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POD: Exam 3 > Immunology > Flashcards

Immunology Flashcards

1
Q

What can break anergy?

A

Infection; increased PAMPs =» increased MHC expression

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2
Q

Autoimmune Lymphoproliferative Disorder (ALPS)

A

Deficiency of Fas-FasL apoptosis

=»Hepatosplenomegaly, lymphadenopathy

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3
Q

Phenotypic Characteristics of T-reg cells

A
  • Expression of Foxp3
  • Expression of CD-25
  • Constitutive and High Expression o CLTA-4
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4
Q

IPEX Syndrome

A

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome

  • Caused by mutation in Foxp3 gene =» deficiency of t-reg cells
  • Triad= Watery diarrhea, eczematous dermatitous, and endocrinopathy
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5
Q

Mechanisms of B-cell peripheral tolerance

A
  1. Anergy (lacks CD40-CD40L bnding)

2 Clonal deletion

  • Can occur w/ repeated stimulation of BCR =» Increased BAFF/Blys requirement for survival
  • Also occurs via mitochondrial and Fas pathway
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6
Q

CTLA-4 polymorphisms

A

Assoc. w/ decreased mRNA levels and Grave’s Disease, Hashimoto’s, and SLE (for example)

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7
Q

C4, C2 deficiencies

A

Leads to deposition of immune complexes in blood vessels activating the alternative pathway&raquo_space; Increased penetration of PMNs into tissue and destruction of tissue

(Type III hypersensitivity)

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8
Q

PTPN22

A

Gene involved in receptor TK formation

-Commonly assoc. w/ RA, IBD, and TD1M

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9
Q

NOD2

A

Gain-of-function mutant of cytoplasmic bacterial sensor commonly assoc. w/ IBD

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10
Q

AI preferential exception for Males

A

Ankylosing spondylitis and Goodpasture’s syndrome

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11
Q

Anergy

A

Occurs when a primary binding event occurs b/w and APC and T-cell but no secondary signal (CD28-B7)

Results in:
1. Decrease in TCR complexes (mediated by Cbl-b degradation)

  1. Engagement of inhibitory receptors (CTLA-4 binds to B7 and PD-1 blocks t-cell activation/pro-inflammatory secretion)
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12
Q

Molecular Mimcry

A

Occurs when an infectious agent expresses a similar epitope to that of a self-Ag =»Autoimmunity

*S. pyogenes =» ARF

EBV =» MS (protein resembles human myelin basic protein)

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13
Q

By-stander activation

A

Basically the same as Molecular Mimicry

BUT

this is caused by activated APCs presenting cross-reactive self-Ag to autoreactive T-cells

RXN IS INITIATED BY SELF-ANTIGEN IN FIRST PLACE

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14
Q

Epitope spreading

A

AI response expands to more self-Ags than just the one the initial Ag that caused the attack

=»Self-perpetuating and flaring up seen w/ conditions like pemphigus

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15
Q

Cryptic epitope

A

Antigenic epitopes not presented to T-cells in sufficient amounts to activate T-cells BUT become abundant after tissue destruction during inflaammation

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16
Q

Conventional Therapy for AI disease

A

Includes corticosteroids (anti-inflammatories) and immunosuppresants that limit t-cell activation

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17
Q

Immunotherapy for AI disease

A

Administration of agents that block pro-inflammatory cytokines and target autoreactive T and B-cells

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18
Q

Radiation oncogenesis

A

UV radiation leads to the formation of pyrimidine dimers that can overwhelm the nucleotide excision pathway =» Melanomas

*High melanin decreases risk for this

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19
Q

Ionizing Radiation

A

Directly fractures the DNA double helix; hematopoietic, thyroid, and breast tissues are especially sensitive

*Bone, GI, and skin are NOT sensitive

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20
Q

CYP1A1 Allele

A

Cytochrome-P450 mutation that converts smoke, an indirect chemical mutagen, into a much more highly potent intermediate

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21
Q

Direct-acting alkylating agents

A

Act as direct chemical carcinogens that are usually assoc. w/ chemotherapy

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22
Q

Polycyclic Aromatic Hydrocarbons

A

Include fossil fuels and cigarette smoke; extremely potent carcinogenic agents that cause a predilection for lymphoma/leukemia

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23
Q

Aflatoxin B1

A

Assoc. w/ Aspergillus that is found on improperly stored nuts

=» Mutation of the p53 gene causing a substitution of serine for arginine @ codon 249; causes hepatocellular carcinoma

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24
Q

Lead Time Bias

A

False, but apparent, improvement in survival time caused by earlier detection of cancer

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25
Q

Length Bias

A

Earlier detection of cancer tends to pick up less aggressive variants

*Is treated the same way as an aggressive variant leading to a perceived increase in survival rate

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26
Q

Paraneoplastic syndromes

A

Hormones not normally made by the tumor tissue cause unusual symptoms; can be the first sign of a metastatic tumor

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27
Q

Carcinoid Syndrome

A

Excess secretion of serotonin and bradykinin leading to hypotension

*Caused by hepatocellular, lung, and pancreatic carcinomas

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28
Q

Lambert-Eaton Syndrome

A

Myasthenia caused by paraneoplastic production of Abs to nerve endings

*Caused by lung cancer

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29
Q

Hypertrophic Osteoarthropathy

A

Excessive new growth of long bones at the ends along w/ arthritis and clubbing of the digits

*Paraneoplasm caused by bronchogenic carcinoma

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30
Q

Trosseau Syndrome

A

Migratory thrombophlebitis that is caused by lung and pancreatic tumors

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31
Q

DIC (paraneoplastic cause)

A

APML, prostate cancer

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32
Q

Nonbacterial thrombotic endocarditis (Marantic)

A

Fibrin growth on valve leaflets caused by mucin-secreting carcinomas
E.g.-pancreatic cancer

  • Also caused by SLE and ARF
  • typically on the mitral valve
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33
Q

Mass Effect

A

(1) - Tumor size grows and compresses structures
- Especially in the skull where there is nowhere for it to go

(2) - Metastasis causes tumors to disrupt fnxn of other organs
(3) - Tumors can cause failure of organ

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34
Q

Pseudomyxoma peritonei

A

Gelatinous mass on the peritoneum originating from a mucous-secreting appendix carcinoma

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35
Q

Skip metastasis

A

Metastasis of a tumor past the first lymph node due to the anastomoses of the lymphatics

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36
Q

Dormancy

A

Prolonged survival of metastasis w/o progression

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37
Q

Pseudotumor

A

Non-neoplastic tumor

E.g.-Swelling from inflammation

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38
Q

Scirrhous

A

Dense desmoplasia making tumors rock hard

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39
Q

Nevus

A

Benign proliferation of melanocytes

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40
Q

Mesothelioma

A

Malignancy of mesothelial cells

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41
Q

Seminoma

A

Malignancy of germ cells; ovarian subtype is called dysgerminoma

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42
Q

Hepatoma

A

Malignant liver tumor

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43
Q

Papillary cystadenocarcinoma

A

Malignant finger-like projections in a tumor derived from glands making a cyst

*True papillary structures will have a central blood vessel

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44
Q

Papillary carcinoma

A

Malignant, finger-like projections?

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45
Q

Keratin pearls

A

Structure seen w/ SCC

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46
Q

Carcinosarcoma

A

Uncommon uterine tumor w/ both malignant glands and stroma

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47
Q

Hamartoma

A

A benign, clonal proliferation where the right cells are seen in the right place BUT w/ the wrong proliferation

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48
Q

Choristoma

A

The wrong cells are seen in the wrong place BUT in the right type of arrangement

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49
Q

Characteristics of Dysplasia

A

Pleomorphism

Loss of polarity

Increased mitotic figures

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50
Q

Carcinoma in Situ

A

Severe Dysplasia; seen w/ marked pleomorphism and thickness changes in the epithelium

*Still does not invade the BM

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51
Q

Tumor Staging

A

(T)umor: Size and extent of invasion

(N)ode: # of lymph nodes involved

(M)etastasis

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52
Q

Warburg Effect

A

Tumors use large amounts of glucose regardless of what is available to the cell but lack ATP production from mitochondria

=»Advantage this gives the cell is that there are increased Krebb cycle intermediates that are available for catabolic metabolism

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53
Q

PET

A

Measures the uptake of 18F-fluorodeoxyglucose by the tumor cell as a sign of the Warburg Effect

=»Also seen w/ increased respiratory activity

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54
Q

MDR-1

A

Multi-drug resistance expressed by tumor cells that make them resilient to chemotherapy

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55
Q

HNPCC

A

Hereditary NonPolyposis Colon Cancer

Mutation in MMR genes

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56
Q

Sporadic Colon Cancer

A

Somatic loss of MMR genes of APC genes

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57
Q

Xeroderma Pigmentosum

A

Cross-linking of pyrimidine residues cannot be repaired due to loss of nucleotide excision mechanisms

=»Terrible skin condition

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58
Q

Advantageous features for a neoplasm

A
  1. Uncontrolled replication
    • Loss of TSGs, contact inhibition, activation of protooncogenes
  2. Immortality
    • Disruption of apoptosis, activation of telomerase
  3. Loss of DNA repair
    • Gatekeeper mutations
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59
Q

p53 mutation

A

Point mutations in this gene are the most genetic alteration in cancer

*Levels will actually be INCREASED as the cell tries to produce more to regain proper fnxn

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60
Q

HPV alteration of p53

A

E6 protein produced binds to p53 and promotes degradation

*E7 protein binds RB and prevents G1 =» S transition

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61
Q

Li-Fraumeni Syndrome

A

One inherited loss of p53 gene followed by a somatic loss

=»Formation of multiple tumors at a young age

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62
Q

APC gene

A

Normally fnxns to downregulate B-catenin, a growth promoter

-Familial adenomatous polyposis occurs w/ one inherited defect along w/ a second mutation

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63
Q

B-catenin

A

Product bound to E-cadherin that when released, moves to the nucleus and upregulates cell-cycle genes

*Loss of cell-cell contact =»Release of B-catenin from E-cadherin

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64
Q

WNT

A

Signal that blocks APC fnxn

*Excessive activation of WNT =» Cell-cycle progression

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65
Q

RET gene

A

Normally functions as a growth hormone receptor to promote cell survival in neuroendocrine cells but point mutations can lead to..

MEN 2A (Extracellular Region): Medullary thyroid carcinoma, thyroid, adrenal carcinoma

Men 2B (Intracellular Region): Medullary thyroid carcinoma

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66
Q

C-kit gene

A

Growth factor receptor that when mutated causes gastrointestinal stromal tumors (GIST)

*Treated w/ TK inhibitors

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67
Q

t(5;12)

A

Translocation assoc. w/ CMML and causes excessive activation of the PDGF receptor

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68
Q

The Philadelphia Chromose

A

t(9;22) (BCR-ABL)

*Major breakpoint=cause of CML

Minor breakpoint= cause of ALL

*Gleevac= inhibitor of BCR-ABL TK; cures CML

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69
Q

Her-2/neu

A

Overexpressed NORMAL growth hormone receptor found in breast cancer

-Treated w/ Tastuzumab

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70
Q

EGFR

A

Gene that is found activated in lung and colon cancer (Outer portion of TK receptor)

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71
Q

Ras mutations

A

GTP-binding proteins that can cause a wide range of carcinomas, melanomas, and lymphomas

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72
Q

BRAF

A

v600E mutation; activated by Ras proteins in normal cascade

  • Common in thyroid, melanomas, and sporadic cancers
  • Target therapies for codon 600 mutations
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73
Q

DNA Methylation

A

Tumors will…

Hypomethylate protooncogenes
-Genetically unstable

Hypermethylate TSGs
-Inactivation in cases like BRCA-1(breast cancer)

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74
Q

Histone Acetylation

A

More negative charge=»More open for transcription (protooncogenes)

Reverse also applies for TSGs

*Chromatid alteration can also change the packing of DNA making it more or less available for transcription

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75
Q

miRNA

A

Binds to the UTR on the 3’end of mRNA making it more unstable and more likely to be degraded; tumors use this to decrease the mRNA of TSGs

-

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76
Q

RISC

A

RNA induced silencing complex that recognizes dsRNA since it may represent viral mRNA, degrades it, and keeps a piece to recognize future pieces of dsRNA

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77
Q

siRNA

A

Binds to the coding region of mRNAs that is used to silence complimentary RNA strands

*DICER, a protein found in cells, will chop up dsRNA to produce siRNA and silence other dsRNA

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78
Q

Evasion of apoptosis by tumor cells

A

Reduced amount of CD95

Increased Bcl-2 (stabilizes the mitochondrial membrane preventing the mitochondrial apoptotic pathway)

Decreased p53

Inhibition of caspases

FLIP(binds to Fas)

Loss of APAF-1

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79
Q

Immunohistochemistry

A

Used to categorize tumors, determine origin of metastases, and form a pronosis

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80
Q

What type of cancer if flow cytometry used to diagnose?

A

Lymphoma/leukemia

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81
Q

X-linked SCID

A

Caused by a mutation in the y-chain receptor for IL-7, 2, and 15
=» no maturation of T-cells

T-cells: Decreased
B-cells: Normal
IG: Decreased

Treatment: Stem-cell transplant ASAP; Introduction of normal y-chain gene into BM using lentivirus (can cause leukemias if placed near an oncogene)

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82
Q

AR SCID

A

Can be caused by a deficiency in ADA or PNP (JAK-3) enzymes leading to a toxic accumulation of dATP and dGTP

APA: All decreased

PNP: Only T-cells decreased

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83
Q

Bruton’s X-linked Agammaglobulinemia

A

Mutation in BTK (Bruton’s TK) gene leads to inability of pre-B cells to mature

Repeated infections include: otitis media, pneumonia, sinusitis
*due to decreased amounts of all Igs

Findings: Will see no CD19 B-cells or plasma cells in the blood
Germinal centers and Peyer’s patches are underdeveloped
Increased AI disease

*Treated w/ gamma globulin injections

84
Q

DiGeorge Syndrome

A

Dysmorphogensis of the third and fourth pharyngeal pouches lead to aplasia of the thymus along w/ heart malformations

  • LNs have depleted paracortical areas
  • Facial abnormalities include low-set ears and wide eyes alongside learning disabilities and cardiac malformations
  • Suggested by presence of neonatal tetany and thymic shadow
85
Q

22q11 deletion syndrome

A

Components of this deletion include DiGeorge Syndrome, schizophrenia, and bipolar disorder

86
Q

X-linked Hyper IgM Syndrome

A

Mutation in CD40L on T-cells =» Lack of class switching that is compensated for by increased levels of IgM

-Additional defects in DTH cause increased susceptibility to intracellular microbes and P. jiroveci

87
Q

Selective IgA deficiency

A

Most common primary deficiency; assoc. w/ decreased IgA levels

=»Frequent sinopulmonary infxns and diarrhea

88
Q

Common Variable Immunodeficiency

A

Failure of B-cells to mature into plasma cells

  • Decreased serum IgA and IgG; serum IgM normal
  • Assoc. w/ gastrointestinal and respiratory infxn by pyogenic organisms
89
Q

Wiskott-Aldrich Syndrome

A

X-linked multi-system deficiency assoc. w/
-Thrombocytopenia, eczema, recurrent infxn

Pts. are unable to respond to bacterial polysaccharides and have decreased IgM levels

-Treat w/ gene therapy

90
Q

Ataxia Telangiectasia

A

Multi-system disorder assoc.w/ a staggering gait(neurologic), abnormal dilation of blood vessels, and decreased T and B-cells

-Pt. will NOT be able to respond to skin tests and have decreased IgA and IgG

91
Q

Chediak-Higashi Syndrome

A

Dysfunctional, giant granules are seen in the pts. PMN

-Due to a protein trafficking defect =»defective phagolysosome formation

NBT (-)

92
Q

Chronic Granulomatous Disease

A

Pts. are unable to from ROIs causing intracellular bacteria to survive via the formation of chronic granulomas

NBT (-)

93
Q

Hereditary Angioedema

A

Deficiency in C1 inhibitor leads to excess activation of C4 and C2

=»Localized edema

94
Q

Paroxysmal nocturnal hemoglobinemia

A

Deficiency of DAF causes excess activation of the complement cascade and excessive intravascular hemolysis

=»Hemoglobinemia

95
Q

Secondary Immunodeficiency causes

A

Malnutrition: Lack of T-cell development

Cancer

Viral/Parasitic Infxn: Measles =» Infects lymphocytes

Drugs: Anti-inflammatories/Immunosuppresants

Splenectomy: Increased susceptibility to encapsulated organisms

AIDS

96
Q

Physiologic Hypogammaglobulinemia

A

Normal neonatal reduction of serum IgG after maternal antibodies expire and infant has not taken over full production

*Transient Hypogammaglobulinemia of Infancy (THI) is a slight longer period (9-15 months) where this condition continues for inexplicable reasons; disorder is self-limiting and infant will react normally to vaccination

97
Q

Immunosenescence

A

Changes in immunity w/ old age that include:

Unsustained memory response
Inability to respond to new Ags
Low-grade inflammation (chronic)
Greater risk for AI response

98
Q

Leukocyte Adhesion Deficiency

A

Defects on leukocytes in selectins and integrins =»decreased migration during inflammation

*Bacterial infxns W/O pus formation

99
Q

Immunological Stages of Tumor Development

A

Elimination

Equilibrium

Evasion

100
Q

NK Response to Tumor Cells

A

NK cells: Activated by a lack of bonding w/ inhibitory receptors or FcyR activation
=»Kill tumor cells via ADCC, cytotoxic product release, and release of IFN-y (activates macrophages)

101
Q

Missing Self Hypothesis

A

Tumor cells hide MHC-I molecules in order to hide from CTLs, however, this leads them open to attack by NK cells

102
Q

Macrophage response to tumor cells

A

M1 macros are activated by tumor Ags, IFN-y, and some microbial products

=»Act thru direct killing w/ cytotoxic granules or TNF-a release (thrombosis of blood vessels)

103
Q

Cross-priming

A

Tumor Ags are ingested by APCs and presented to naive T-cells to form CTLs

-CTLs also activated by cytokine release from CD4+ cells

104
Q

Tumor evasion of Immune System

A
  1. Lack of recognition: Tumors lose MHC-I expression
  2. Inhibitory cytokine secretion: CTLA-4, PD-1, and TGF-B
  3. Recruitment of T-reg cells
105
Q

Dendritic-cell based tumor vaccine

A

Approved for use against prostate cancer; made by pulsing APCs w/ tumor Ag or transfecting them w/ tumorigenic genes

106
Q

Cytokine-enhanced tumor cell vaccines

A

Vaccination is given w/ cytokines (IL-2) or co-stimulators (B7) for T-cell fnxn

107
Q

LIK

A

Lymphokine activated killer cells

NK cells cultivated w/ IL-2 to activate them against tumor cells

108
Q

TIL

A

Tumor infiltrating lymphocytes

Lymphocytes taken from a pt, expanded in culture via IL-2 and inactivated tumor cells

=»enriched for tumor-specific activity

109
Q

Graft vs. Leukemia effect

A

Lymphocytes from healthy donors are given to cancer pts. who also receive radiation therapy

=»Health donor lymphs attack leukemia cells against pts. HLA

110
Q

Anti-tumor antibodies

A

Formed either thru humanization of mouse antibodies or conjugation with tumorigenic toxins

111
Q

Familial Retinoblastoma

A

AD inheritance of a faulty TSG that allows unregulated progression thru the cell cycle

=»Multiple, bilateral tumors that occur at a young age if there is a LOH

*Treat w/ cryotherapy and monitor pt.

112
Q

GSTM/GSTT1

A

Defects in either of these genes result in reduced ability to handle aromatic hydrocarbons

GSTM1- Conjugates epoxides on polycyclic aromatic hydrocarbons

GSTT1- Conjugates monohalomethans on polycyclic aromatic hydrocarbons

113
Q

ERS

A

Cancers that have a higher “Extra Risk Score” are more highly assoc. w/ environmental or inherited risk factors

  • Includes colorectal, basal cell carcinoma, and lung cancer
  • Low scores (or negative scores) are assoc. w/ stochastic DNA replicative occurrences
114
Q

Juvenile Polyposis

A

AD caused by mutations in the SMAD4/DPC3 gene that is assoc. w/ large polyps, but less numerous that FAP, on the colon that usually appear around puberty

115
Q

Cowden Syndrome

A

Assoc. w/ inherited mutations in the PTEN TSG; pts. will develop multiple hamartomas and have an increased risk in developing breast, uterine cancer

116
Q

Turcot’s Syndrome

A

Variant of FAP that is also assoc. w/ brain tumors

117
Q

Attenuated FAP

A

Version of FAP w/ less polyps but more highly assoc. w/ colon cancer

118
Q

Von-Hippel Lindau Disease

A

Caused by an inheritance in the VHL gene and assoc. w/ the development of hemangioblastomas in parts of the nervous system; also assoc. w/ an increased risk for kidney cancer

119
Q

CC for Hodgkin’s Disease

A

MOPP

=»If MOPP (R), then use ABVD

120
Q

CC for Non-Hodgkin’s Lymphoma

A

CHOP

121
Q

CC for Breast Cancer

A

CAF or CMF

122
Q

CC for small lung cancer

A

PACE

123
Q

CC for germ cell carcinoma

A

VIP

124
Q

CC for cervical cancer

A

BIP

125
Q

CC for Ovarian Cancer

A

BEP

126
Q

CC for Pheochromocytoma

A

CVD

127
Q

CC for Testicular Cancer

A

PEB

128
Q

p-glycoprotein

A

Upregulated protein in cancer cells that promotes the efflux of chemotherapeutics out of the cell

129
Q

Melphalon

A

Is taken up by a cell due to its similarity to phenylalanine and then induces its toxic effect

130
Q

Mechloroethamine

A

Alkylating agent that binds to the n-7 guanine on DNA cross-linking two strands

Part of MOPP; is not excreted at all

131
Q

Cyclophosphamide

A

Alkylating agent that must be activated by CYP-450 enzymes in the liver

*Causes hemorrhagic cystitis and SIADH

=»Pts. undergo extensive rehydration therapy to flush the drug out and prevent damage to the bladder; pts. also have hyponatremia and hypervolemia due to extensive water retention and get confusion, N/V, and possible cerebral edema

132
Q

Na-2-mercaptoethanesulfate

A

Reacts w/ cyclophosphamide to neutralize its toxicity and prevent its binding to the bladder wall

=»decreased possibility of hemorrhagic cystitis

133
Q

Chloarmbucil

A

Least toxic alkylating agent; causes only a little hepatotoxicity

=»Used for CLL

134
Q

Estramustine phosphate

A

Combination of nitrogen mustard and estradiol w/ increased water solubility; used in aggressive prostate cancer

*Has anti-mitotic capabilities by binding to B-tubulin

135
Q

Busulfan

A

Used to treat CML; toxicities include pulmonary fibrosis and hyperpigmentation

136
Q

Procarbazine

A

Nitrosurea that produces free radicals that damage DNA; part of MOPP

  • Must avoid MAOs and alcohol w/ this drug; combined effect will =»hypertension
  • also cause breakage of chromosomes and inhibit G1-S transition
137
Q

Carmustine, lomustine, semustine

A

Nitrosureas that have increased lipid solubility making them the first line of defense against brain tumors

*Toxicities= pulmonary fibrosis, nephrotoxicity

138
Q

Decarbazine

A

Methylates DNA preventing its transcription; part of ABVD

*No toxicities

139
Q

Temozolomide

A

Methylates DNA and RNA preventing transcription; used in gliomas

*No toxicities

140
Q

Cisplatin

A

Binds to n-7 guanine in DNA but forms crosslinks on the same DNA strand; interferes w/ DNA replication and mitosis

  • Has severe nephrotoxicity and Ototoxicity
  • can administer to furosemide as a diuretic to limit renal damage
141
Q

Doxorubicin/Daunorubicin

A

Intercalates b/w the two strands of DNA blocking the action of topoisomerase II; also causes histone eviction all of which =»dysregulation of transcriptional machinery

  • Has severe cardiotoxicity
  • Part of AVBD (Adiamycin=Doxorubicin)
142
Q

Zexrazoxane

A

Used in conjunction w/ Doxorubicin to prevent cardiotoxicity if the pt. is at an increased risk

143
Q

Mitoxantrone

A

Binds to DNA preventing the action of topoisomerase II but is less frequently cardiotoxic than doxorubicin or daunorubucin

*When it is toxic, it is worse

144
Q

Etoposide

A

Forms a ternary complex w/ topoisomerase II; used for testicular tumors in conjnxn w/ cisplatin and bleomycin

-Prevents the re-ligation of DNA (no S-G2 transition)

145
Q

Camptothecin, irinotecan, topotecan

A

Binds to topoisomerase I and prevents DNA replication

Irinotecan/Topotecan =» Severe diarrhea

Irinotecan- prodrug that must be activated by carboxyesterases

*CCS-S

146
Q

Bleomycin

A

Bind to free iron in cells and produce radicals

Toxicities= Pulmonary fibrosis and pneumonitis; low-grade fever

*Used for advanced testicular tumors along w/ Vinblastine and Cisplatin

147
Q

Dactinomycin

A

Intercalates b/w purine-pyrimidine pairs; *most potent anti-tumor agent

Toxicities: Oral/GI ulcers

USES: MTX-(R) Choriocarcinoma
Wilm’s Tumor
Rhabdomyosarcoma

148
Q

MTX

A

Folate analog that binds to DHFR; blocks the biosynthesis of pyrimidines

*No FH4 is ever formed (important for DNA synthesis)

Used for choriocarcinoma and maintenance of ALL in children

*CCS-S

149
Q

Leucovorin “Rescue”

A

Minimizes the toxic effects of FH4 loss in cells produced by MTX by skipping the metabolic block in DHFR; administered 24-36 hours after first MTX

*Is not taken into malignant cells because it cannot bind with the transporters

150
Q

Capecitabine

A

Pro-drug transformed into 5-FU by carboxyesterases in the liver

151
Q

Fluorouracil

A

Decreases DNA synthesis by binding to thymidylate synthase in the FdUMP form; can also be converted to the FdUTP form which will bind directly to DNA or RNA

  • Toxicity= Stomatitis/GI Ulcers =» STOP at earliest signs of diarrhea and stomatitis
  • Used for solid tumors
152
Q

Cytarabine

A

Inhibits DNA Polymerase-a; causes less ulcers than 5-FU

153
Q

Mercaptopurine

A

Inhibits the synthesis of A and G thru “pseudo-feedback inhibition”

*Metabolism is blocked by allopurinols =»reduce dose if pt. is being treated for gout otherwise could develop cholestasis/ulcers

154
Q

Pentostatin, Cladribine, Fludarabine

A

Adenosine Deaminase inhibitors

155
Q

DOC for Hairy Cell Leukemia

A

Cladribine

156
Q

Vincristine, Vinblastine

A

Vinka alkaloids that bind to tubulin and prevent the polymerization of microtubules arresting the cell in metaphase (CCS); part of ABVD

*Toxicities= Peripheral neuropathy (especially vincristine) alopecia, nephrogenic SIADH

157
Q

Paclitaxel, Docetaxel

A

Yew alkaloids that bind to tubulin and prevent its depolymerization arresting the cell in metaphase (CCS); used for advanced ovarian and breast cancer

Toxicity is dose-limiting

158
Q

IFN-a

A

Works directly on cancer cells and also stimulates immune cells such as NK cells, macros, and T-cells

*Used for Kaposi’s Sarcoma, Hairy cell leukemia, non-Hogkin’s lymphoma

159
Q

Tamoxifen

A

Anti-estrogen drug used in metastatic breast cancers that contain receptors responsive to steroidal hormones

160
Q

Anti-androgen therapy

A

Includes drugs like bicalutamide and flutamide that prevent steroidal binding to a tumor cell

161
Q

Total Androgen Ablation

A

Uses Leuprolide, an LHRH agonist, to block the release of *LH along with anti-androgen therapy drugs

162
Q

Bevuczimab

A

Blocks VEGF and prevents angiogenesis

  • Antibody therapies end in -ab
  • Also have NO TOXICITY
163
Q

Denusomab

A

Blocks RANK-RANK ligand binding in osteosarcomas

164
Q

Trastuzumab

A

(Herceptin)

Blocks the Her-2/Neu receptor in metastatic breast cancer

*Must be Her-2/Neu (+)

165
Q

Imatinib

A

(Gleevac)

Blocks Bcr-Abl kinase; treats CML

166
Q

Crizotinib

A

Blocks ALK-1 kinase in non-small cell lung carcinoma

*MUST BE (+) FOR EML4-ALK1

167
Q

Venetoclax

A

Inhibits Bcl-2 =»Destabilization of mitochondrial membranes =»apoptosis

*Used for REFRACTORY CLL

168
Q

Vorinostat/Romidepsin

A

HDAC inhibitors; used for REFRACTORY T-cell lymphoma

169
Q

OLAPARIB

A

PARP-1 inhibitor

170
Q

PARP-1

A

Performs “DNA rescue” thru base excision; inhibition of this pathway

=»apoptosis

171
Q

TGF-B

A

Sources: Platelets, T-cells, macrophages, endothelial cells

Action: Stimulates ECM synthesis after injury; suppresses acute inflammation

172
Q

Vitamin C deficiency effects on wound healing

A

Inhibition of collagen synthesis =» Decreased healing

173
Q

Glucocorticoid effects on wound healing

A

Inhibits the secretion of TGF-B; an important factor that promotes collagen synthesis

174
Q

Dehiscence

A

Rupture of wound due to inadequate formation of granulomatous tissue

*common after abdominal surgeries

175
Q

Desmoids

A

Aggressive fibrous overgrowth during wound healing over cutaneous tissue

176
Q

Allergy March

A

Newborns who present w/ eczema and GI disorders tend to have an increased disposition towards developing asthma later in life

177
Q

Type I skin test

A

Observe for wheal and flare after ~15 mins

=»is due to leakage of fluid into the tissue

178
Q

Indications for total IgE evaluation

A

Prediction of allergy development in pediatric pts.

Evaluate immunodeficient pts.

179
Q

Immunotherapy for Type I Hypersensitivity

A

Pt. is subject to increasing doses of an allergen leading to an ultimate rise in neutralizing IgG levels and decreasing IgE levels

180
Q

DAT

A

Direct Coomb’s Test

Detects ab-coated RBCs in vivo

181
Q

IDAT

A

Indirect Coomb’s Test

Tests pt. serum for the presence of antibodies

182
Q

Hemolytic Disease of the Newborn

A

At the first pregnancy, an Rh(-) mother forms antibodies against an RH(+) fetus; on subsequent pregnancy, mothers abs can attack fetal RBCs

*Will see hyperbilirubinemia, hepatosplenomegaly, and (+) DAT

=»Prevent by giving mother injections of anti-D

183
Q

Drug-induced Hemolytic Reaction

A

Drugs (such as Penicillin) act as a hapten and bind Igs to RBCs

=»Complement mediated lysis and phagocytosis

184
Q

Pemphigus vulgaris

A

Antibodies are formed against epidermal cadherins

=»Interruption of cell-cell connections causing bullae

*Epidermis will stain in a FISHNET pattern

185
Q

Goodpasture’s Syndrome

A

IgG antibodies are formed against kidney glomeruli and BM of alveoli

=»AGN and Pulmonary hemorrhage; mostly in ~30 yr olds

*Presence of anti-GM antibodies in serum and glomerular tissue will IFA stain LINEAR

TREATMENT: Plasmapharesis of anti-GM

186
Q

Pernicious Anemia

A

Can be caused by anti-IF =»decreased Vitamin B12 absorption

*Causes macrocytic anemia and faulty erythropoiesis

187
Q

Myasthenia Gravis

A

Antibodies formed against Ach-receptors

*Seen w/ ptosis, progressive muscle weakness, and respiratory issues

188
Q

Grave’s Disease

A

Caused by anti-TSH-R antibody that chronically stimulates the thyroid to produce more hormone

=»Exophthalmos, myxedema, enlarged thyroid

189
Q

Serum Sickness

A

Excess formation of Ag-Ab complexes end up getting deposited in tissue and =» decreased complement levels

  • Manifests as a rash, fever, and arthralgia
  • IFA pattern= Lumpy-bumpy
190
Q

Rheumatoid Arthritis

A

Formation of IgM-RF binds IgG and gets deposited in tissues at joints

191
Q

SLE

A

Chronic inflammatory disease in which antibodies are made against dsDNA; most commonly affects women

  • Will see “Butterfly rash,” glomerulonephritis, arthritis, and vasculitis
  • Assoc. w/ HLA-DR3 inheritance or C4,C2 deficiencies
192
Q

Polyarteritis nodosa

A

Immune complexes formed w/ Hep-B antigen get deposited in arterial walls

=»Infiltrates composed of PMNs and macros

193
Q

Arthus Reaction

A

Test done for Type III hypersensitivity

-Checking for inflammatory reaction after a few hours

194
Q

Hydatiorm mole

A

Benign proliferation of placental epithelium

195
Q

AFP

A

Tumor marker used to track the progression of liver cell cancer

196
Q

CA-125

A

Tumor marker used to monitor ovarian cancer

197
Q

CA 19-9

A

Tumor marker used to monitor colon and pancreatic cancer

198
Q

CA 15-3

A

Tumor marker used to monitor breast cancer

199
Q

Normal BRCA function

A

Tumor suppressor in gene repair

200
Q

Gardner’s Syndrome

A

Form of FAP assoc. w/ development of osteomas and desmoids

*Still involves mutation in APC gene

201
Q

Pemetrexed

A

MTX drug that also inhibits thymidylate synthase

202
Q

Choriocarcinoma treatment

A

MTX and Dactinomycin (90% success rate)

203
Q

Paraneoplastic Cushing Syndrome

A

Can be caused by lung small cell carcinoma, pancreatic tumor, or neural tumors

=»Excess ACTH

204
Q

Paraneoplastic SIADH

A

Caused by lung small cell carcinoma or intracranial neoplasms

=»Increased ADH or ANP

205
Q

Paraneoplastic polycythemia

A

Caused by gastric, renal, hepatocellular, or cerebreal hemangioma

=»Increased EPO

206
Q

RET gene

A

Necessary for survival of neuroendocrine cells

  • Normally functions w/ signal transduction and is “rearranged during transfection”
  • MEN genes are normally TSGs
207
Q

Most aggressive type of Breast tumor

A

BRCA-1

*Typically are Grade 3 tumors

POD: Exam 3 (2 decks)

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