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Block 3b1 PHM > Lung Cancer, BCM & Paraneoplastic Syndromes > Flashcards

Lung Cancer, BCM & Paraneoplastic Syndromes Flashcards

1
Q

Describe the pathogenesis of paraneoplastic syndromes (5)

A

Tumor production of protein hormones, enzymes, or fetal proteins

Tumor stimulation of antibody production

Metabolism of steroids by the tumor

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2
Q

What is a neurological paraneoplastic syndrome?

A

Immune mediated attack on central, peripheral, autonomic nervous systems

“Auto-antibodies” may be involved, mainly vs intracellular antigens; the presence of which indicates w/ certainty that there is an associated malignant tumor

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3
Q

After CXR, what other diagnostic tests might you might do if neurological paraneoplastic syndrome is suspected?

A

Imaging: PET, CT, MRI*esp for neurological symptoms

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4
Q

What do you test & what do you test for in neurological paraneoplastic syndromes?

A

Spinal fluid: 80% will have “onconeural antibodies”

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5
Q

What are the 2 main autoantibodies in neurological paraneoplastic syndromes? Antigen? Associated syndromes & symptoms and cancers?

A
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6
Q

What are the clinical presentations of Anti-NMDA receptor encephalitis?

A

Neurological paraneoplastic syndrome w/ flu like prodrome followed by psychiatric sx, behavioral abnormalities, memory deficits, seizures, progressive loss of consciousness

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7
Q

What 2 conditions are associated w/ Anti-NMDA receptor encephalitis?

A

(Ovarian) teratoma & lymphoma

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8
Q

What is the pathogenesis of subacute cerebellar degeneration?

A

Neurological paraneoplastic syndrome involving Anti-Hu and Anti-Yo antibodies

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9
Q

How does subacute cerebellar degeneration present clinically?

A

Ataxia, dysarthria (motor speech disorder), nystagmus (eye bounce at periphery)

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10
Q

What are malignancies associated w/ subacute cerebellar degeneration?

A

Lung, Ovarian & Breast Cancer

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11
Q

What paraneoplastic syndrome is associated w/ Non-Hodgkin’s Lymphoma & what autoantibodies are involved?

A

Subacute Cerebellar Degeneration; anti-Tr

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12
Q

How does Limbic Encephalitis present clinically?

A

Seizures, short term memory & behavioral deficits

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13
Q

Which antibodies are involved in Limbic Encephalitis & their respective malignancies?

A

GABA receptor antibodies: lung cancer (adults)

Anti-Hu: SCLC

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14
Q

Which malignancy is associated w/ Opsoclonus Myoclonus in children specifically?

A

Neuroblastoma

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15
Q

How does Lambert-Eaton Myasthenic Syndrome present clinically?

A

Progressive proximal weakness, diminished reflexes, autonomic symptoms

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16
Q

Which antibodies are associated w/ Lambert-Eaton Myasthenic Syndrome?

A

VGCC-P/Q ab’s

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17
Q

Which malignancy is Lambert-Eaten Myasthenic Syndrome associated with?

A

SCLC

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18
Q

If Myasthenia Gravis is paraneoplastic, what conditions is it associated with? How might it present clinically?

A

Thymoma & Pure Red Cell Aplasia

Ptosis

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19
Q

Which paraneoplastic syndrome does this person present with?

A

Poly/dermatomyositis

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20
Q

In an elderly male patient with anemia/iron deficiency, what might you recommend?

A

Colonoscopy

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21
Q

What is pemphigus & what other diseases might it resemble?

A

Autoimmune blistering disease

Erythema multiforme, graft vs. host disease, lichen planus

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22
Q

Describe the pathogenesis of pemphigus

A

Autoantibodies target desmoplakin, bullous pemphigoid antigen, envoplakin, periplakin plectin

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23
Q

Which malignancy is pemphigus associated w/ and what is the prognosis?

A

Lymphoproliferative diseases; poor prognosis

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24
Q

How does Sweet Syndrome present clinically?

A

Cutaneous plaques on neck, face, upper extremities w/ fever & neutrophilia

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25
Q

What might a biopsy in suspected Sweet Syndrome reveal?

A

Just neutrophilic infiltrate, biopsy may not show malignancy

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26
Q

What is the type of associated malignancy in Sweet Syndrome? Give 1 ex

A

Hematologic; MDS

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27
Q

How does acanthosis nigricans maligna present? & What are its associated malignancies?

A

Grey brown hyperpigmented plaques

Adenocarcinoma of GI tract, but also lung, breast, lymphoma, myeloma

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28
Q

How does a neuropathic itch present & what is its associated malignancy?

A

Just itch, no rash

Hodgkin Lymphoma

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29
Q

What do the blue & red circles reveal in the CT respectively?

A

Blue: mass obstructing bronchus

Red: post-obstructive pneumonia

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30
Q

What is the pathogenesis of Cushing’s Syndrome & its associated malignancies?

A

Inappropriate ACTH secretion

SCLC, Bronchial Carcinoid, Thymic Carcinoma, Pancreatic Cancer, Pheochromocytomas (hormone secreting tumor in adrenal glands), Medullary Thyroid Cancer, GI Carcinoid

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31
Q

How does Syndrome of Inappropriate Anti-diuretic Hormone (SIADH) present clinically? Which malignancy is it most commonly associated with?

A

Water retention & low Na-> fatigue, anorexia, altered mental status

SCLC association

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32
Q

What is the pathogenesis of Hypercalcemia?

A

PTHrP

Calcitonin secreting tumors

Bone metastasis

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33
Q

How does Hypercalcemia present clinically?

A

Constipation, confusion, bone pain

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34
Q

What malignancies are associated w/ Hypercalcemia?

A

Lung, Carcinoid, Colorectal, Breast, Medullary Thyroid Cancer

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35
Q

What does the red circle identify on this CT? What is the consequence?

A

Mass in upper pole of R kidney

Excess EPO secretion

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36
Q

What kind of paraneoplastic syndrome is erythrocytosis? & What is the associated malignancy?

A

Hematologic; Increased EPO secretion

Associated w/ renal cell cancer

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37
Q

What kind of paraneoplastic syndrome is Pure Red Cell Aplasia? & What is its associated malignancy?

A

Hematologic; Thymoma

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38
Q

What kind of paraneoplastic syndrome is DIC? & What are its associated malignancies?

A

Hematologic; Metastatic Adenocarcinoma, Acute Promyelocytic/Monocytic Leukemia

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39
Q

Which malignancy is the paraneoplastic syndrome Autoimmune Hemolytic Anemia associated with?

A

Low grade lymphoproliferative disease

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40
Q

What group of malignancies is the paraneoplastic syndrome Thrombophlebitis associated w/?

A

Adenocarcinomas

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41
Q

Which malignancies is the hematologic paraneoplastic syndrome “Acquired Factor VIII Deficiency” associated w/?

A

Solid & Plasma Cell Tumors, Multiple Myeloma

42
Q

What are 2 ex’s of paraneoplastic syndromes related to the heart?

A

Carcinoid Heart Disease & Marantic Endocarditis

43
Q

What is the pathogenesis of the cardiac paraneoplastic syndrome marantic endocarditis?

A

Central arterial embolization-> cerebral & myocardial infarctions

44
Q

What is Meigs Syndrome associated with?

A

NOT cancer

Benign ovarian fibroma w/ hydrothorax

45
Q

How is Meigs Syndrome treated?

A

Removal of benign tumor-> fluid elimination

46
Q

What might paraneoplastic syndromes signify?

A

Presenting signs/symptoms when cancer recurs

47
Q

How are paraneoplastic syndromes treated generally?

A

1st treat the acute problem

Then, treat the malignancy

48
Q

How is hypercalcemia treated acutely?

A

Fluids, corticosteroids, furosemide (Lasix)

49
Q

How is Hyponatremia in SIADH treated acutely?

A

Fluid restriction, hypertonic saline

50
Q

How is erythrocytosis treated acutely?

A

Phlebotomy

51
Q

What are 2 examples of epigenetic modifications & how do they differ?

A

Acetylation: releases DNA from histones by changing charge; loosening effect

Methylation: tightens DNA making DNA inaccessible to transcription; silencing effect

52
Q

What is the function of miRNA?

A

Degrades/translationally inhibits DNA

Can decrease expression of tumor suppressor genes in tumor cells

53
Q

What types of DNA damage call for base excision repair?

A

O2 radicals, deamination, spontaneous base loss, gamma irradiation & alkylating agents

54
Q

What are the consequences of DNA damage that call for BER?

A

Damaged bases/SSB

55
Q

What types of DNA damage call for NER?

A

UV radiation, smoking, Platinum drugs

56
Q

What are the consequences of DNA damage that call for NER?

A

Pyrimidine dimers, bulky adducts

57
Q

What are the main players in BER?

A

DNA glycosylase

APE1 Endo

DNA polymerase beta

LigaseIII and XRCC1 (X Ray Cross Complementation Protein I)

58
Q

How is the 8-oxo-guanine base lesion repaired?

A

OGG1 glycosylase removes GO- when it is paired w/ C

MutY removes A when paired w/ GO: backup if OGG1 doesn’t repair

59
Q

What clinical condition results if MutY fails to repair base lesion 8-oxo-guanine?

A

MutYH-associated polyposis colon cancer

60
Q

Which 2 compounds from cigarette smoke can impair DNA structure?

A

Nitrosamines & Benzo[a]pyrene

61
Q

How does UV radiation induce DNA damage?

A

Mutations in dypyrimidine sequences

62
Q

Describe the steps in NER

A

TFIIH complex (helicases + endonucleases) recognize site of intrastrand cross-link

Deoxynucleotides

DNA Polymerase & DNA Ligase

63
Q

What is an example of a disease due to impaired NER?

A

Xeroderma Pigmentosum

64
Q

What is an ex of a platinum chemotherapeutic drug & what is its MOA?

A

Cisplatin: forms intrastrand crosslinks between G’s

65
Q

What are 2 ex’s of TKI’s that inhibit EGFR?

A

Gefitinib & Osimertinib

66
Q

What is the issue w/ the problematic TKI of EGFR?

A

Secondary EGFR mutation: T790M

Prevents inhibition by Gefitinib

67
Q

What drug can be used to work around the EGFR mutation that confers resistance vs. Gefitinib?

A

Osimertinib: can inhibit EGFR w/ the T790M mutation

68
Q

What is the most common mutation of BRAF & what is the consequence?

A

BRAFV600E

Induction of MEK & ERK pathways

69
Q

What is the acronym & the steps to remember the MAP Kinase pathway?

A

Righteous (RTK)

Raisins (RAS)

Raffle & (RAF)

Make (MEK)

Ergonomics (ERK)

70
Q

What is the drug that can be used to work around the BRAF V600E mutation?

A

Vemurafenib inhibits BRAFV600E

“Very fed up with him”

71
Q

What drug can be given in combination w/ Vemurafenib to reduce the chance of melanoma remission in the face of BRAF mutation?

What is this drug’s MOA?

A

Trametinib: inhibits MEK downstream from RAF

72
Q

In the PI3K/AKT pathway, what is AKT activated by?

A

pDK & mTOR

73
Q

What are 3 general capabilities of AKT when it phosphorylates various products?

A

Cell cycle progression: stabilizes cyclin D1 via phosphorylation of GSK3B

Growth/Proliferation: phosphorylates mTOR

Inhibits apoptosis: phosphorylates MDM2, NF-KB, etc

74
Q

What is the pathogenesis of Cowden’s Disease & the clinical consequences?

A

LOF mutation in PTEN, PIP3 accumulates-> cancer

High risk of multiple cancers (ie: breast, thyroid, endometrium & kidney)

75
Q

What is the most common oncogenic ALK fusion protein?

A

EML4-ALK

76
Q

What is the first-line Tx vs. ALK rearrangements? 1 other ex?

A

Alectinib: 1st line vs. ALK rearrangements

Crizotinib

77
Q

What drug is given to treat Malignant Hyperthermia?
What is its MOA?

A

Dantrolene: muscle relaxant that decreases Ca release

78
Q

What is the genetic polymorphism that can cause 6 mercaptopurine to accumulate and lead to myelosuppressive effects when the minor pathway of metabolism is also inhibited?

A

Thiopurine Methyltransferase Deficiency (TPMT)

79
Q

What is the minor pathway in metabolizing myelosuppressive drugs like 6 mercaptopurine & why might this pathway be inhibited?

A

Xanthine Oxidase may be inhibited by Allopurinol to treat concomitant gout

80
Q

What is the pathogenesis of Acute Intermittent Porphyria?

A

Accumulation of Amino Levulinic Acid (ALA) and Porphobilinogen

81
Q

What genetic polymorphism causes ALA and Porphobilinogen to accumulate in Acute Intermittent Porphyria?

A

HMB Synthase

82
Q

What are the clinical presentations of Acute Intermittent Porphyria?

A

5 P’s
Painful Abdomen

Port wine-colored urine

Polyneuropathy

Psychological Disturbances

Precipitated by drugs (cytochrome P450 inducers), alcohol, estrogen/progesterone*

83
Q

How is Acute Intermittent Porphyria treated?

A

Glucose & Heme can treat AIP, which inhibits ALA Synthase

84
Q

How is the chemotherapy drug Irinotecan metabolized?

A
  • *Carboxylesterase** converts Irinotican (prodrug) into
  • *SN-38** (active drug)-> conjugated metabolite->bile
85
Q

What is the genetic polymorphism that converts Irinotecan’s active form SN-38 into conjugated metabolites that can be excreted into bile?

What is its MOA?

A

UGT1A1 involved in glucorinidation of SN-38

86
Q

What can be done before a drug like Irinotecan is administered to ensure proper metabolism?

A

Genetic testing vs. polymorphisms like UGT1AL1 to inhibit myelosuppresive effects from accumulating

87
Q

Which stains (+) in SCLC?

A

AE1/E3, CD56, Leukocyte Common Antigen (LCA)

Metastatic: also BER-EP4 and Synaptophysin

88
Q

Which stains (+) in NSCLC-adenocarcinoma?

A

TTF-1 & Napsin-A

89
Q

What stains (+) in mesothelioma?

A

Calretinin

90
Q

What should be done to address a brain tumor?

A

Steroids (ex: dexamethasone) can decrease H2O in brain & sx

Whole brain radiation therapy

Targeted therapy if there is an ALK rearrangement

91
Q

What are 2 Tx options for brain metastases in NSCLC, for ex?

A

Resection for single brain metastasis

Whole brain radiation therapy, for multiple disease sites beyond scope of Stereotactic Radiosurgery

92
Q

Categorize the type of brain metastasis in this MRI

A

Dural based metastasis

93
Q

What are the top 3 types of cancers to develop in 15-29 year olds?

A

1) Lymphomas (20%)
2) Invasive Skin (15%)- 76% Melanoma
3) Endocrine System (11%)- 96% Thyroid

94
Q

If a PET scan reveals a right lower lobe nodule, what is the diagnostic test to consider?

A

CT guided biopsy

95
Q

What is standard of care to test in metastatic disease?

A

Genetic driver mutations (ie: EGFR, ALK, ROS, RET, BRAF)

96
Q

What are the 3 things that are tested for to check for driver mutations in metastatic disease?

A

Blood, Urine, Tissue

97
Q

What are 3 techniques to test for driver mutations in metastatic disease in tissue?

A

Next Generation Sequencing

Immunohistochemistry for Proteins

Florescence in Situ Hybridization

98
Q

What 2 changes might you expect to see in the EGFR gene in metastatic cancer?

A

Exon 19 deletion

Point mutation L858R

99
Q

Which change might you expect to see in ALK and ROS1 genes in metastatic cancer?

A

Rearrangement

100
Q

Who decides what is a good screening test?

A

US Preventative Services Task Force, American Cancer Society, among other groups

Block 3b1 PHM (5 decks)

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