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Step 1 Pharm > Heme/onc > Flashcards

Heme/onc Flashcards

1
Q

Activator of antithrombin;􏰀thrombin and􏰀 factor Xa. Short half-life.

A

Heparin

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2
Q

Uses of Heparin?

MOA?

A

Immediate anticoagulation for pulmonary embolism (PE), acute coronary syndrome, MI, deepvenous thrombosis (DVT). Used during pregnancy (does not cross placenta).

Follow PTT.

MOA: activator of antithrombin: decrease thromibn and factor Xa activity

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3
Q

Pt comes in with DIC.. you provide a medication that acts as a cofactor for antithrombin.

BAD shits starts happening!!!

what (-) rxns does this drug cause?

How do we undo the damage??

A

Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions.

For rapid reversal (antidote), use protamine sulfate (positively charged molecule that binds negatively charged heparin).

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4
Q

Wht are examples of Low molecular wt Heparins?

What are their benifits?

A

Enoxaparin, Dalteparin, while fondaparinux act more on f_actor Xa_, have better bioavailability, and 2–4 times longer half-life; can be a_dministered subcutaneousl_y and without laboratory monitoring.

(-)Not easily reversible.

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5
Q

Most severe rxn to Heparin and what’s its mechanism?

A

Heparin-induced thrombocytopenia (HIT)—development of IgG antibodies against heparin- bound platelet factor 4 (PF4).

Antibody-heparin-PF4 complex a_ctivates platelets􏰂–> thrombosis and thrombocytopenia._

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6
Q

What is the mechanis of Argatroban and Bivalrudin?

A

from leeeeches!

INHIBIT thrombin DIRECTLY; used instead of heparin for antigoag in pts w/ HIT

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7
Q

All ya know about Heparin

A

Large, anionic

Parenteral (IV, SC) admin

rapid actication

activates antithrombin to decrease IIa and factor Xa

Lasts hours, safe for preggers

reveresed with protamine sulfate

moniotor PTT

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8
Q

All ya know about warfarin

A

Small-lipid monlecues

Oral admin

acts in liver

slow, limited by 1/2 lives of normal clot factors

Impair synthesis of Vit K: diSCo in 1927

Chroinc duration

Crosses placenta (tereatogenic)

OD use IV vit K or FFP

monitor with IRN and PT (extrnisic pathway)

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9
Q

Interferes with γ-carboxylation of vitamin K– dependent clotting factors II, VII, IX, and X, and proteins C and S.

A

Warfarin

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10
Q

Why do some people respod to Warfarin differently?

A

Metabolism affected by polymorphisms in the gene for vitamin K epoxide reductase complex (VKORC1). In laboratory assay, has effect on EXtrinsic pathway and􏰁 incase PT. Long half-life.

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11
Q

Use of Warfarin

How do we monitor it?

A

Chronic anticoagulation (e.g., venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation).

Not used in pregnant women (because warfarin, unlike heparin, crosses placenta).

Follow PT/INR

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12
Q

What toxicities do we worry about in warfarin?

What is the pathology of bleeding we see?

A

Bleeding, teratogenic, skin/tissue necrosis
A , drug-drug interactions. Proteins C and S have shorter half-lives than clotting factors
II, VI, IX, and X, resulting in early transient hypercoagulability with warfarin use.

Skin/tissue necrosis believed to be due to small vessel microthromboses.

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13
Q

How do you use heparin and warfarin together?

A

For reversal of warfarin, give vitamin K.
For rapid reversal, give fresh frozen plasma. Heparin “bridging”: heparin frequently used

when starting warfarin. Heparin’s activation of antithrombin enables anticoagulation during initial, transient hypercoagulable state caused by warfarin. Initial heparin therapy reduces risk of recurrent venous thromboembolism and skin/tissue necrosis

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14
Q

Apixaban, rivaroxaban: what is their mechanism and use?

A

bind directly to Xa

Treatment and prophylaxis for DVT and PE (rivaroxaban); stroke prophylaxis in patients with atrial fibrillation.

Oral agents do not usually require coagulation monitoring.

(-) bleeding with NO reversible agent

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15
Q

What is the MOA of Alteplase (tPA), reteplase (rPA), streptokinase, tenecteplase (TNK-tPA). Use?

A

Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots.

Increase 􏰁PT, Increase 􏰁PTT, no change in platelet count.

Use: Early MI, early ischemic stroke, direct thrombolysis of severe PE.

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16
Q

What pts should NOT recieve Thrombolytics: Alteplase, retelpase (tpA or rPa?

How do you tx toxicity?

A

Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension.

Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis.

Fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies.

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17
Q

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation.

Platelets cannot synthesize new enzyme, so effect lasts until new platelets are produced: 􏰁bleeding time,􏰀TXA2 and prostaglandins. No effect on PT or PTT.

A

Aspirin

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18
Q

Neg sides of Aspirin

A

Gastric ulceration, tinnitus (CN VIII).

Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye syndrome in children with viral infection.

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19
Q

What do we see in Asprin OD?

A

Overdose initially causes hyperventilation and respiratory alkalosis, but transitions to mixed metabolic acidosis–respiratory alkalosis.

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20
Q

What type of drugs are: Clopidogrel, prasugrel, ticagrelor (reversible), ticlopidine.

MOA?

A

ADP recepotr inhibitors

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21
Q

When do we use ADP Receptor inhibitors (lopidogrel, prasugrel, ticagrelor (reversible), ticlopidine )

What is their toxicity?

A

Acute coronary syndrome; coronary stenting. 􏰀 Decrease incidence or recurrence of thrombotic stroke.

Neutropenia (ticlopidine). TTP may be seen.

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22
Q

What is the MOA of Cilostazol and dipyrimadole?

Uses?

Toxicity?

A

Phosphodiesterase III inhibitor;􏰁cAMP in platelets, resulting in inhibition of platelet aggregation; vasodilators.

Use: Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.

Toxicity: Nausea, headache, facial flushing, hypotension, abdominal pain.

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23
Q

Bind to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation Use:Unstable angina

A

Abciximab, eptifibatide, tirofiban.

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24
Q

Cell cycle review

A
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25
Q

We use this drug to tx RA, IBD, psoriasis, and ectopic preggers

Cancers: Leukemia, lymphoma, choriocarcionoma

Side: Myelosuppression

Drug and MOA

A

Methotrexate

Folic acid analog that competitively inhibits dihydrofolate reductase–>

Decreased 􏰂􏰀dTMP􏰂􏰀–> DECREASED DNA synthesis.

26
Q

This drug inhibits dihydrofolate reducates and results in myelosuppresion

What can we use to prevent negative side effects?

A

Methotrexate

Use Leucovorin to resuce (folinic acid)

also see macrovesicular fatty change to liver

27
Q

Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid.

This complex inhibits thymidylate synthase 􏰂􏰀:

DECREASED dTMP􏰂􏰀—> Decreased DNA synthesis.

A

5-FU

Myelosuppression, which is not reversible with leucovorin (folinic acid).

28
Q

Commonly used on basal cell carcinoma topically or actinic keratosis to prevent trasnformation

Taken systemically causes myelosuppression that can’t be reveresed.

A

5-FU

29
Q

Purine (thiol) analogs: DECREASE de novo purine synthesis (no A or G)

Activated by HGPRT.

What drugs are these?

What are they used for?

A

Azathioprine, 6-mercaptopurine (6-MP), 6-thioguanine (6-TG)

Preventing organ rejection, rheumatoid arthritis, IBD, SLE; used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease.

30
Q

What is the MOA of Azothioprine and 6-MP

What toxicity do we worry about?

A

Purine (thiol) analogs to inhibit de novo purine synthesis.

Activated by HGPRT. Azathioprine is : into 6-MP.

Toxicity:

Myelosuppression, GI, liver.

31
Q

You have a pt with hx of gout that just received a new liver. You need to put him on some meds but what drugs do we need to be carefull of prescribing to this pt?

A

Asothiprine, and 6-MP all are metabolized by xanthine oxidase which is inhibited by allopurinol thus you will increase the BM and GI, liver toxicity

32
Q

What do we use the following drugs for:

Azothioprine:

6-MP

6-thiogranine

A

Preventing organ rejection, rheumatoid arthritis, IBD, SLE; used to wean patients off steroids in chronic disease and to treat steroid-refractory chronic disease.

33
Q

MOA of Cytarabine and uses?

A

Pyrimidine analog􏰂–> inhibition of DNA polymerase.

Sides: pancytopenia, leukopenia, thrombocytopeni

34
Q

Use to treat Testicular cancer and Hodkin lymphoma

Side: pulmonary fibrosis

What drug, what mechanism?

A

Bleomycin

INduces free radical formation–> get breaks in DNA strands

35
Q

Use of dACTomycin

MOA

Sides?

A

Children ACT out: Wilms tumor, Ewing sarcoma, rhabdomycosarcoma (childhood tumors)

MOA: Intercalates into DNA

Sides: Myelosuppression

36
Q

Child comes in recently dx with Ewing sarcoma. Started on medication to help and his white cells tank. What drug does this?

A

Dactomycin (for childhood cancers)

intercalates into DNA

37
Q

Used to tx SOLID tumors and leukemia/lymphoma

Causes Dilated cardiomyopathy, some myelosuppresion

What is the drug and it’s MOA?

Can we prevent the sides?

A

Doxorubins and Danuorubicin

Generates free radicals–> intercalates into DNA–> get breaks in DNA and Decrease replication

Give Dexrazoxane (iron chelator) to prevent cardiotoxicity

38
Q

Drugs that cause cardiotoxicty and how can we prevent it

A

Doxorubisin and Danorubicin

Give Dexrazaxoxe (iron chelation)

39
Q

What is the MOA of Busulfan?

When do we Px it?

A

Cross links DNA (alkylating agent)

CML.

Also used to ablate patient’s bone marrow before bone marrow transplantation

40
Q

Alkylating agent that cross links DNA

Sides: Severe myelosuppression (in almost all cases), pulmonary fibrosis, hyperpigmentation.

A

Busulfan

41
Q

Cross-link DNA at guanine N-7. Require bioactivation by liver.

Drug

Use?

A

Cyclophosphamide, ifosfamide –> both alkylating agents

Use: Solid tumors, leukemia, lymphomas.

42
Q

What side effects do we worry about when prescribing Cyclophosphamide to pt

What can we do to prevent or limit toxicity?

A

Myelosuppression; hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolites).

43
Q

Nitrosoureas (carmustine, lomustine, semustine, streptozocin)

What is teh MOA?

What is their uses?

Toxicity?

A

Require bioactivation. Cross blood-brain barrier to CNS. Cross-link DNA.

Use: Brain tumors (including glioblastoma multiforme).

CNS toxicity (convulsions, dizziness, ataxia).

44
Q

MOA of Paclitaxel

Side effects

A

Hyperstabilize polymerized microtubules in M phase so that mitotic spindle cannot break down (anaphase cannot occur).

“It is taxing to stay polymerized.”

Sides: Myelosuppression, alopecia, hypersensitivity.

45
Q

Vinca alkaloids that bind β-tubulin and inhibit its polymerization into microtubules 􏰂 prevent mitotic spindle formation (M-phase arrest).

What drugs do this?

What are their side effects?

A

Vinblastine and Vincristine

Blastine Blasts bone marrow = bone marrrow suppresion

Cristine= peripheral neuropathy

46
Q

What is the MOA Cisplatin?

What toxicities are associated with it?

How do you prevent sides

A

Cisplatin SPLATS your kidneys

Crosslinks DNA

*Nephrotoxic, acoustic nerve damage

*use amifostine (free radical scavenger) to prevent sides

47
Q

What is the mech of Etoposide?

What side effects are concerned with?

What cancers does it help with?

A

inhibits topoisomerase II􏰂􏰁: INCREASE DNA degradation.

Myelosuppresion, GI

for: solid tumors: testicular)

48
Q

Inhibit topoisomerase I and prevent DNA unwinding and replication.

Drug and uses and sides

A

Ironotecan and Topotecan: S phase specifc

Severe myelosuppression:

49
Q

Inhibits ribonucleotide reductase to DECREASE 􏰂􏰀DNA Synthesis (S-phase specific).

Uses?

Side effects?

A

Hydroxyurea!

Uses: Sickel Cell pts (increase HbF), Melanoma and CML

Side: BM suppresion and GI

50
Q

What is teh MOA and use of hydroxyurea?

A

Inhibits ribonucleotide reductase to DECREASE 􏰂􏰀DNA Synthesis (S-phase specific).

51
Q

Use, mechanism and sides of Prenisone and prednisalone

A

Various; bind intracytoplasmic receptor; alter gene transcription.

Most commonly used glucocorticoids in cancer chemotherapy.

Used in CLL, non-Hodgkin lymphoma (part of combination chemotherapy regimen). Also used as immunosuppressants (e.g., in autoimmune diseases).

Cushing-like symptoms; weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psych

52
Q

Monoclonal antibody against VEGF. Inhibits angiogenesis.

What’s drug?

Use?

Sides?

A

Drug: Bevacizumab

Solid tumors (colorectal cancer, renal cell carcinoma).

Sides: Hemorrhage, blood clots, and impaired wound healing.

53
Q

Imatinib:

Use?

MOA?

Sides?

A

Tyrosine kinase inhibitor of BCR-ABL (Philadelphia chromosome fusion gene in CML) and c-kit (common in GI stromal tumors).

Use: GI and stromal cell tumors and CML

get edema

54
Q

When would we Rx Rituximab and what’s it’s MOA?

A

Monoclonal antibody against CD20, which is found on most B-cell neoplasms.

Ri-TWO-X-imab (two x X = 20)

Uses: Non-Hodgkin lymphoma, CLL, IBD, rheumatoid arthritis.

sides: 􏰁risk of progressive multifocal leukoencephalopathy.

55
Q

What drug 􏰁increass risk of progressive multifocal leukoencephalopathy?

What’s it’s MOA?

A

Rituximab

monoclonal antibody against CD20

56
Q

MOA or Tamoxifen and Raloxifene?

What is their differences?

When would you use one vs the other?

A

Selective estrogen receptor modulators (SERMs)—receptor antagonists in breast and agonists in bone. Block the binding of estrogen to ER ⊕ cells.

Tamoxifen for breast cancer treatement

Both for prevention of breast cancer

**Raloxifen for prevention of osteopotosis

57
Q

What toxicity profile do we worry about in Tamoxifen?

A

Tamoxifen—partial agonist in endometrium, which􏰁 Increases the risk of endometrial cancer; “hot flashes.”

Raloxifene—no increase 􏰁in endometrial carcinoma because it is an estrogen receptor antagonist in endometrial tissue.

58
Q

Monoclonal antibody against HER-2 (c-erbB2), a tyrosine kinase receptor. Helps kill cancer cells that overexpress HER-2, through inhibition of HER2-initiated cellular signaling and antibody- dependent cytotoxicity.

A

Herceptin or Trastuzumab

59
Q

What drug can we use to tx Her-2 + Breast cancer or gastric cancer?

What side effect to we worry about?

A

Herceptin or Trastuzumab

Sides: CARDIOTOXICTY; Herceptin herts the hert

60
Q

What is Chemo-Tax man?

Cisplatin/Carboplatin–>

Vincristine–>

Bleomycin,Busulfan–>

Doxorubisin–>

Trastuzumab–>

Cyclophosphamide–>

5-FU, 6MP, MTX–>

A

Cisplatin/Carboplatin–> acoustic nerve damage and nephrotoxic

Vincristine–> peripheral neuropathy

Bleomycin,Busulfan–> pulmonary fibrosis

Doxorubisin–> Cardiotoxic

Trastuzumab–> Cardiotoxic

Cyclophosphamide–> hemorrhagic cystitis

5-FU, 6MP, MTX–> myemlosuppresion

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