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VTS ECC 2024 > Immunology/Oncology > Flashcards

Immunology/Oncology Flashcards

1
Q

Chemotherapy

A

“the management of illness by chemical means”
– affects dividing cells through disruption of DNA replication and/or cell division

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2
Q

Exmaples of Innate immunity

A

chemical: stomach acid and saliva pH
physical barriers: skin, tracheal mucus, mucosal endothelial surfaces, tears, and some cells of the immune system such as natural killer and phagocytic cells

Cytokines and enzymes are also part of innate immunity

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3
Q

Adaptive immunity

what is it mediated by?

A

term used for the body’s response to specific antigens.
– mediated by lymphocytes

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4
Q

Antibodies

A

immune response tailored to each type of antigen
– immune cells can produce specific immune proteins against spefic antigens
– retain a memory of the antigen in preparation for future encounters

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5
Q

Cytokines

what are they secreted by? What is their purpose?

A

– immune cells communicate using cytokines
– hormone‐like molecules secreted by lymphocytes, macrophages, and endothelial cells.
– Cytokines kill viruses and bacteria, stimulate hematopoiesis, mediate inflammatory responses, and activate the complement system.

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6
Q

Immunity classifications

x5

A
  1. innate or natural,
  2. acquired,
  3. passive,
  4. non‐specific or specific,
  5. cellular or humoral
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7
Q

Acquired immunity

Type of cells and types of immunity components

A

develops following exposure to various antigens
– specialized lymphocytes to produce antibodies that are specific for a particular antigen
– specialized B and T lymphocytes are activated by specific antigens and produce cell clones that attack foreign proteins
– Two components: humoral immunity and cellular immunity

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8
Q

Humoral immunity

A

– major defense system against bacterial infections.
– the function of activated B lymphocytes, known as plasma cells, that produce immunoglobulins (antibodies) which in turn activate the complement system to attack and neutralize antigens
– antigen–antibody complex → activates B lymphocytes
– As a B lymphocyte becomes an activated B lymphocyte, it undergoes many mitotic divisions to make numerous clones of itself

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9
Q

Cellular immunity

3 types of cells involved
x3 examples of this immunity

A

– mediated by T lymphocytes and is responsible for delayed allergic reactions, transplant rejection, and defense against viruses and neoplastic mutations.
– T lymphocytes have specific antigen receptors unique for single antigens.
– cloned, activated T lymphocytes make up three distinct populations:
1. killer T lymphocytes,
1. helper T cells, and
1. suppressor T cells.

Celluar = “T” mobile

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10
Q

Passive immunity

A

– defined by the transfer of antibodies from one individual to another, such as through the ingestion of colostrum or through placental circulation
– give the infant some protective and transient immunity but can cause significant illness if they fail – for example, failure of passive transfer in foals

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11
Q

Anaphylaxis definition

A

linically severe and life‐threatening type I hypersensitivity reaction with an acute onset following antigen exposure.
– caused by exposure to drugs, vaccines, food substances, reptile venom, insect venom, incompatible blood products, contrast agents, or ingested foreign material

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12
Q

three‐part classification system for anaphylactic reactions

A
  1. immunological IgE mediated,
  2. immunological non‐IgE mediated (IgG)
  3. non‐immunological
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13
Q

Immunological IgE‐mediated reactions

A

most commonly caused by insect stings and bites, reptile envenomation, food antigens, and drugs
– IgE antibodies are produced that bind to high‐affinity sites on mast cells in the tissue and basophils in the circulating pool

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14
Q

Immunological non‐IgE‐mediated reactions

A

commonly caused by immunoglobulin transfusions, complement activation, autoimmune disease, and coagulation cascade activation
– allergic response is mediated by IgG and macrophages
– much more antibody and antigen than the IgE‐mediated pathway
– These reactions do not release histamine

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15
Q

Non‐immunological reactions

A

caused by drugs such as chemotherapeutic agents or opioid analgesics and independent physical factors such as cold, heat, or exertion
– basophils and mast cells degranulate without the involvement of immunoglobulins

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16
Q

Pathophysiology of anaphylactic reactions

A

early response is clinically occult or undetectable but if the patient is re‐exposed to the antigen, → cross‐linking of the antibody molecules causes changes in the plasma membranes of the cell that permit an influx of extracellular calcium
– releases various stored and rapidly synthesized mediator products, including histamine, platelet activating factor (PAF), and cytokines, that potentiate the clinical signs of an anaphylactic reaction.

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17
Q

Histamine

where is it stored?

A

stored in the granules of mast cells.

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18
Q

Cardiovascular effects of anaphylaxis

A

rapid‐onset, refractory hypovolemic and distributive shock due to increased vascular permeability and vasodilation that causes swift and significant fluid shifts from the intravascular to the extravascular compartment

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19
Q

K9 “shock organs”

A

Liver and GIT
– histamine release within the GIT into portal vein induces hepatic vasodilation and an increase in hepatic blood flow.
– results in hepatic congestion and decreased venous outflow, further compromising blood flow from the hepatic circulation into the rest of the GIT
– reduced gastrointestinal venous return affects cardiac output and contributes to a global state of hypotensive and distributive shock
– Alters endothelial membrane permeability in the intestines → organ edema, fluid loss, hemorrhagic enteritis (that can start within minutes to hours following antigen exposure)
→ further contributing to hypovolemic shock

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20
Q

Feline “shock organs”

A

lungs and respiratory tract

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21
Q

Effects of Epinephrine for Anaphylaxis

A

– increase peripheral vascular resistance, counteracting vasodilation, and has positive effects on both blood pressure and coronary perfusion
– may have mast cell stabilizing properties and act as a PAF antagonist. It may also relieve respiratory distress and address some elements of shock

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22
Q

Chemotherapy‐Associated Neutropenia

A

– neutropenia typically secondary to overwhelming infection, neoplasia, or the myelosuppressive effects of parvovirus or chemotherapy
– Neutropenia secondary to chemotherapy commonly occurs in the 5–10 days following administration, although this is dependent on the agent administered
– graded 1- 4

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23
Q

Grade 1 neutropenia

A

neutrophil count at nadir is between normal for their species and 1500/μL

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24
Q

Grade 2 neutropenia

A

grade 2 (moderate) neutropenia is present when the neutrophil count is between 1500/μL and 1000/μL.
– Prophylactic broad‐spectrum antibiotic coverage can be considered at this point,
– CBC should be checked prior to the next dose of chemotherapy with a target neutrophil count of >3000/μL.

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25
Q

Grade 3 neutropenia

A

grade 3 (marked) neutropenia have a neutrophil count between 1000/μL and 500/μL and have an increased risk of secondary illness
– Antibiotics should be continued or initiated in these patients to prevent sepsis.
– next dose of chemotherapy should not be administered without a CBC done with neutrophil count seen above 3000/μL,
– dose should be reduced by 25%.
– best treated as outpatients if care is required, since hospitalization increases their risk of acquired illness

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26
Q

Grade 4 neutropenia

A

– severe with neutrophil count below 500/μL.
– at significant risk of sepsis and other secondary illness, even if they have been receiving antibiotic therapy

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27
Q

Chemotherapy

Gastrointestinal toxicity

A

two main ways that chemotherapy can cause gastrointestinal signs: centrally mediated nausea and direct injury to the stem cells of the intestinal crypts.

28
Q

Chemotherapy

Crypt cells

A

crypt cells of the intestines commonly affected by chemotherapy
–causes GI side effects

29
Q

Tumor Lysis Syndrome definition

A

oncological emergency that occurs following the death of tumor cells due to chemotherapy, radiation therapy, or spontaneous lysis
– sequel to chemotherapeutic or radiation therapy of hematological (i.e. lymphoma, leukemia) and solid tumor malignancies, most commonly within 48 hours of the initial therapy

30
Q

Tumor lysis syndrome diagnosis

A

separated into laboratory and clinical syndromes
– “Laboratory” tumor lysis syndrome is diagnosed based on derangements in uric acid, potassium, phosphorus, and calcium
– “clinical” tumor lysis syndrome is diagnosed when laboratory tumor lysis syndrome is present along with elevated creatinine, seizure, cardiac arrhythmias, or acute death

31
Q

Oncology

ATLS is characterized by

A

hyperkalemia,
hyperphosphatemia
metabolic acidosis

32
Q

PathPhys of Tumor Lysis Syndrome

A

After cancer cells die they rupture and release previously intracellular products into the circulation, primarily calcium, nucleic acids, phosphorus, and potassium
= hypocalcemia, hyperkalemia, and hyperphosphatemia; hyperkalemia results in bradycardia cardiac arrhythmia
– rapid release of cellular byproducts overwhelms the body’s ability to clear and recycle waste → AKI common result from calcium and phosphorus precipitation → Hypocalcemia commonly occurs secondary to hyperphosphatemia and acute kidney injury (AKI) is a common sequalae of ATLS.

Tumor cells can contain up to four times the normal quantity of phosphorus

33
Q

AKI from ATLS

A

– rapid release of cellular byproducts overwhelms the body’s ability to clear and recycle waste → AKI common result from calcium and phosphorus precipitation →
– Hypocalcemia commonly occurs secondary to hyperphosphatemia and acute kidney injury (AKI) is a common sequalae of ATLS.

34
Q

Urate nephropathy

A

– results when the purines adenine and guanine are metabolized into xanthine that is then metabolized into uric acid
– calcium phosphate salts may be deposited in the renal tubules.
– Coupled with damage by other nephrotoxins and volume depletion, this can result in oliguric renal failure

35
Q

Treatment: Tumor lysis syndrome

A

– IVF essential but cautiously in the face of renal oliguria or anuria
– 0.9% saline and diuretics used to promote calciuresis
– treatment for hyperkalemia if indicated

36
Q

Antihyperuricemic therapy for tumor lysis syndrome

A

– goal to lower uric acid levels
– xanthine oxidase inhibitors such as allopurinol or febuxostat and the recombinant urate oxidase enzyme rasburicase
– Allopurinol prevents the conversion of hypoxanthine to xanthine and hence xanthine to uric acid; however, it has many potential adverse drug reactions

37
Q

Paraneoplastic Syndromes definition

A

any systemic illness that is induced by neoplasia but occurs in a body system far from and unrelated to the primary tumor
– illness can be acutely more serious than the primary disease and can be the first indication of the primary neoplasia.

38
Q

Most common paraneoplastic syndromes in dogs

A

– caused by the production of polypeptide hormones that lead to endocrine‐like effects such as hypercalcemia and hypoglycemia.
– others include: anemia, thrombocytopenia, fever, cachexia, cutaneous abnormalities, and neurological signs.

39
Q

Paraneoplastic syndrome

Several types of anemia are associated with neoplasia

A

affects 30% of dogs with cancer
– may be related to chronic disease, blood loss, immune‐mediated hemolysis, chronic chemotherapy, or pure red cell aplasia

40
Q

Paraneoplastic syndrome

Anemia of chronic disease

A

– most common abnormality and results from decreased iron availability, shortened erythrocyte life span, and decreased erythropoiesis.
– characterized as normocytic, normochromic, and non‐regenerative.
– Iron replacement therapy will enable hemoglobin synthesis, help correct the anemia, and replenish iron stores (along with treating source of chronic blood loss)

41
Q

Paraneoplastic syndrome

Blood loss anemia

A

– observed with bleeding tumors (e.g. hemangiosarcoma) and is generally microcytic, hypochromic, and can be either regenerative or non‐regenerative.

42
Q

Paraneoplastic syndrome

IMHA and ITP as paraneoplastic syndromes

Can be seen with which neoplasia?

A

can be seen with K9 lymphoma
– secondary to protein production by malignant lymphocytes that either bind to or mimic antigens on red blood cells or platelet membranes, resulting in immune‐mediated destruction of red blood cells
– thrombocytopenia can be caused by the production of antiplatelet antibodies by the tumor, and cross‐reactivity between tumor antigens and platelet antigens

43
Q

Other paraneoplastic complete blood count abnormalities

A

eosinophilia, considered a marker for systemic or intestinal mast cell neoplasia

44
Q

Paraneoplastic syndrome

Leukocytosis

A

– A leukocytosis without obvious infection or other inflammatory causes has been associated with lymphoma and with tumors of the lungs, gastrointestinal tract, and genitourinary system
– thought to be from cytokine production that enhances the production of granulocytes and their release from bone marrow into the peripheral blood

45
Q

Chemistry abnormalities associated with paraneoplastic syndromes

A

– hypercalcemia and hypoglycemia
– Hypercalcemia of malignancy occurs secondary to tumor cell production of a parathyroid hormone‐related peptide (PTHrp) and is the most common metabolic emergency seen in veterinary patients with cancer.

46
Q

7

Malignancies that can cause hypercalcaemia

A
  1. lymphosarcoma,
  2. anal gland adenocarcinoma,
  3. carcinoma of the thyroid, prostate, or mammary glands,
  4. thymoma,
  5. bone neoplasia,
  6. multiple myeloma,
  7. leukemias
47
Q

Paraneoplastic hypoglycemia

A

often associated with insulinoma and other tumors such as:
1. adenocarcinoma,
1. lymphoma,
1. hepatomas,
1. leiomyomas
1. leiomyosarcomas,
1. carcinomas,

although any tumor can induce hypoglycemia

48
Q

mechanisms of paraneoplastic hypoglycemia

3 possible mechanisms

A

secretion of insulin‐like peptides,
– glucose consumption by tumor cells,
– and impaired or altered gluconeogenesis and glycogenolysis in the liver

49
Q

ALKYLATING Chemo Agents

x5

A
  1. Chlorambucil (Leukeran)
  2. Cyclophosphamide (Cytoxan)
  3. Procarbazine
  4. Melphalan (Alkeran)
  5. Lomustine CCNU
50
Q

ANTHRACYCLINES Chemo Agents

A
  1. Doxorubicin (Adriamycin)
  2. Mitoxantrone (Novantrone)
51
Q

ANTIMETABOLITES Chemo Agents

x3

A
  1. 5-Fluorouracil (5-FU)
  2. Cytosine arabinoside (Cytarabine, Cytosar-U,)
  3. Gemcitabine (Gemzar)
52
Q

ANTITUBULIN Chemo Agents

x2

A
  1. Vinblastine
  2. Vincristine
53
Q

PLATINUM Chemo Drugs

x2

A
  1. Carboplatin
  2. Cisplatin
54
Q

TYROSINE KINASE INHIBITORS

A

Toceranib (Palladia)

55
Q

MISCELLANEOUS Chemo Agents

x3

A
  1. L-asparaginase (Elspar)
  2. Imiquimod 5% cream (Aldara)
  3. Prednisone/prednisolone
56
Q

Chemo agents that can possibly cause Allergic reactions

A

L-asparaginase, etoposide, and doxorubicin, and taxanes such as paclitaxel may cause IgE-mediated type I hypersensitivity reactions.

57
Q

Bone marrow toxicity

A

Myelosuppression is a common side effect of chemotherapy but can also occur secondary to cancer, either by myelophthisis or paraneoplastic immune-mediated processes.

58
Q

How soon can you see myelosuppression after chemo?

A

neutrophil nadir varies somewhat depending on the chemotherapy agent administered but most often occurs around 7 to 10 days after treatment.

59
Q

Cardiotoxicity

A

Doxorubicin may cause cardiotoxicity in dogs and the resulting disease is similar to dilated cardiomyopathy (DCM).

60
Q

Hepatotoxicity

after which chemo?

A

Hepatoxicity secondary to CCNU (lomustine) administration is relatively common in dogs
– CCNU-induced hepatoxicity is rare in cats.

61
Q

Neurologic toxicity

A

5-Fluorouracil (5-FU) is extremely neurotoxic in cats and should never be administered in any form; results in a fatal reaction that may include excitability, blindness, tremors, dysmetria, and death
– toxicities in dogs have been reported after ingestion of these topical creams.
– grand mal seizures, tremors, dyspnea, and vomiting

62
Q

Pulmonary toxicity

A

– Respiratory complications of cancer are generally due to advanced staged metastatic disease
– there are rare reports of chemotherapy drugs causing pulmonary pathology
– Cisplatin can cause fatal pulmonary edema in cats and should not be administered to this species
– Bleomycin has been reported to cause intestinal pneumonia and pulmonary fibrosis, and case reports exist of pulmonary fibrosis secondary to alkylating agents such as CCNU

63
Q

Tranfusion Medicine

Immune Complex Formation; Type III hypersensitivity

A

– formation and depositing of immune complexes in areas such as the glomeruli, endothelial cells, lymph nodes, and synovium,
– can lead to neutrophil migration, activation, and inflammation resulting in glomerulonephritis, vasculitis, lymphadenitis, and immune‐mediated arthritis within hours to weeks of exposure
– use of protein concentrates such as human serum albumin is suspected to cause type III hypersensitivity

64
Q

acute type 1 hypersensitivity response

A

– allergica reaction to antigen
– range from life-threatening to mild reaction
– typically occur within 1 hr of exposure
– may be localized to cutaneous manifestations such as angioedema, erythema, urticaria, and pruritus. Gastrointestinal signs such as vomiting and diarrhea may be also seen with generalized or systemic allergic reactions
– recently recognized signs of canine anaphylaxis include elevated alanine transaminase and increased gallbladder wall thickness

65
Q
A

VTS ECC 2024 (17 decks)

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