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Pharmacology > Heme Lymph > Flashcards

Heme Lymph Flashcards

1
Q

Oncogenes

A

Ras

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2
Q

Tumor suppressor

A

P53

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3
Q

Go G1 S and g2 M

A

M mitosis
Go resting phase of G1
G1has restriction point whihc activation of oncogenes overrides
S synthesis dna replication phase
G2 has dna replication checkpoint which tumor suppressor genes p53 override

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4
Q

Primary chemo

A

Chemo is the primary treatment in advanced cancer with no alternative treatment

Relieve tumor related symptoms, improve quality of life, prolong time to tumor progression

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5
Q

Curable cancer with primary chemo

A

Hodgkin and non Hodgkin lymphoma, choriocarcinoma, germ cell cancer, and acute myelogenous leukemia

Kids-burkitts, wilms, embryonal rhabdomyosarcoma, ALL

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6
Q

Neoadjuvant chemotherapy

A

For localized cancer in adjunct ro other methods whihc are less than completely effective

Reduce size of primary tumor to make surgery easier or spare vital organs

Chemo given for time after surgery as ADJUVAnT therapy

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7
Q

ADJUVAnT chemotherapy

A

After surgery

Reduce incidence of local adhd systemic recurrence and improve overall survival of patients

Prolong disease free survival and overal survival

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8
Q

What is the log kill hypothesis

A

Symptoms high number of cancer cells/death -Infrequent treatment, treatment started too late , prolongation of survival with eventual death

Diagnosis pretty high cancer cells- Combination chemotherapy, intensive treatment schedule, therapy continued after clinical evidence of cancer disappears, cure

Surgery lower number-Early surgery combines with intensive adjuvant therapy

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9
Q

Primary/inherent chemotherapeutic resistance

A

Drug resistance int he absence of prior exposure to available standard agents

Genomic instability of cancer p53

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10
Q

Acquired chemo drug resistance

A

Develops in response to exposure to a given cancer drug

Genetic change-amplification or suppression fo a particular gene

Increasing heterogeneity over time ->tumor continues to proliferate and is no resistant to treatment x

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11
Q

P-glycoproteins, PGP

A

On tissues with barrier functions including the kidney, liver and GI tract
Pharmacological barrier sites including the blood brain barrier and the placental blood barrier

High baseline expression of PGP correlates wit hprimary/inherent resistance to natural products

Can be overprexpressed leading to acquired drug resistance

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12
Q

Therapeutic index

A

TD50/ED50

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13
Q

Chemo therapeutic index

A

Close ED50 and TD50 when desired is low ED50 and high TD50

High doses are required ot maximize rapid cancer cell death

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14
Q

AE chemo

A 
Non cancerous proliferating cells
—bone marrow precursors of blood cells(cytopenias, myelosuppression)
—intestinal epithelial cells
—oral mucosa
—gonadal cells
—hair follicles-alopecia
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15
Q

MOA alkylation agents

A

Transfer of alkyl groups to DNA leading to DNA cross linking

Arrest in late G1, early S phase

Individual drugs vary in how they do this-cisplastin versus cyclophosphamide

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16
Q

What cells are most susceptible to alkalyating agents

A

Replicating cells

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17
Q

Resistance alkalyating agents

A

Increased capability to repair DNA lesions through increased expression of activity of DNA repair enzymes

Decreased cellular transport of alkyating drug

Increased expression or activity of glutathione and glutathione associated proteins
—these are needed to conjugate the alkyating agents

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18
Q

Alkylation agents adverse effects

A 
Primarily occur in rapidly growing tissue 
-bone marrow
—myelosuppression
-GI tract
—diarrhea
-reproductive system

N/V
Blistering at the site of administration

Carcinogenic-increased risk of secondary malignancies AML

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19
Q

MOA antimetabolites

A

Methotrexate-folic acid metabolite

5-FU uracil analog

Cytosine arabinoside-cytosine deoxyriboside

Mimic and/or reduce the essential components needed for the formation of DNA, RNA and proteins
Arrest and/or DNA damage often occurs during S phase

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20
Q

Cells most susceptible to antimetabolites

A

Replicating

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21
Q

Resistance antimetabolites

A

Inhibition of metabolism intoactive metabolites-cytarabine and the active metabolite of art-ctp

Decrease drug transport
-methotrexate and the reduced folate carrier or folate receptor

Decreased formation of poly glutamate metabolites by folyl polyglutamate synthase (FPGS)
-important for methotrexate, pemetrexed and pralatrexate

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22
Q

Ae antimetabolites

A

Myelosuppression
N/v
GI toxicity(5-FU)

Hand foot syndrome

  • painful erythema and swelling of the hands and feet
  • pemetrxed
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23
Q

Natural products MOA

A

Tubules polymerization disrupted by vinblastine, vincristine, vinorelbine and enhanced by paclitaxel, docetaxel, and cabazitaxel

Topoisomerase inhibitors
Topoisomerase 1 topotecan, irinotecan
Topoisomerase 2-etoposide

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24
Q

Mechanism of resistance natural products

A

P-glycoproteins mediated drug efflux

Point mutations ind rug binding (topo 1 and 2)

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25
Q

AE natural products

A 
Myelosuppression
N/v
Neurotoxicity
-vincristine
Hypersensitivity
-paclitaxel and docetaxel
Diarrhea
-topotecan and irnotecan
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26
Q

MOA antitumor antibiotics

A

Inhibition of topoisomerase 2, generation fo free radicals (DNA damage), DNA intercalated
-anthracyclines (doxorubicin)

Induce DNA cross links
-mitomycin

DNA fragmentation and single/double strand breaks due to free radical formation
-bleomycin

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27
Q

Mechanism of resistance antitumor antibiotics

A

Point mutations in topo2, suppression of apoptotic signaling
-doxorubicin

Increased expression f multidrugresistant efflus pumps
-doxorubicin and mitomycin

Upregulation of bleomycin hydrolase enzyme
-inhibits bleomycin iron binding and limits its cytotoxic effects

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28
Q

Antitumor ae

A 
Myelosuppression
N/v
Free radical mediated cardiotoxicity
-doxorubicin
Blue fingernails, sclera, urine
-mitoxantrone
Pulmonary toxicity
-bleomycin
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29
Q

Tyrosine kinase and growth factors receptor inhibitors MOA

A

Inhibit growth factor receptor signaling

Inhibit tyrosine kinase activity

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30
Q

Resistance tyrosine kinase and growth factors receptor inhibitors

A

Point mutations in drug binding sites

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31
Q

AE tyrosine kinase and growth factor receptor inhibitos

A

N/v

Acneform skin rash and hypersensitivity
-cetuximab

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32
Q

Immune checkpoint inhibitors

A

Nivolumab and pembrolizumab

  • PD1 inhibitors
  • melanoma, NSCLC, hodgkins

Atezolizumab, avelumab, durvalumab
-PD-L1 inhibitor-bladder cancer, NSCLC, meckel cell skinc ancer

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33
Q

Molecular background immune checkpoint inhibitors

A

T cell activated by dendritic cells within lymph node

Activated T cell penetrates the tumor microenvironment
-tumor microenvironment includes tumor cells, macrophages, and t regulatory cells

The tumor may possess PD-L1; activated T cells may induce PD-L1 upregulation on tumor cells, macrophages and t reg cells through the release of interferon y

An activated T cell inactivated when it binds PD-L1
-B7.1 and PD-1: receptors on T cell forPD-L1

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34
Q

Mechanism resistance immune checkpoint inhibitors

A

Primary or acquired
Insufficient generation of anti tumor T cells
Inadequate function of tumor specific T cells
Impaired formation of T cell memory

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35
Q

AE immune checkpoint inhibitors

A

Fatigue, nausea, loss of appetite, itching
Can allow the immune system to attack normal organs (serious problem)
-lungs, intestines, liver kidneys

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36
Q

Point of immune checkpoint inhibitors

A

New class of chemo that boosts immune system mediated tumor clearance

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37
Q

The leukemia’s

A

ALL
AML
CML
CLL

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38
Q

ALL

A

Acute childhood leukemia
Most common ancer in kids

Discovery of methotrexate increase survival

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39
Q

Treat all

A

6-merceptopurine, cyclophosphamide, vincristine, and danorubicin

Enter remission with combination prednisone with vincristine

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40
Q

When circulating leukemia cells migrate to sanctuary sites located int he brain and testes

A

Intrathecal methotrexate to prevent CNS leukemia (prophylaxis)
-major mechanism of relapse

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41
Q

AML

A

Most common leukemia in adults

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42
Q

Treat AML

A

Cytarabine most active
Best used in combo with anthracycline
But idarubicin is preferred

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43
Q

Intensive support care during period of induction of chemo with AML

A

Platelet transfusions to prevent bleeding
G-CSF , filgrastim to shorten periods of neutropenia
Antibiotics to combat infections

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44
Q

How get remission of aml

A

Allergenic bone marrow transplant

-preceded by high dose chemo and total body irradiation followed by immunosuppression

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45
Q

After remission

A

Consolidation chemo with high does cytarabine or hematopoietic cell transplant

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46
Q

At what age do ppl respond less to chemo for aml

A

60 tolerance to aggressive therapy and their resistance to infection are lower

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47
Q

CML

A

BCG-Abl fusion oncoprotein
-Philadelphia chromosome t9:22

Get constitutive expression of Bcr-Abl fusion oncoprotein

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48
Q

How treat CML

A

Reduce granulocytes to normal levels, raise hemoglobin concentration to normal, relieve disease related symptoms,

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49
Q

Treat CML

A

Imatinib first line in previously untreated most exhibit a complete hematologic response

Dasatinib and nilotinib initially approved for patients intolerant to imatinib
Currently each shows clincial activity and now both are indicated as first line treatment of chronic CML

Busulfan and other oral alkyating agents also are effective

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50
Q

CLL

A

High risk disease or the presence of disease related symptoms means treatment warranted

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51
Q

How treat CLL

A

Chlorambucil and cyclophosphamide alkylation gets agents

  • chlorambucil with prednisone
  • COP-cyclophosphamide combined with vincristine and prednisone
  • CHOP-cyclophosphamide combined with vincristine, prednisone and doxobrucin

Bendamustine also approved
-monotherapy or combination with prednisone

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52
Q

CLL

A

Fludarabine is also effective

  • monotherapy
  • combination with (cyclophosphamide) and with (mitoxantrone and dexamethasone) or it is combined with (rituximab)

Rituximad is an anti-CD20 antibody
-enhances chemotherapy and is effective when resistance to chemopay has emerged
R CHOP

Ofatumumab is fully human IgG1 antibody that binds to different CD20 epitope than rituximab

  • maintains activity in rituximab-resistant tumors
  • approved for CLL that is refractory to fludarabine therapy
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53
Q

Hodgkin’s lymphoma

A

A complete staging evaluation is needed before treatment plan can be formulated

Biggest change is int he stage I and stage IIA disease

  • combined-modality therapy with a brief course of combination chemotherapy and involved field radiation
  • ABVD-doxorubicin , bleomycin, vinblastine, dacrabazine

50-60% of patients with Hodgkin’s lymphoma are cured of disease

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54
Q

Changes in treat for advanced stage II and IV Hodgkin’s lymphoma

A

MOPP-mechlorethamine, vincristine, procarbazine, and prednisone
—high complete response rates (80-90%); cures in 60% of patients

ABVD-doxorubicin, doxorubicin, bleomycin, vinblastine, mechlorethamine, vincristine, bleomycin, etoposide, and prednisone
—alternative regimen, followed by involved radiation therapy

Over 80% of previously untreated patients with advanced disease (stages III and IV) are expected to go into complete remission
-complete remission=disappearance of all disease-related symptoms and objective evidence of disease

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55
Q

Non Hodgkin’s lymphoma- diffuse

A

Combination chemotherapy is the standard for patients with diffuse non Hodgkin’s lymphoma

CHOP-cyclophosphamide, doxorubicin, vincristine, and prednisone
—best treatment in terms of initial therapy

CHOP+rituximab (R-CHOP)
-clinical studies show increased response rate , disease free survival and overall survival versus CHOP alone

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56
Q

Non hodgkin lymphoma follicular

A

Initiation of chemotherapy at the onset of symptoms

  • watchful waiting
  • bendamustine+rituximab
  • R-CHOP
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57
Q

Multiple myeloma

A

Most patients symptomatic at time of initial diagnosis

Requires treatment with cytotoxic chemotherapy

MP protocol-melphalan+prednisone

  • standard regimen for 30 years
  • 40% of patients respond and the median duration of remission is 2-2.5 years
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58
Q

Stage I breast cancer

A

Small primary tumor and negative axillary lymph node dissections
Treat with surgery alone
80% chance of a cure

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59
Q

Stage II breast cancer (1-3 nodes node +)

A

High risk of both local and systemic recurrence (micrometastasis)

Postoperative use of systemic adjuvant combination chemotherapy reduces the relapse rate and prolongs survival

CMF-cyclophosphamide, methotrexate, and 5-FU
FAC-5-FU, doxorubicin, cyclophosphamide

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60
Q

Prostate cancer

A

Advanced prostate cancer becomes refractory

Mitoxantrone and prednisone

  • approved for hormone refractory prostate cancer
  • provides palliative int hose experiencing significant. Bone pain

Docetaxel+prednisone has become stand of care for hormone refractory prostate cancer*

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61
Q

Colorectal cancer

A

High risk stage II and III candidates for adjuvant chemo

  • FOLFOX-folinic acid (leucorvin)+5-FU+oxaliplatin
  • XELOX-capecitabine+oxalplatin
  • used for 6 months following surgical resection
  • reduces recurrence rate after surgery by 35%
  • improves patient survival compared with surgery alone
62
Q

Metastatic colorectal cancer

A

FOLFIRI-folinic acid (leucovorin)+5-FU+irinotecan
-ziv-aflibercept added if progression has been observed with oxaliplatin based chemo

FOLFOX or FOLFIRI+(bevacizumab or cetuximab/panitumumab) results in sig improved clincial efficacy

TAS-102 approved for the chemo refractory disease setting
-limited by significant toxicities ,clincial efficacy and low response rates

63
Q

Non small cell lung cancer

A

ADJUVAnT platinum based chemo provides survival benefit in patients with pathological stage IB II and IIIA

Radiation can be used ot relieve pain, airway obstruction or bleeding
-less aggressive , used in patients that cant tolerate more aggressive

64
Q

Chemo non small cell lung cancer

A

Bevacizumab
-used in combination with carboplatin and paclitaxel in patients with good performance status and non squamous histology, standard treatment option

Patient not a good candidate for bevacizumab or squamous cell histology present(cisplastin or carboplatin)+ cetuximab

Maintance chemo=pemetrexed used in patients that have stabilized after four cycles of platinum based first line chemo

65
Q

Erlotinib NSCLC

A

First line in advanced NSCLC patients with sensitizing EGFR mutations

66
Q

Afatinib NSCLC

A

First line of metastatic NSCLC whose tumors have EGFR exon 19 deletions or exon 21 mutations

67
Q

Osimertinib NSCLC

A

Approved for the treatment of metastatic EGFR T790M mutant NSCLC following progression on or after EGFR TKI therapy

Overcomes resistance fromt he T790M gatekeeper mutation
-this mutation can happen de novo or after prior TKI therapy

68
Q

Squamous cell

A

Platinum based chemo
Cisplastin and gemcitabine combined with necitumumab

Nivolumab-if progressed on or after standard platinum based

69
Q

Small cell

A

Initially sensitive to platinum based combination regimes
(Cisplastin+etoposide) or (cisplastin + irinotecan)

Drug resistance develops in nearly all patients with extensive disease
If diagnosed early it is curable using combined chemotherapy and radiation

Topotecan used as a second line monotherapy in patients that have failed based regimen

70
Q

Ovarian cancer stage I

A

Whole abdomen radiotherapy

Cisplastin and cyclophosphamide

71
Q

Ovarian stage III and IV

A

Carboplatin and paclitaxel

72
Q

Recurrent ovarian cancer

A

Topotecan or liposomes doxorubicin

73
Q

Testicular cancer

A

PEB-Cisplastin , etoposide, bleomycin

High risk disease-high dose cisplastin+etoposide+bleomycin

74
Q

Malignant melanoma

A

Curable with surgical resection when it presents locally

Once metastasis has occurred it is onee of most difficult to treat

Dacarbazine, temozolomide and cisplastin most active -low response rate

Biological agents IFNa and IL2 have greater activity than traditional agents, treat with a high dose IL2

75
Q

Malignant melanoma

A

Nivolumab and pembrolizumab

76
Q

Brain cancer

A

Nitrosoureas most active

  • cross BBB
  • carmustine sued as a single agent
  • PCV-procarbazine+lomustine+vincristine

Alkyating agent temozolomide
-patients with new glioblastoma multiforme

Oligodendroglioma chemosensitive
-PCV regimen is treatment of choice

Bevacizumab alone or in combination ith chemo has documented clincial activity in adult GBM

77
Q

Drugs for neutropenia

A

Filgrastim
Pegfilgrastim
Sargramostim
Plerixafor

78
Q

Drugs for thrombocytopenia

A

Oprelvekin
Romiplastin
Eltrombopag

79
Q

Iron therapy from food

A

Meat fish poultry well absorbed

Poorly from veggies, grain, milks and eggs

80
Q

Oral iron 200-400 mg for microcytic anemia

A

Ferrous in divided doses with only water/juice food inhibits absorption

81
Q

AE iron therapy

A

Nausea, constipation, anorexia, heartburn, vomiting, and diarrhea and dark stools

82
Q

Parenteral iron

A

For iron malabsorption, intolerance of oral therapy, noncompliance

-iron dextran, sodium ferric gluconate complex and iron sucrose

83
Q

When get iron effects

A

Reticulocytosis in a few days and increase Hb in a 2 weeks

84
Q

Acute iron toxicity

A

Young kids
Necrotizing gastroenteritis with vomiting, abdominal pain and bloody diarrhea->shock, lethargy, dyspnea

Suggestion of improvementthen severe metabolic acidosis, coma, death

85
Q

Treat acute iron toxicity

A

Deferoxamine (potent iron chelating)

86
Q

Chronic iron toxicity

A

Hemochromatosis
Deposits in heart, liver, pancrease->organ failure and death

Hereditary hemochromatosis an dpatients who receive many red cell transfusions over a long period of time

87
Q

B12

A

Animal products
Fortified breakfast cereals -for vegetarians

Need 2 microgram/day

Body stores 2-5 mg
-takes years to become deficient

88
Q

Why take years to become b12 deficient

A

Normal body stores greatly exceed daily requirement

89
Q

NO inhaled analgesia and B12

A

Inactivated cyanocobalamin

-normally rapidly replenished from body store

90
Q

If body store of B12 depleted

A

Rapid onset neurological dysfunction (paresthesia s, weakness, spasticity) that may not fully reverse

91
Q

Absorption b12

A

IF from parietal cells and absorbed in ileum

92
Q

Pernicious anemia

A

Elderly
Autoantibody blocks IF-Cbl interaction or IF-Cbl receptors in ileum

Gastrectomy or gastritis
H pylori

93
Q

Treat b12 defiency

A

Oral b12 supplementation in pernicious anemia

Parenteral therapy if neurological symptoms are present

94
Q

Folate what in

A

Yeast, liver, kidney, green leafy

95
Q

Usual cause of folate defiency

A

Inadequate dietar intake or alcoholism

96
Q

Treat folate defiency

A

1 mg a day for 4 months

97
Q

High doses folate

A

Hypotension, hypoglycemia

98
Q

Treat megaloblastic anemia

A

Improve within a few days
Should see reticulocytosis in 2-5 days
HCG up in 2 months

Neurological symptomslonger to improve an dmay be irreversible but not worsen

99
Q

Folate supplementation for elderly?

A

Increases risk of masking megaloblastic anemia caused by b12 defiency

100
Q

Epoetin alfa moa

A

165 aa erythrpopiesis stimulating glycoproteins

  • from recombinant DNA
  • identical aa sequence of isolated natural erythropoietin
101
Q

Effects epoetin Alfa

A

Stimulated erythropoiesis
Increase reticulocytosis count<10 days
Increase RBC could and hemoglobin and hematocrit

Usually include irona nd folate

102
Q

Clincial epoetin Alfa

A

Anemia from chronic kidney disease, cancer chemo, zidovudine treatment for HIV

Reduce allergenic rbc transfusions in patients undergoing elective surgery

Use banned by international Olympic

103
Q

Pharm epoetin alfa

A

Administered IV or subcutaneously

Half life of 4-13 horus

104
Q

AE epoetin alfa

A

DAP>10 mmHg

Death, MI, stroke, venous thromboembolism,, thrombosis of vascular access and tumor progression or recurrence

-cough HA, muscle pain, spasm, joint or bone pain, spasms, vomiting, insomnia wight loss

105
Q

Darbepoetin alfa

A

3x longer HL 21 hours

106
Q

Hydroxyurea moa

A

Targets ribonucleotide reductase results in s phase cell cycle arrest

Somehow. Boosts the levels of fetal hemoglobin mechanism unknown

107
Q

Effects hydroxyurea

A

Lowers concentration of Hb S within a cell_> less polymerization of the abnormal hemoglobin

108
Q

Celincal applciation hydroxyurea

A

Sickle cell!!!!!

109
Q

Pharmacokinetics sickle cell

A

Orally
Wide distribution. Concentrates in erythrocytes and leukocytes

Has multiple metabolic pathways also excreted unchanged by kidney

110
Q

AE hydroxyurea

A

Cough, hoarseness, fever, chills, low back pain, painful difficult urination

111
Q

Eculizumab moa

A

Monoclonal antibody that specifically binds to complement protein C5 with high affinity

Inhibits its cleavage to C5a and C5b

Prevents generation of terminal complement complex C5b-9

112
Q

Effects eculizumab

A

Inhibits terminal complement mediated intravascular hemolysis in PNH…RBC lack enough CD59 and CD55 to prevent MAC mediated destruction

Inhibits complement mediated thrombotic miccroangiopathy in patients with atypical HUS

113
Q

Clincial eculizumab

A

PNH

Atypical HUS

114
Q

Pharmacokinetics eculizumab

A

IV over 35 min

Maintence dose

EXPENSIVE 444,000/yr but so effective

115
Q

AE eculizumab

A

Infections herpes influenza like

Meningococcal infections must have menigococcal vaccine 
Immunogenicity
URI
MSK pain
Anemia, leukopenia
HTN HA
Insomnia fatigue UTI
116
Q

Filgrastim moa

A

G-CSF made by recombinant DNA

117
Q

Effects filgrastim

A

G-CSF regulates production neutrophils in bone marrow

118
Q

Clincial filgrastom

A

Decrease infection from febrile neutropenia in patients with nonmyeloid malignancies receiving myelosuppression anticancer drugs or in those receiving a bone marrow transplant

Mobilize hematopoietic progenitor cells into peripheral blood for collection by leukapheresis

119
Q

Pharmacokinetics filgrastim

A

IV infusion continuous wait 24 hours after chemo since dividing cells most vulnerable

120
Q

AE filgrastom

A

Well tolerated

Allergic reaction

Bone pain

Splenic rupture
Acute respiratory distress

121
Q

Pegfilgrastim

A

Longer lasting version of filgrastim due to conjugation with monomethoxypolyethylene glycol

122
Q

Sargramostim moa

A

Recombinant form of granulocytes macrophage

GM-CSF made in year

123
Q

Effects sargramostim

A

In bone marrow to increase production of neutrophils, eosinophils and monocytes//macrophages

124
Q

Clincial sargramostim

A

Accelerate recovery of myeloid cells after autologous bone marrow transplantation
-allogenic too

Mobilize HSC into peripheral blood for collection via leukapheresis

Induction chemo with AML to shorten time to neutrophil recovery/decreased incidence of severe infections

125
Q

Pharmacokinetics sargramostim

A

IV ro SC

126
Q

AE sargramostim

A

Benzyl alcohol can cause fatal gasping syndrome in premature infants

Causes fluid retention typically->edema but can cause pleural effusion, pericardial perfusion

Sequesteration fo granulocytes in pulmonary circulation has caused dyspnea

Occasional supraventricular tachycardia

Renal hepatic

127
Q

Filgrastim vs sargramostim vs cost benefit analysis

A

Filgrastim fewer ae so filgrastim/pegfilgrastim wine

-filgrastim speed recovery from severe neutropenia but little evidence of impact on clincial outcomes

128
Q

Plerixafor moa

A

Partial agonist of the CXCR4 receptos, important for the homing of hematopoietic stem cells to the bone marrow

129
Q

Effects plerixafor

A

Mobilizes HSC from the bone to plasma

130
Q

Clincial plerixafor

A

Not mobilizing stem cells for autologous transplant with just G CSF

Expensive

Lymphoma, multiple myeloma

131
Q

Pharmacokinetics plerixafor

A

Sq

132
Q

AE plerixafor

A

Hypersenstivity reaction is main concern

Has potential to mobilize leukemia cells, contaminate apheresis product

133
Q

Oprelvekin moa

A

Recombinant for IL-11

Unknown moa

134
Q

Effects eprelvekin is-11

A

Increases platelet levels by promoting the formation and maturation of megakaruocytes

135
Q

Clincial applications oprelvekin is-11

A

Can be sued to treat thrombocytopenia in patients undergoing myelosuppressive chemotherapy for non myeloid cancers…DOES NO HAVE A MAJOR CLINCIAL USE

136
Q

Pharmacokinetics is-11

A

Given sq once/day

137
Q

AE oprelvekin

A

Edema from volume expansion cardiac dysrhythmias, severe allergic reactions and bloodshot eyes

138
Q

Romiplstim moa

A

Peptibody compose dof two disulfide bonded human IgG1 kappa heavy chain constant regions (an Fc fragment), each of which is covalently bound at residue 228 with two identical peptide sequences linked via polyglycine that bind to the TPO receptor

No TPO homologous

139
Q

Effects romiplostim

A

Increased the platelet count in

-health individuals, patients with ITP, patients with myelodysplastic syndrome

140
Q

Clincial applications romiplostim

A

Excess platelet destruction due to idiopathic thrombocytopenic purpura
66 ITP cases/1,000,000 per year

141
Q

Pharmacokinetics romiplostim

A

Administered weekly as a sq injection

142
Q

AE romiplostim

A

Well tolerated most serious is allergic reaction

143
Q

Eltrombopag moa

A

Potent, orally available non peptide TPO receptor agonist

144
Q

Effects eltrombopag

A

Increases the platelet count in:
Healthy individuals
-patients with ITP
-thrombocytopenia due to hepatitis C

145
Q

Clincial eltrombopag

A

Excess platelet destruction due to idiopathic thrombocytopenic purpura

Cirrhosis due to hepatitis C

146
Q

Pharmacokinetics eltrombopag

A

Oral once day

147
Q

AE eltrombopag

A

Hepatotoxicity if sued with interferon in patients with chronic hepatitis C

148
Q

Drugs causing hemolytic. Anemia

A

Cephalosporins-most common cause, espicially ceftriaxone an cefetetan

Penicillin, piperacillin

149
Q

Drug induced thrombocytopenia

A

Heparin

Quinidine quinine

150
Q

Drugs causing aplastic anemia

A

Cancer chemo (alkylation agents, antimetabolstes, cytotoxic antibiotics

Chloramphenicol-antibiotic

Benzene-aplastic anemia

Pharmacology (52 decks)

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