkalemia, as well as arrhythmias

107
Q

how do you treat tumor lysis syndrome

A

Includes IV hydration and correction of electrolyte abnormalities
May require emergency hemodialysis

108
Q

what types of effusions could be initial findings in a patient with cancer

A

Pleural, pericardial, or peritoneal space

109
Q

what are pleural and pericardial effusions most commonly caused by

A

lung and breast cancers

110
Q

what are malignant ascites associated with

A

ovarian, colorectal, stomach, and pancreatic cancers.

111
Q

what determines the degree of hemodynamic stability in pericardial effusion or cardiac tamponade

A

The rate of accumulation and distensibility of the sac

112
Q

what are the s/s of pericardial effusion or cardiac tamponade

A

Patient may present with fatigue, chest heaviness, dyspnea, palpitations, cough and syncope

113
Q

what are the physical exam findings for pericardial effusion/cardiac tamponade

A

Tachycardia, narrowed pulse pressure, hypotension, distended neck veins, muffled heart sounds, and pulsus paradoxus

114
Q

how do you diagnose pericardial effusion or cardiac tamponade

A

Chest x-ray may demonstrate an enlarged cardiac silhouette and pleural effusion
EKG may show sinus tachycardia, low QRS voltage and electrical alternans
Transthoracic echocardiogram is diagnostic tool of choice and will demonstrate pericardial effusion with RA systolic collapse and RV diastolic collapse (tamponade)

115
Q

what is the treatment for pericardial effusion/cardiac tamponade

A

Treatment of choice is echo-guided percutaneous pericardiocentesis under local anesthesia

116
Q

what is superior vena cava syndrome

A

The result of direct obstruction of the superior vena cava by malignancies such as compression of the vessel wall by right upper lobe tumors or thymoma and/or mediastinal lymphadenopathy

117
Q

what is the most common malignancy causing SVC syndrome

A

bronchogenic carcinoma

118
Q

how would patients present with SVC syndrome

A

Patients may present with a gradual onset of dyspnea, chest pain, cough and, facial and arm swelling; cerebral edema is rare

119
Q

what are the physical exam findings for SVC syndrome

A

Distended neck, arm and chest veins, nonpitting edema of the neck, arm swelling, tongue and facial swelling and cyanosis

120
Q

How do you diagnose SVC syndrome

A

Chest x-ray may show a widened mediastinum
Chest CT with contrast is diagnostic test of choice

121
Q

how do you treat SVC syndrome

A

Glucocorticoids (such as prednisone or methylprednisolone) decrease the inflammatory response to tumor invasion and edema surrounding the tumor.
Glucocorticoids are most helpful if the tumor is steroid-responsive, such as lymphomas

Intravascular stenting, chemotherapy and radiation are also effective depending on the tumor type

122
Q

what factors make patients with cancer more susceptible to thromboembolic events

A

Malignancy causes a hypercoagulable state
Neoplastic cells and chemotherapy can cause intimal injury
Obstructive tumors cause venous stasis

123
Q

what are the S/S of a thromboembolic event

A

Patients may present with hx of dyspnea, fever, cough, DOE, pleuritic chest pain, leg pain or swelling, and rarely hemoptysis

124
Q

what are the PE findings of a thromboembolic event

A

can include low-grade fever, tachypnea, tachycardia, pleural rub and unilateral lower extremity swelling

125
Q

How do you diagnose thromboembolic events

A

Ventilation-perfusion scan and spiral chest CT with contrast are diagnostic modalities to confirm diagnosis

126
Q

how do you treat thromboembolic events

A

Anticoagulation should be initiated immediately, unless contraindicated, with heparin full-dose bolus and infusion or LMWH (enoxaparin) 1mg/kg subQ Q12 hours
Xarelto (rivaroxaban) 15 mg po BID for 21 days, followed by 20mg daily is an alternative

Thrombolytic therapy may be necessary with hemodynamic compromise and severe RV failure on echo

Clinical medicine A (32 decks)

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