FMS Weeks 6 & 7 Flashcards

Pathology

1
Q

What are ERBB1 and ERBB2?

A

EGFR and HER growth factor receptors

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2
Q

What neoplasias are Actinomycin D used for?

A

choriocarcinoma, Wilm’s tumor, testicular tumors, Kaposi’s sarcoma

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3
Q

What type of tumors are steroid hormones used in?

A

HR+ tumors

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4
Q

What type of drug is Mechlorethamine?

A

alkylating agent

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5
Q

What are the 5 big tumor suppressor genes?

A

P53, RB, APC, PTEN, CDH1

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6
Q

What typ of drug is Bortezomib?

A

Proteosome inhibitor

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7
Q

What are the 6 hallmarks of cancer?

A

SERIE A

SUSTAINING proliferative SIGNALING

EVADING growth SUPRESSORS

RESISTING cell DEATH

INDUCING ANGIOGENESIS

ENABLING replicative IMMORTALITY

ACTIVATING INVASION/METASTASIS

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8
Q

What type of drug is danazol?

A

Androgen agonist

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9
Q

What is the target of Bevacizumab?

A

VEGF

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10
Q

What type of drug is Lenalidomide?

A

angiogenesis inhibitor

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11
Q

what is desmoplasia?

A

firm abundant collagen in many malignant tumors

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12
Q

characteristics of coagulative necrosis

A

gross architecture is preserved, firm texture, all organs except the brain

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13
Q

What does the tissue in this slide display?

A

coagulative necrosis

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14
Q

What is the mechanism of fat necrosis?

A

Leaking digestive enzymes (such as lipases from the pacreas) destroy cells, causing fatty deposits through saponification, calcium deposits, and inflammatory reaction

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15
Q

How do tumors enable replicative immortality?

A

upregulated telomerase activity

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16
Q

What are the typical toxicities of bleomycins?

A

skin lesions, hyperpigmentation, dose-limiting pulmonary fibrosis

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17
Q

What is the mechanism of topoisomerase inhibitors?

A

bind to DNA/topoisomberase II and stabilize dsDNA; results in double stranded breaks

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18
Q

What is type C Niemann-Pick?

A

lysosomal storage disease; mutations affecting enzyme in cholesterol trafficking

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19
Q

what are renal tubule resorbtion droplets?

A

reversible accumulations of protein that are absorbed into the cytoplasm of proximal tubular cells; seen in proteinuria conditions

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20
Q

What are the toxicities of lenalidomide?

A

severe neutropenia, thromboembolism

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21
Q

What type of drug is Trastuzumab?

A

Monoclonal anitibody

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22
Q

What are the main causes of hemosiderosis?

A

overload of iron: increased dietary absorbtion, hemolytic anemias, repeated blood transfusions

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23
Q

What is the mechanism of antineoplastic alkaloids?

A

disaggregate mitotic spindles (metaphase arrest)

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24
Q

What type of drug is Paclitaxel?

A

taxane

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25
Q

What type of drug is tamoxifen?

A

Estrogen antagonist

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26
Q

What kind of drug is Nivolumab?

A

monoclonal antibody (checkpoint inhibitor)

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27
Q

describe metastatic calcification

A

less common; otherwise normal tissues; associated with hypercalcemia and or some abnormality in Ca metabolism

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28
Q

What does the tissue in this slide display?

A

liquifactive necrosis

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29
Q

what are the toxicities of Bortezomib?

A

Therapeutic index around 1; peripheral neruopathy, hypotension, GI, asthenia, myelosuppression

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30
Q

What type of drug is Irinotecan?

A

topoisomerase inhibitor

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31
Q

With what type of necrosis is pus associated?

A

liquefactive

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32
Q

What type of drug is 6-mercaptopurine?

A

Purine analog

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33
Q

Use of retinoic acid in neoplasias?

A

high concentrations stimulate repressed (broken) RA receptors; especially in myelocytic leukemia (APL)

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34
Q

How does proteasome inhibition work?

A

they block the proteasome, producing conflicting regulatory signals; cancer cells are more sensitive to proapoptotic effects and undergo apoptosis more than normal cells

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35
Q

Mechanism of purine analogs as antineoplastics?

A

prodrug that inhibits ATP/GTP synthesis

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36
Q

what are the types of necrosis?

A

coagulative, liquefactive, caseuous, fat necrosis, and fibrinoid necrosis

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37
Q

What kind of drug is this?

A

Alkylating agent (mechlorethamine); nitrogen mustard

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38
Q

How do aromatase inhibitors work?

A

Inhibit aromatase (used in estrogen production); used in combination with estrogen inhibitors like tamoxifen for ER+ tumors

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39
Q

What type of drug is Leuprolide?

A

GnRH agonist

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40
Q

What is a fibroadenoma?

A

benign, biphasic (fibroblasts&glandular) neoplasm of the breast

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41
Q

what are the toxicities of vinblastine?

A

MYELOSUPPRESSION, peripheral neuropathy

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42
Q

What type of drug is Pomalidomide?

A

angiogenesis inhibitor

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43
Q

What type of drug is Degarelix?

A

GnRH antagonist

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44
Q

What is hemosiderin?

A

an endogenous pigment derived from hemoglobin, seen in tissues of both physiological/pathological blood cell breakdown

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45
Q

what are the main causes of metastatic calcification?

A

hypercalcemia: increased secretion of PTH, increased bone resorbtion, vitamin D disorders, renal failure

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46
Q

What is the classical toxicity of Thalidomide?

A

teratogen, peripheral neuropathy

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47
Q

What is the classical toxicity of checkpoint inhibitors?

A

immune suppression

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48
Q

What type of drug is Dactomycin?

A

Antineoplastic antibiotic

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49
Q

What is the philadephia chromosome?

A

a t(9,22) that leaves ABL gene (Bcr-Abl TK) constituativelyl activated

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50
Q

what is the limiting toxicity of cisplatin?

A

nephrotoxicity

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51
Q

What are “-tinibs”?

A

kinase inhibitors

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52
Q

What is unique about Bleomycins?

A

inactivated except in skin and lung tissue (does not suppress bone marrow)

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53
Q

what are asbestos bodies?

A

deposition of calcium and iron salts on asbestos fibers

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54
Q

What type of drug is Pertuzumab?

A

monoclonal antibody

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55
Q

what is Bevacizumab used for?

A

colon cancer and vasculopathy of the eye

56
Q

What type of drug is cyclophosphamide?

A

alkylating agent

57
Q

what are “-mabs”?

A

monoclonal antibody drugs

58
Q

What is KRAS?

A

G protein

59
Q

what are the toxicities of Actinomycin?

A

Classical antineoplastic toxicities

60
Q

What is steatosis?

A

fatty accumulation/change in cells that are not able to package/process triglycerides

61
Q

Key aspects leading to irreversible cell injury?

A

inability to correct mitochondrial dysfuntion and major disturbances in membrane function

62
Q

What are the toxicities of pyrimidine analogs?

A

classical, CNS and MYELOSUPPRESSION, GI, skin

63
Q

What are Psammoma bodies?

A

dystrophic accumulation of calium layers with a lamellated appearance

64
Q

What is the antineoplastic mechanism of taxanes?

A

mitotic spindle inhibitors; stabilizes microtubules leading to metaphase arrest

65
Q

How do antineoplastic antibiotics work?

A

Intercalation and generation of free radicals causing DNA damage (also transcription and replication inhibition at high doses)

66
Q

what is a leiomyoma?

A

a benign tumor of the smooth muscle

67
Q

What is alpha 1 anti-trypsin deficiency?

A

an accumulation of abnormal endogenous proteins (partially folding) in the ER of liver cells; circulating enzyme deficiency causes emphysema

68
Q

What type of drug is Adriamycin?

A

antineoplastic antibiotic

69
Q

What type of drug is Etoposide?

A

topoisomerase inhibitor

70
Q

what is Bortezomib typically used for?

A

multiple myeloma and mantle cell lymphoma

71
Q

What type of drug is Nivolumab?

A

monoclonal antibody

72
Q

What type of drug is Bevacizumab?

A

monoclonal antibody; angiogenesis inhibitor

73
Q

What type of drug is Vorozole?

A

Aromatase inhibitor

74
Q

What type of drug is Letrozole?

A

aromatase inhibitor

75
Q

What type of drug is Ipilimumab?

A

monoclonal antibody

76
Q

What type of drug is Vincristine?

A

vinca analog

77
Q

What type of drug is imatinib?

A

Tyrosine Kinase Inhibitor

78
Q

What are the main toxicities of Trastuzumab?

A

CARDIOTOXICITY

long half life; rigors, cytokine release syndrome, tumor lysis syndrome,

79
Q

What type of drug is Cisplatin?

A

platium analog

80
Q

What are the toxicities of Adriamycin (Doxorubicin)?

A

Classical toxicities and CARDIOTOXICITY

81
Q

Why do tumors need to enable angiogenesis?

A

they outgrow their blood supplies

82
Q

Describe tyrosine kinase inhibitors?

A

“-tinibs”; inhibit tyrosine kinases associated with neoplasias, metabolized by CYP3A4 (common drug interations), hard to predict toxicities

83
Q

What is the typical example of fibrinoid necrosis?

A

“immune complexes” and fibrin deposited on the walls of blood vessels

84
Q

What are the 2 features of reversible cell injury seen in light microscopy?

A

cell swelling and fatty change

85
Q

What type of drug is docetaxel?

A

taxane

86
Q

What are the toxicities of Paclitaxel?

A

myelosuppression, peripheral neurophathy, cardiac block and arrythmias

87
Q

what are “-rafenibs”?

A

raf kinase inhibitors

88
Q

What type of drug is retinoic acid?

A

Vitamin A

89
Q

What is the mechanism of cyclophosphamide?

A

activated to reactive carbocation (carbonium) by CYP450s; given near tumor site, creates adducts across DNA strands

90
Q

what is VEGF associated with?

A

angiogenesis regulation

91
Q

What is Thalidomide used for as an antineoplastic?

A

multiple myeloma and other malignancies

92
Q

What type of drug is Flutamide?

A

androgen antagonist

93
Q

What is the angiogenesis action of thalidomide?

A

inhibits VEGF and bFGF

94
Q

What are the two components of tumors?

A

parenchyma (neoplastic cells ) and reactive stroma (connective tissue)

95
Q

What does Bortezomib act on?

A

inhibits ubiquitin-proteosome pathway (26S inhibitor)

96
Q

How do platium analog antineoplastics work?

A

they crosslink DNA

97
Q

What are the toxicities of alkylating agents?

A

classical neoplastic toxicities; purine crystalluria

cyclophosphamide: hemorraghic cystitis

Busulfan: pulmonary fibrosis

98
Q

What type of drug is Carfilzomib?

A

proteosome inhibitor

99
Q

What are the toxicities of topoisomerase inhibitors?

A

SECONDARY LEUKEMIA (AML), bone marrow suppression, hepatic

100
Q

What are the toxicities associated with TK inhibitors?

A

multiple hard to predict toxicities (skin reactions, hepato, hypertension, myelosuppression, edema, CHF)

101
Q

What is the classic example of caseous necrosis?

A

lung tissue in tuberculosis

102
Q

What are “-zomibs”?

A

proteasome inhibitors

103
Q

What are glycogenoses?

A

glycogen storage diseases; defective enzymes in synthesis/breakdown of glycogen, causes cell injury/death

104
Q

Where does trastuzumab act?

A

HER2-EGFR protein

105
Q

what is a rhabdomyosarcoma?

A

a malignant tumor of the striated msucle

106
Q

what are “-anibs”?

A

angiogenesis inhibitors

107
Q

What are the toxicities of 6-Mercaptopurine?

A

MYELOSUPPRESSION

classical toxicities, hepatotoxicity, inhibition of xanthine oxidase (necessitates dose reduction with allopurinol)

108
Q

What type of drug is Gefitinib?

A

Tyrosine Kinase Inhibitor

109
Q

What type of drug is Thalidomide?

A

angiogenesis inhibitor

110
Q

how might a cell adapt to ER stress from misfolded proteins?

A

decreased protein synthesis and increased chaperone production; otherwise apoptosis

111
Q

What is anaplasia?

A

poorly differentiated

112
Q

What are xanthomas?

A

accumulation of foamy macrophages in connective tissue

113
Q

what are russell bodies?

A

distended ER in areas of chronic inflammation (plasma cells active synthesizing immunoglobulins)

114
Q

What type of drug is Vinblastine?

A

Vinca alkaloid

115
Q

What are the toxicites of vincristine?

A

PERIPHERAL NEUROPATHY, myelosuppression

116
Q

What type of drug is Actinomycin D?

A

Antineoplastic antibiotic

117
Q

What is the difference between GnRH agonists and antagonists?

A

GnRH antagonists are better drugs because they cause drop in LH and FSH without initial surge (GnRH agonists cause initial surge in LH & FSH as receptor numbers increase; require androgen/estrogen antagonists concurrently)

118
Q

What type of drug is Erlotinib?

A

Tyrosine Kinase Inhibitor

119
Q

What category would best descrive glycogen storage diseases?

A

Accumulation of abnormal endogenous substance due to genetic or acquired defects

120
Q

What are the immunomodulatory activities of thalidomide?

A

T-cells are stimulated; B-cells undergo apoptosis

121
Q

What type of drug is estradiol?

A

estrogen agonist

122
Q

two types of pathologic calcification?

A

dystrophic and metastatic

123
Q

How do monoclonal antibodyies work?

A

They are mediators of receptor blockades and antibody-dependent cellular toxicity (driving apoptosis)

124
Q

What type of necrosis is most associated with the central nervous system?

A

liquefactive

125
Q

What is NMYC?

A

a trascription activator

126
Q

what is an infarct?

A

a localized area of coagulative necrosis

127
Q

What type are Pompe disease and von Gierke disease?

A

glycogen storage disorders

128
Q

What is BRAF?

A

RAS signal transducer

129
Q

What is the effect of the Philadelphia chromosome?

A

constituatively activated TK ABL

130
Q

What type of drug is 5-Fluorouracil?

A

pyrimidine analog

131
Q

What phenomenon is featured in this slide?

A

artherosclerosis

132
Q

What is a leimyosarcoma?

A

a malignant (mesenchymal) tumor of the smooth muscle

133
Q

How to ‘classical’ antineoplastics work?

A

they inhibit nucleic acid synthesis: binding to DNA or interfering with nucleic acid pathways

134
Q

describe dystrophic calcification

A

more common type of calcification; locally in dying/abnormal tissue (also breast tissue); normal serum levels and calcium metabolism

135
Q

What type of drug is Bleomycin?

A

antineoplastic antibiotic