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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

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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

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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

Cell autophagy/lysosomal and Ca2+-dependent protein degradation pathways, ER stress and mitochondrial dysfunction are involved in muscle protein degradation in cancer cachexia

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4
Q

Most common cause of paraneoplastic GI ulceration?

A

MCT with histamine the main driver

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5
Q

Tx for GI ulceration?

A

H2 blockers, PPIs, misoprostol, sucralfate, rehydration

prophylactically rec for advanced stage disease

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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

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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

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8
Q

Tumors associated with hyperestrongenism in order of commonality?

A

Sertoli cell, seminoma, interstitial cell, granulosa cell

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9
Q

Cause of acromegaly?

A

pituitary tumor (cat)

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10
Q

Which tumor has been associated with paraneoplastic ectopic ACTH release?

A

primary lung tumors

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11
Q

Most common cause of hyperglobulinemia?

A

MM

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12
Q

What else can cause a monoclonal gammopathy?

other than cancer

A

Leishmania, Erhlichia

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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
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14
Q

Tumors associated with pareneoplastic anemia? Thrombocytopenia?

A

LSA, leukemias, HSA, others

same for PLT and hct

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15
Q

Paraneoplastic erythrocytosis?

A

renal tumors, nasal fibrosarcoma, laeiomyosarcoma, schwannoma, tvt

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16
Q

Paraneoplastic neutrophilic leukocytosis caused by wat cancers?

A

lung tumors, LSA

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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
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18
Q

% of cats with thrombocytopenia that is cancer related?

A

39% - LSA most common

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19
Q

Mechanisms of cancer related thrombocytopenia?

A
  • Platelet destruction
  • Sequestration
  • Consumption
  • Decreased production
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20
Q

Tumors associated with DIC?

A
  • HSA
  • inflammatory mammary carcinoma
  • pulmonary carcinoma
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21
Q

Nodular dermatofibrosis associated tumor?

A

renal cystadenoma/carcinoma

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22
Q

Which tumor causes superficial necrolytic dermatitis?

A

glucagonoma

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23
Q

Tumors associated with feline paraneoplastic alopecia?

A

pancreatic carcinoma, biliary carcinoma

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24
Q

Which tumor can cause exfoliative dermatitis in a cat?

A

thymoma

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25
Q

Tumors associated with glomerulonephritis?

A

primary erythrocytosis, lymphocytic leukemia

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26
Q

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

A

thymoma

  • OSA, biliary carcinoma, LSA, oral sarcoma
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27
Q

Tumors commonly associated with peripheral neuropathy?

A

insulinoma, lung tumors, mammary tumors

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28
Q

Most common cause of HO?

A

pulmonary metastasis from OSA > primary lung tumor

urinary tract tumors, esophageal tumors

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29
Q

Blood work for primary hyperparathyroidism? Most common cause?

A
  • High iCa, normal or high PTH
  • functional benign parathyroid adenoma or adenomatous hyperplasia
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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

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31
Q

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

A

TNF, IL-1, 6, calcitriol

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32
Q

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

A

IL1, 6, TNFa/b, RANKL

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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

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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
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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
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36
Q

Fluid choice for hyperCa of malignancy? Why?

A

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

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37
Q

TX mild hyperCa with minimal CS?

A

0.9% NaCl rehydration SQ or IV

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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
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39
Q

Which bisphosphanate is less nephrotoxic, zoledronate or pamidronate?

A

zoledronate though more (100x) more potent

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40
Q

Aminobisphosphonates bine strongly to hydroxyapatite at which site?

A

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

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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
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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
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43
Q

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

A

insulin binding by monoclonal immunoglobulin

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44
Q

% of dogs with Sertoli cell tumors with hyperestrogenism?

A

25-50% - TX by removing tumor

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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
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46
Q

MOA of steroids for hypoglycemia?

A
  • Increases gluconeogenesis
  • Decreases peripheral tissue glucose utilization
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47
Q

MOA diazoxide?

A
  • Inhibits insulin secretion
  • Increases epinephrine release –-> inhibits glucose uptake by cells
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48
Q

MOA octreotide?

A

Somatostatin analogue that inhibits release of insulin

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49
Q

TX for ectopic ACTH secreting lung tumor?

A
  • remove if possible
  • Trilostane
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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
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51
Q

Affects of Bence Jones proteinuria?

A

light chain tubular casts–> interstitial nephritis and renal failure

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52
Q

Causes of hyper viscosity syndrome?

A

monoclonal gammopathy, polycythemia vera, paraneoplastic erythrocytosis

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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
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54
Q

TX for hyper viscosity syndrome?

A
  • plasmapheresis if d/t serum proteins
  • phlebotomy and IV fluids if d/t erythrocytosis
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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)

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