Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Onco boards 2024 > Management of Patients AB 18% > Flashcards

Management of Patients AB 18% Flashcards

1
Q

Which interleukins send anorexigenic and orexigenic signals?

A

IL1 & IL6 - contribute to cancer cachexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define cancer cachexia.

A

profound destructive process characterized by skeletal m wasting with or w/o loss of fat mass and harmful abnormalities in fat and CHO metabolism in spite of adequate intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pathways involved in cancer cachexia

A

NF-kb –> ubiquitin proteasome pathway

TNFa up regulates myostatin (TGFb) that negatively regulates muscle mass

TNFa also interferes with anabolic effects of GH and IGF1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Most common cause of paraneoplastic GI ulceration?

A

MCT with histamine the main driver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tx for GI ulceration?

A

H2 blockers, PPIs, misoprostol, sucralfate, rehydration

prophylactically rec for advanced stage disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tumors associated with hypercalcemia in dog? Cat? (in order of commonality)

A

Dog - LSA (35-55%), AGASACA (25%), MM, parathyroid, thymoma, melanoma, mammary tumors, multiple others

Cat- LSA, SCC, MM, others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tumors associated with hypoglycemia in order of commonality?

A

insulinoma, HCC, leiomyosarcoma/oma, HSA, LSA, lymphocytic leukemia, mammary carcinoma, melanoma, plasma cell, renal adenocarcinoma, salivary adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Tumors associated with hyperestrongenism in order of commonality?

A

Sertoli cell, seminoma, interstitial cell, granulosa cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cause of acromegaly?

A

pituitary tumor (cat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which tumor has been associated with paraneoplastic ectopic ACTH release?

A

primary lung tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Most common cause of hyperglobulinemia?

A

MM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What else can cause a monoclonal gammopathy?

A

Leishmania, Erhlichia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Most common cause of hypercalcemia in cats (non-neoplastic v. LSA and myeloma)?

A

Options were: neoplasia 33%, idiopathic not listed

  • Idiopathic 42%, CKD 35%, neoplasia 13% (LSA most common neoplasia, SCC second most)
  • Confusing b/c Withrow – 1/3 (30%) cats w hypercalcemia was from malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tumors associated with pareneoplastic anemia? Thrombocytopenia?

A

LSA, leukemias, HSA, others

same for PLT and hct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Paraneoplastic erythrocytosis?

A

renal tumors, nasal fibrosarcoma, laeiomyosarcoma, schwannoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Paraneoplastic neutrophilic leukocytosis?

A

lung tumors, LSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Thrombocytopenia in tumor-bearing dogs typically secondary to?

A
  • Chemotherapy
  • As high as 36% in tumor-bearing dogs
  • 58% in dogs w lymphoid neoplasia
  • Also common in vascular splenic tumors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

% of cats with thrombocytopenia that is cancer related?

A

39% - LSA most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mechanisms of cancer related thrombocytopenia?

A
  • Platelet destruction
  • Sequestration
  • Consumption
  • Decreased production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tumors associated with DIC?

A
  • HSA
  • inflammatory mammary carcinoma
  • pulmonary carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Nodular dermatofibrosis associated tumor?

A

renal cystadenoma/carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which tumor causes superficial necrolytic dermatitis?

A

glucagonoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tumors associated with feline paraneoplastic alopecia?

A

pancreatic carcinoma, biliary carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which tumor can cause exfoliative dermatitis in a cat?

A

thymoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Tumors associated with glomerulonephritis?

A

primary erythrocytosis, lymphocytic leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which tumor is most likely to cause myasthenia gravis? Others?

A

thymoma

  • OSA, biliary carcinoma, LSA, oral sarcoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tumors commonly associated with peripheral neuropathy?

A

insulinoma, lung tumors, mammary tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Most common cause of HO?

A

pulmonary metastasis from OSA > primary lung tumor

urinary tract tumors, esophageal tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Blood work for primary hyperparathyroidism? Most common cause?

A
  • High iCa, normal or high PTH
  • functional benign parathyroid adenoma or adenomatous hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Case presented had increased TCa, increased Crea, N phos, N PTH, USG 1.011 =

A

inconclusive - either primary hyperparathyroidism or hypercalcemia of malignancy need more info

HARD IONS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Mechanism of hypercalcemia in osteolytic lesions (e.g. MM)?

A

TNF, IL-1, 6, calcitriol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Paracrine factors that increase osteoclast # and activity in bony metastasis?

A

IL1, 6, TNFa/b, RANKL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Most common CS of hyperCa in Dogs? Cats?

A

Dog - PU/PD d/t impaired action of ADH on renal tubular cells of collecting duct

Cat - anorexia, vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Blood work for hypercalcemia of malignancy?

A
  • low PTH, high OR normal PTHrp
  • calcitriol is expected to be normal but can be high or low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When to tx hyperCa of malignancy?

A
  • Always removal of cause or chemo induction if possible
  • tCa > 16 mg/dL x phosphate (mg/dL) product > 60
  • if p is ill or azotemia
  • if p will not respond to sx or chemo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Fluid choice for hyperCa of malignancy? Why?

A

0.9% NaCl - competes with Ca for renal tubular absorption further enhancing calciuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

TX mild hyperCa with minimal CS?

A

0.9% NaCl rehydration SQ or IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Moderate to severe hyperCa tx?

A
  • 0.9% NaCl over 4-6 hours rehydration then at 100-125 mg/kg/d (1.5-2x maintenance)
  • Lasix 2-4 mg/kg q 8-12 IV, SC, PO ONLY IF HYDRATED
  • Prednisone 1-2 mg/kg q12-24h PO if diagnosis made
  • Pamidronate 1-2 mg/kg in 250 mL of NaCl IV over 2 hours
    or
  • Zoledronate 0.1-0.25 mg/kg diluted in 60 mL of NaCl IV over 15 mins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Which bisphosphanate is less nephrotoxic, zoledronate or pamidronate?

A

zoledronate though more (100x) more potent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Aminobisphosphonates bine strongly to hydroxyapatite at which site?

A

R1
- R2 determines amino-BP (ex.zol) vs nonamino-BP (ex. clodronate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

MOA of zoledronate?

A
  • Mevalonate pathway –> inhibit farnesyl pyrophosphate
  • interfere with post translational prenylation of GTP-binding proteins (Ras, Rho, and Rac)
  • inhibit bone resorption w/o inhibiting mineralization
  • induction of apoptosis net attenuation of pathologic bone resorption
  • synthetic analogs of inorganic pyrophosphates with preferential absorption at sites of active remodeling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Most common mechanism of hypoglycemia in non-islet cell (insulin secreting) tumors?

A

IGF-2 secretion

  • others: IGF-1 or somatomedins, hypermetabolism of glucose, production of substances stimulating insulin release, production of hepatic glucose inhibitor, insulin binding by monoclonal immunoglobulin, insulin receptor proliferation, ectopic insulin production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the MOA of hypoglycemia associated with plasma cell tumors?

A

insulin binding by monoclonal immunoglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

% of dogs with Sertoli cell tumors with hyperestrogenism?

A

25-50% - TX by removing tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

TX for hypoglycemia?

A
  • Oral karosyrup–0.5-1.0ml/kg
  • 50%dextrose–1ml/kgIV; Maintain with 2.5-5.0% dextrose CRI
  • Small frequent meals
  • Treat underlying disease
  • Low dose glucocorticoids (0.5mg/kg SID)
  • Diazoxide, octreotide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

MOA of steroids for hypoglycemia?

A
  • Increases gluconeogenesis
  • Decreases peripheral tissue glucose utilization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

MOA diazoxide?

A
  • Inhibits insulin secretion
  • Increases epinephrine release –-> inhibits glucose uptake by cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MOA octreotide?

A

Somatostatin analogue that inhibits release of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

TX for ectopic ACTH secreting lung tumor?

A
  • remove if possible
  • Trilostane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

In MM the M component is most likely to cause monoclonal gammopathy. How does the M component interfere with coagulation?

A
  • coats PLT inhibiting aggregation to damaged endothelial surfaces
  • release of PLT factor 3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Affects of Bence Jones proteinuria?

A

light chain tubular casts–> interstitial nephritis and renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Causes of hyper viscosity syndrome?

A

monoclonal gammopathy, polycythemia vera, paraneoplastic erythrocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Why is IgM macroglobulinemia most likely to cause hyper viscosity?

A

high molecular weight pentamer

  • in MM the M component is more commonly IgA (dimer) than IgG (monomer); IgA will polymerize
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

TX for hyper viscosity syndrome?

A
  • plasmapheresis if d/t serum proteins
  • phlebotomy and IV fluids if d/t erythrocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Feline MCT paraneoplastic?

A

anemia, erythrocytosis

56
Q

What are paraneoplastic syndromes with leiomyosarcoma?

A

Hypoglycemia, Nephrogenic diabetes insipidus, 2nd erythrocytosis

57
Q

What is paraneoplastic syndrome for TVT?

A

Erythrocytosis

58
Q

What testicular tumor has a paraneoplastic syndrome and is it reversible?

A

Sertoli-hyperestrogenism, reverses 1-3months post-op unless mets

59
Q

MOA of paraneoplastic severe leukocytosis?

A

producing of granulocyte stimulating factor G-CSF and/or granulocyte-macrophage colony stimulating factor GM-CSF

60
Q

Tumors associated with eosinophilia?

A
  • MCT, T-cell LSA via IL-5
61
Q

MOA of heparin release causing clotting issues?

A

heparin acts as a cofactor for anti-thrombin III to inactivate clotting factors XII, XI, X, and IX

62
Q

Gene associated with nodular dermatofibrosis?

A
  • German Sheperds
  • Birt-Hogg- Dube (BHD) gene on chromosome 5
63
Q

TX for nodular dermatofibrosis and renal cystadenocaricnoma?

A
  • none; sx usually not possible as bilateral renal tumors, can consider for ulcerative/painful nodules
  • MST 2.5 yr from CS
64
Q

TX for superficial necrolytic dermatitis in dogs with glucagonomas?

A
  • typically limited since most metastatic
  • octreotide and AA infusions have been reported
65
Q

MOA acquired paraneoplastic myasthenia gravis?

A

Ab formed against nicotinic acetylcholine receptors on the postsynaptic sarcolemmal surface within the neuromuscular jxn

66
Q

How to dx myasthenia gravis?

A
  • definitive circulating Ab against AcH receptors
    • edrophonium chloride challange test is helpful in dogs with generalized to support
67
Q

TX for myasthenia gravis?

A

pyridostigmine bromide - rec. prior to SX and/or RT especially if megaesophagus d/t risk of aspiration

  • in recent studies neither MG or megaesophagus affected prognosis in dogs or cats with thymoma but aspiration is a common perioperative morbidity and mortality
68
Q

Most common cause of HO?

A

Pulmonary mets (OSA), primary lung tumor

if no lung pathology then tumors of urinary system (renal UC, nephroblastoam, botryoid rhabdo, etc)

Cat - renal adrenocortical carcinoma and renal adenoma

69
Q

Non-neoplastic causes of HO?

A

dirofilaria immitis, bacterial endocarditis, PDA with L to R shunt, spirocerca lupi esophageal granulomas, esophageal FB, congenital megaesophagus

70
Q

CS HO?

A

swelling and edema of peripheral limbs, lameness, painful/warm to touch, symmetric, serous to mucupurulent bilateral ocular and nasal d/c, respiratory changes

71
Q

TX for HO?

A
  • remove primary tumor if solitary or few mets
  • chemotherapy if sensitive tumor
  • bisphosphonates
  • vagotomy has been described
72
Q

Fever is primarily mediated by?

A

TNF-a, IL-1, IL-6 on the hypothalamus –> activate arachidonic acid cascade –> prostaglandin E production –> thermoregulatory center

73
Q

DX of paraneoplastic fever?

A

must r/o other causes (sepsis, infection, etc)

74
Q

TX for fever?

A
  • tx underlying cancer
  • NSAIDs and steroids if not cancer directed therapy
75
Q

VCOG LSA response

A

CR: disappearance of all target lesions (LN)
PR: >30% decrease mean sum
PD : >20% increase in mean sum or relevant new lesion
SD: neither PR or PD

76
Q

Minimum size for consistently measurable LN?

A

1 cm

77
Q

Minimum single LN increase to warrant PD?

A

5 mm

78
Q

What is the minimum size of a target single LN pre-treatment to be used to monitor response?

A

2 cm

  • can use sum if using individual LN should not be included for response if <2cm
  • minimum of 1 and max of 5 target lesions
79
Q

Direction to measure LN with LSA?

A

longest diameter

80
Q

What are considered non-measurable lesions?

A

LN <1cm, bone marrow, hypercalcemia or other lab parameter, effusions, CXR lesions

81
Q

When LN are normal in size/non-palpable which value should be assigned to them?

A

5 mm

82
Q

What size must a new PLN be to be considered a new lesion representing PD?

A

1.5 cm

  • otherwise likely represents an overlooked lesion
83
Q

Does VCOG recommend bone more assessment at baseline for LSA?

A

No

  • only if significant infiltration e.g. concern for leukemia and going to change TX recommendations
  • additional can only be used as a Yes/No in monitoring response to tx (e.g. to confirm a CR)
  • only used for PD if new cytopenias developed and then performed otherwise infiltration considered equivocal
84
Q

VCOG follow up recommendations LSA?

A

monthly monitoring q1 mo for 1.5 years then q2 mo thereafter

85
Q

VCOG solid tumor minimum size recommendations for monitoring?

A
  • tumor 1 cm via caliper long axis with photo documentation
  • CT/MRI: 1 cm with maximum slice thickness 5 mm
  • CXR: 2 cm
  • LN > 1.5 cm SHORT AXIS
  • U/S: 2 cm (not a preferred modality)
86
Q

Can bone scan be used to measure lesions according to VCOG solid tumor response?

A

No - only yes/no for lesions

  • same for PET-CT
87
Q

Which imaging modality is preferred for response monitoring?

A

CT > MRI or CXR

88
Q

How to monitor multiple target lesions solid tumors?

A

create baseline sum of the longest diameter of all lesions and compare

89
Q

Short axis size for a LN to be considered non-pathological?

A

1 cm

90
Q

VCOG solid tumors response

A
91
Q

RECIST grade 1-5 general

A

1: Mild; asymptomatic or mild symptoms; clinical signs or diagnostic observations only; intervention not indicated.

2: Moderate; outpatient or non-invasive intervention indicated; moderate limitation of Activities of Daily Living (ADL).

3: Severe or medically significant but not immediately life threatening; hospitalization or prolongation of
hospitalization indicated; disabling; significantly limiting Activities of Daily Living (ADL).

4: Life-threatening consequences; urgent interventions indicated

5: Death related to AE Death can be defined as either euthanasia or natural death, according to the investigators’ discretion.

92
Q

Neutropenia grading

A

1: lower limits of normal - 1,500

2: 1,000-1,499

3: 500-999

4: <500

5: dead

93
Q

GI tox grading generalities

A

1: self limiting with outpatient care

2: >24h

3: requires hospitalization

4: life threatening

5: dead

94
Q

Published neutrophil cut off for ABX?

A

750

95
Q

Prednisone cardiovascular effects?

A
  • reduce capillary permeability and enhance vasoconstriction
96
Q

Prednisone cellular effects?

A
  • inhibit fibroblast proliferation, macrophage response to migration inhibiting factor, sensitization of lymphocytes, and the cellular response to mediators of inflammation
  • stabilize lysosomal membranes.
97
Q

Prednisone CNS effects?

A
  • lower the seizure threshold, alter mood and behavior, diminish response to pyrogens, stimulate appetite, and maintain alpha-rhythm
  • COMMONLY USED FOR CNS tumors
98
Q

Prednisone endocrine effects?

A
  • suppress the release of ACTH from the anterior pituitary, which reduces or prevents the release of endogenous corticosteroids.
  • suppress TSH release
  • inhibit osteoblast function
  • release ADH
  • inhibit insulin
99
Q

Prednisone effect on fluids and electrolytes?

A

-increase renal potassium and calcium excretion
- sodium and chloride reabsorption
- diuresis

100
Q

Prednisone effect on GI/hepatic system?

A
  • increase the secretion of gastric acid, pepsin, and trypsin
  • alter the structure of mucin and decrease mucosal cell proliferation
  • Iron salts and calcium absorption are decreased, whereas fat absorption is increased
  • increased fat and glycogen deposits in hepatocytes and increased serum levels of ALT, GGT, ALP
101
Q

Prednisone hematopoetic effects?

A
  • increase the number of circulating platelets, neutrophils, and RBCs
  • Inhibit PLT aggregation
  • Decreased amounts of lymphocytes (peripheral), monocytes, and eosinophils are seen because glucocorticoids can sequester these cells into the lungs and spleen and can prompt decreased release from bone marrow
  • Glucocorticoids can cause involution of lymphoid tissue
102
Q

Prednisone immune effect?

A
  • decrease circulating levels of T-lymphocytes
  • inhibit lymphokines
  • inhibit neutrophil, macrophage, and monocyte migration
  • reduce production of interferon
  • inhibit phagocytosis, chemotaxis, antigen processing, and intracellular killing
  • antagonize the complement cascade
103
Q

Prednisone metabolic effects?

A
  • stimulate gluconeogenesis. - Lipogenesis in abd
  • Fatty acid mobilization and oxidation
  • Plasma levels of triglycerides, cholesterol, and glycerol are increased
  • Protein is mobilized from most areas of the body (not the liver).
104
Q

Prednisone musculoskeletal effects?

A
  • muscular weakness, atrophy, and osteoporosis
  • Bone growth inhibited via growth hormone and somatomedin inhibition
  • increased calcium excretion, and inhibition of vitamin D activation
  • enhanced reabsorption of bone
  • Fibrocartilage growth inhibition
105
Q

Prednisone respiratory effects?

A
  • increase the number of beta-adrenergic receptors as well as their binding affinity
  • inhibit beta-adrenergic receptor down-regulation, preventing tachyphylaxis and potentiating beta-adrenergic agonist effects on bronchial smooth muscle
106
Q

When should prednisone be avoided?

A

with NSAID, without diagnosis, if liver disease, DM, acute infection

107
Q

Alternative to prednisone in the event of significant liver disease?

A

Prednisolone

108
Q

Prednisone uses in oncology?

A
  • Direct cell killing in LSA
  • anti-inflammatory
  • CNS/nerve tumors
109
Q

Which factor helps optimize APC presentation?

A

GM-CSF

110
Q

What are hematopoietic GF?

A

cytokines that regulate the growth, development, and function of hematopoietic lineages

111
Q

Hematopoietic GF to stimulate erythroid lineage development?

A

EPO, SCF (stem cell factor), IL-3, and GM- CSF

112
Q

Hematopoietic GF to stimulate monocytes lineage development?

A

IL-3, GM-CSF, G-CSF, and M-CSF

113
Q

Hematopoietic GF to stimulate eosinophil lineage?

A

IL-3, GM-CSF, and IL-5

114
Q

Which GF stimulate uncommitted progenitor cells such as stem cells and multipotent progenitors?

A

SCF, IL-3, and GM- CSF

115
Q

GF with growth-promoting and possibly differentiative cytokine with effects on pre-B cells and immature thymocytes?

A

IL-7

116
Q

Functions of hematopoietic GF?

A

Direct:
- changes in membrane structure and function
- modulation of receptor expression
- inhibition of migration of the cells being stimulated or affected

Indirect:
- enhanced chemotaxis
- enhanced phagocytosis
- enhanced oxidative metabolism
- enhanced cytotoxicity
- increased arachidonic acid release
- increased leukotriene B4 synthesis
- change in calcium flux and pH within and around the cell
- potentiation of antigen processing

117
Q

EPO uses?

A
  • myelodysplasia
  • CKD
  • HCT <25% dog, <20% cat
118
Q

EPO risks?

A
  • transform myelodysplasia to overt neoplasia
    -can cause anti-EPO Ab resulting in transfusion dependency (less with Darbepoietin)
  • pure red blood cell aplasia
119
Q

What is darbepoietin?

A

hyperglycosylated synthetic human recombinant erythropoietin analogue

  • less immunogenic
  • issue with all hemoatpotic GF is species specific
120
Q

G-CSF is produced by?

A

monocyte macrophage cells and by fibroblasts and endo- thelial cells in response to IL-l, tumor necrosis factor, and bacteria

121
Q

What is Neupogen?

A
  • cytokine that primarily increases the proliferation, differentiation, and activation of progenitor cells in the neutrophil-granulocyte line in BM
  • human product
122
Q

Neupogen uses?

A
  • severe infection
  • BM transplant
  • should not be given within 24 hours of chemo
  • increase dose intensity by counteracting neutropenia with chemo/RT
  • same for GM-CSF but not clinically available as far as I can tell
123
Q

Neupogen risks?

A
  • hypersensitivity
  • severe neutropenia from Ag development (less if species specific)
  • irritation at injection site
  • Bone or musculoskeletal pain, splenomegaly (including splenic rupture), glomerulonephritis, capillary leak syndrome, and hypotension have been reported in human
124
Q

Steroids MOA in pain modulation?

A
  • inhibition of collagenase and pro inflammatory cytokines
  • trigger lipocortin and block production of eicosanoids (e.g. prostaglandin)
125
Q

What is the ideal first line treatment for cancer pain?

A

NSAIDs

126
Q

Differences in toxicity COX 1 vs COX2 inhibitors?

A
  • GI more common with COX 1
  • similar with renal & liver
127
Q

MOA grapiprant?

A

selective EP4 prostaglandin PGE2 receptor antagonist

128
Q

COX 1 selective inhibitors?

A

Aspirin

129
Q

COX 2 preferential (non-selective) inhibitors? Selective?

A
  • Piroxicam, meloxicam, carprofen
  • deracoxib, firocoxib, robenacoxib
130
Q

When is multimodal pain therapy PROVEN to be effective?

A

Only in immediate operative period however extrapolated to be beneficial for chronic pain

131
Q

Drugs that can result in hypersensitivity?

A

Doxorubicin, Taxol, Etoposide, L-asparaginase during or shortly after tx

132
Q

TX for hypersensitivity?

A
  • Discontinue infusion
  • Ensure patent airway
  • Establish vascular access – initial fluids at shock dose if necessary
  • Dex-SP at 0.5-2.0 mg/kg IV
  • Diphenhydramine at 2 mg/kg IM
  • Epineprhine (0.1 to 0.3ml of a 1:1,000 solution) can be given IV or IM if severe
  • If reaction was hypersensitivity alone – may be possible to resume infusion once clinical signs subside – give at slower rate
133
Q

What are electrolyte abnormalities with acute tumor lysis?

A

Hyperphosphatemia, hyperkalemia, hypocalcemia, acidosis, hyperuricemia

134
Q

TX/monitoring for tumor lysis syndrome?

A
  • IV fluid diuresis
  • EKG monitoring
  • VBG: (K+, Ca2+, PO4-)
  • phosphate binder
  • hypertonic dextrose/insulin to drive K/P intracellular
  • anti-emetics
  • may need blood products if DIC
  • my need Bicarb supplemenation
135
Q

What is used in humans for acute tumor lysis treatment?

A
  • Allopurinol (xanthine oxidase inhibitor; purine analog)
  • Blocks conversion of xanthine/hypoxanthine to uric acid
  • ↓ risk of hyperuricemia-induced ARF
136
Q

Who is at increased risk for acute tumor lysis

A
  • Advanced disease / large tumor burden
  • High proliferative fraction (hematopoietic tumors)
  • Abdominal involvement
  • Pre-existing renal insufficiency
  • dehydration
  • Dalmatians/English Bulldogs (lack uricase)
  • Renal clearance is primary mechanism for excretion of P / K /uric acid

Onco boards 2024 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions