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Pharmacology > Lecture 8 (hem/onc)-Exam 4 > Flashcards

Lecture 8 (hem/onc)-Exam 4 Flashcards

1
Q

Venous thromboembolism txt:
* What are the parenteral agents-indirect inhibitors? (3)

A
  • Unfractionated heparin
  • Low molecular weight heparins
  • Fondaparinux
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2
Q

Venous thromboembolism txt:
* What are the oral anticoagulants? (3)

A
  • Vitamin K antagonists (warfarin)
  • Direct factor Xa inhibitors (rivaroxaban, apixaban)
  • Direct thrombin inhibitors (dabigatran)
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3
Q

Venous thromboembolism txt:
* What is the thrombolytics/fibrolytics?

A

tPA

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4
Q

What is primary hemostasis? Secondary hemostasis?

A
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5
Q

Extrinsic pathway
* What is activated and how?
* What is the cascade?
* What lab is ordered to monitor the extrinsic pathway?

A
  • Tissue damage causes activated platelets from primary hemostasis to release tissue factor (TF) and Ca+
  • TF and Ca+ bind to activated factor VII
  • The TF/Ca+/VIIa complex cleaves factor X into activated factor X (Xa)
  • Laboratory monitoring:Prothrombin time / INR
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6
Q

Intrinsic pathway
* When does it initiate?
* What is the cascade?
* What is the lab order to monitor?

A
  • Initiated when blood is exposed to negatively charge surface
  • Factor XII activated to XIIa
  • Cleaves XI to XIa
  • Cleaves IX to IXa
  • IXa binds with Ca+ and VIIIa
  • IXa/Ca+/VIIIa complex cleaves X to Xa
  • Laboratory monitoring: Activated partial thromboplastin time
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7
Q

Common pathway
* What happens after X is activated?

A
  • Xa cleaves factor V to Va
  • Xa bind with Va and Ca+ to form prothrombinase complex
  • Prothrombinase complex cleaves factor II (prothrombin) into IIa (thrombin)
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8
Q

Thrombin has several functions: (4)

A
  • Cleaves fibrinogen (I) to fibrin (Ia) – platelet plug stabilization
  • Binds to platelets – platelet activation
  • Activates factors – V, VIII, XI (positive feedback)
  • Cleaves stabilizing factor (factor XIII) into XIIIa
    * Binds to Ca+ and forms fibrin cross links
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8
Q

Clot retraction
* Thrombin not directly at the site of injury binds to what?
* What happens after this? (2)

A

Thrombin not directly at the site of injury binds to thrombomodulin
* Thrombomodulin forms a complex with protein C and protein S
* The complex inhibits factor V and factor VIII activation and slows down clotting

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9
Q
  • Antithrombin III (ATIII) binds what?
  • What is the cascade after that?
A

Antithrombin III (ATIII) binds to thrombin and factor Xa making them unavailable for clotting
* Inhibits factors VII, IX, XI, and XII
* Low affinity

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10
Q

Fibrinolysis
* Plasminogen is activated by what?
* What happens to fibrin?

A
  • Plasminogen is activated by tissue plasminogen activator (tPA) to form plasmin
  • Fibrin gets broken down to fibrin degradation products by plasmin
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11
Q

What is the coagulation cascade?

A
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12
Q

Heparin, LMWH, fondaparinux: Indirect inhibition
* Heparin and low molecular weight heparins (LMWH) bind to what?
* What is ATIII?

A
  • Heparin and low molecular weight heparins (LMWH) bind to antithrombin III and accelerates its activity
  • ATIII is a natural anticoagulant that inactivates factors Xa and thrombin
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13
Q

What is the MOA:
* Heparin:
* LMWH:
* Fondaparinux:

A

Heparin
* Accelerates Xa and thrombin inactivation

LMWH
* Selectively accelerates Xa inactivation; minimal effects on thrombin

Fondaparinux
* Specifically accelerates Xa inactivation; no effects on thrombin

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14
Q

How does heparin, and LMWH look like?

A
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15
Q

What can the large molecule (unfractionated)-> Heparin do?

A

able to interact with both antithrombin III and thrombin

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16
Q

What are the indications of heparin? (4)

A
  • Short-term anticoagulation (cont infusion)
  • Immediate anticoagulation – rapid onset (seconds)
  • MC life or limb threatening clots; surgical bridging therapy, DVT prophylaxis if other medications contraindicated
  • Safe in pregnancy – does not cross the placenta (since so big)
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17
Q

What is the dosing of heparin?

A
  • IV or subcutaneously (SC)
  • IV: given as bolus plus continuous IV infusion (short half-life)
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18
Q

What are the monitoring parameter of heparin?

A
  • aPTT [goal = 1.5 to 2.5 times normal (30 to 40 seconds)]
  • Antifactor Xa level (goal=0.3 to 0.7)
  • CBC (hemoglobin, hematocrit, platelets)
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19
Q

What are the adverse effects of heparin?

A
  • Bleeding
  • Osteoporosis – long-term therapy
  • Heparin induced thrombocytopenia
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20
Q

What is the antidote for heparin?

A
  • Protamine sulfate 1mg neutralizes ~ 100 units heparin
  • Continuous infusions: use heparin dose from preceding 2 to 3 hours
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21
Q

How much antidote do you need to give if you give 1200 units of heparin per hour?

A
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22
Q

Heparin induced Thrombocytopenia
* What happens with the immune system? What does that cause?

A

Immune system makes antibodies that bind to heparin-platelet factor 4 complexes
* Platelet activation – aggregation (clumping)
* Clots
* Thrombocytopenia

Platelets are dropping but clots are forming

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23
Q

Heparin induced Thrombocytopenia
* What are the risk?
* What is the onset?
* How do you dx it? (3)

A
  • Risk: unfractionated heparin > 7 to 10 days (also occurs with LMWH)
  • Onset: 5 to 10 days after heparin initiation

Diagnosis:
* Check 4T score – probably of HIT
* Low score (≤ 3 rules out HIT); look for additional diagnoses
* High score; stop heparin, give alternative, order additional testing

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24
HIT – alternative treatments * What do you give more critcally ill patients? * What do you give stable patients?
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Discontinue heparin
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Warfarin * What is the moa?
* Factors II, VII, IX and X dependent on vitamin K for synthesis * Warfarin inhibits vitamin K recycling and synthesis * Not available for factor production
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Warfarin * What are the indications? (2)
* DVT, atrial fibrillation, prosthetics valves * **Only oral anticoagulant indicated for patients with mechanical heart valves**
29
Warfarin-Pharmacokinetics: * What is half life? What is onset? * Requires what? * How is metabolized?
* Generally long half-life; prolonged onset * Requires bridging therapy with heparin or LMWH-> if INR therapeutic for two days then then you can stop * Metabolized by CYP2C9 – many drug interactions
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CYP2C9 inducers and inhibors? What do they cause to the levels of warfarin?
31
Monitoring Warfarin * What levels do you need to look at? * Adjuct dose to what? * _ algorithms * initial dose for most patients? * What do you need to check daily intil therapeutic?
PT/**INR** – goal 2 to 3 in most cases * Adjust dose to INR * Evidence-based algorithms * Initial dose for most patients: 5mg PO daily * INR daily until therapeutic (then decrease interval of checking)
32
What are the diet issues with warfarin?
Vit K needs to be stabilized with txt * for example: winter vs summer months
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Warfarin * What are the SE? (3) * What is CI (1)?
34
Warfarin overdose: * Txt based on what?
Treatment depends on INR level and if patient is bleeding
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Warfarin overdose: * What do you with a patient who is not bleeding? (3)
* Hold warfarin * Give vitamin K (1 to 5 mg PO) * Resume warfarin at lower dose once INR is 2 to 3
36
Warfarin overdose: * What do you with a patient who is bleeding? (2)
* 4-factor prothrombin complex concentrate [PCC (Kcentra)] plus vitamin K -> PCC will not work without vit k OR * Fresh frozen plasma (FFP)
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Fresh frozen plasma
38
Direct inhibitors * What are the two types and their MOA?
Factor Xa inhibitors * Directly bind factor Xa * Prevent conversion of prothrombin to thrombin Thrombin inhibitors * Bind to and inhibit thrombin
39
Direct oral anticoagulants (DOACS) * First oral agent since what? * What is dadigratran? * What are the types of oral factor Xa inhibitors (4)
40
Direct oral anticoagulants (DOACS) * What are the benefits over warfarin?
* Faster onset of action * **No direct monitoring required** * Minimal drug-food interactions * Comparable bleeding rate * Less drug-drug interactions * **Fixed dose per indication** – varies by indication, age, renal and hepatic function * ± parenteral anticoagulation bridging
41
Direct oral anticoagulants (DOACS)-Indications * Reduce risk of what? * What does it treat? * Prophylaxis if what? * Not recommened as alternative when? * Contraindicated when? ⭐️
* Reduce risk of stroke any systemic embolism in patients with nonvalvular atrial fibrillation * Treat DVT and PE * Prophylaxis if DVT (hip and / or knee replacement) * Not recommended as alternative to UFH or LMWH in patients with PE who are hemodynamically unstable * **Contraindicated as anticoagulation for mechanical heart valves**
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DOACs – drug interactions * What does P-glycoprotein mediate? * Inhibits do what? Examples * Inducers do what? Exampes?
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DOACs – drug interactions * What does CYP3A4 mediate? * Inhibits do what? Examples * Inducers do what? Exampes?
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Fill in for DOACS
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Anticoagulation for treatment of VTE * Oral anticoagulant monotherapy with what? * Start parenteral anticoagulant then what? * Start parenteral anticoagulant x 5 days then switch ? * Start parenteral* anticoagulant and what?
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Fill in for Venous Thromboembolism treatment
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ANTICOAGULATION TRANSITIONS * What is complex? * What exist? * What is recommended?
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Anticoagulation bleeding * Anticoag are CI with what? * What is major bleeding?
**Anticoagulants contraindicated with any active bleeding** Major bleeding * Gastrointestinal bleeding (MC) – mortality 5% * Intracranial hemorrhage – less common – mortality 50% * Patients can be risk stratified by age, organ function, comorbidities
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Anticoagulation bleeding * What is minor bleeding?
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CONTRAINDICATIONS TO ANTICOAGULATION * What are absolute?
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CONTRAINDICATIONS TO ANTICOAGULATION * What are relative?
53
Treatment of severe vte: Life-threatening pulmonary embolism with hemodynamically unstable patient * What is first line and second line?
* First-line: IV thrombolytic therapy * Second-line: Catheter-directed thrombolytic therapy
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Massive proximal lower extremity thrombosis or ilio-femoral thrombosis associated with severe symptoms (< 14 days duration) * What is first line?
First-line: Catheter-directed thrombolytic therapy
55
Treatment of severe vte * What is last line?
Embolectomy
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Tissue plasminogen activator (tpa) * What is the MOA? * What is the half-life? * How do you dose it?
MOA * binds fibrin in a thrombus and converts plasminogen to plasmin; plasmin lyses fibrin and fibrinogen breaking up the clot Pharmacokinetics: * Short half-life; less than 5 minutes; 80% cleared within 10 minutes * Bolus dose followed by continuous infusion
57
Tissue plasminogen activator (tpa) * What are the adverse effects?
Bleeding * Increased risk with recent hemorrhage, trauma, surgery; uncontrolled hypertension or advanced age
58
Von Willebrand Disease * Deficiency or inhibition of what? * What are the types? * Usually what? * What is there is a history of? * What is rare? What is it associated with?
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Von Willebrand disease: * Deficiency in what? * VW stored where? * VW released when? * vWF attaches to what? * vWf also carries what?
* Deficiency in quantity or quality of von Willebrand factor * Stored in epithelial cells and megakaryocytes * Released in response to tissue injury * vWF attaches to exposed collagen fibers and binds to platelets via glycoprotein 1b receptors; helps bind platelets together to form platelet plug * vWf also carries factor VIII; protects it from early degradation by proteins C and S
60
Von Willebrand disease * What is prolonged?
Bleeding time may be prolonged; aPTT may be mildly elevated
61
Von Willebrand disease Inherited subtypes: Type 1 * What type of disease? * What are the sx?
Type 1 (75%) * Autosomal dominant; quantity low, function normal * Mild disease – bruising, bleeding gums, epistaxis, menstrual bleeding
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Von Willebrand disease Inherited subtypes: Type 2 * What type of disease? * What are the sx?
Type 2 (20%) * Autosomal dominant * Variable severity; quantity good, function not good
63
d disease Inherited subtypes: Type 3 * What type of disease? * What are the sx?
Type 3 (5%) * Autosomal recessive; no vWF and factor VIII deficiency * Severe disease – joint, muscle, GI bleeding
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vWD treatments * What is first line for type 1 and 2? * What is the MOA? * How long do you use it for?
Desmopressin (DDAVP) * Type 1 and Type 2 disease * Stimulates endothelial cells and macrophages to release more vWF * Used only for short periods to help control bleeding or peri-operative
65
Desmopressin (DDAVP) * What is the dosing? * What route is recommended and what is the dose?
Dosing: * 2 hours prior to procedure and every 8 to 12 hours as needed; no more than 3 to 5 days Intranasal spray recommended: * < 50 kg – 150 mcg (1 spray) in single nostril * ≥ 50 kg – 100 mcg (1 spray) in each nostril (total dose = 300 mcg)
66
Vwd type3 treatments * What is the first line txt? * What are examples?
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vWF /antihemophilic factor & complexes vWF and factor VIII replacement * What is the dose and goal?
* Dose: variable; dependent on disease and bleeding severity * Goal: VWF: RCo activity > 50%
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D. Bleeding time platelets / platelet aggregometry
69
B. DDAVP
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Hemophilia * What type of disease? * What is type A and B? * What are the sxs?
* X-linked recessive - clotting factor deficiency * Type A is factor 8 deficiency, type B is factor 9 deficiency * Signs/symptoms: severe bleeding, spontaneous hemarthroses, muscle hematomas, GI bleeding, **bleeding with circumcision procedure**
71
Hemophilia * What are the labs? * What is the txt?
* Labs: Prolonged PTT with normal PT; Factor 8 or 9 assay diagnostic * Treatment/Management: factor 8 or 9 infusions, DDAVP, aminocaproic or tranexamic acid, avoid blood thinners, avoid trauma/contact sports if severe 
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Hemophilia treatment-Prophylaxis: * Prevent what? (2) * Geneally how many transfusions a week? * Dependent on what? * Given where?
## Footnote sereve patients
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Hemophilia treatment * _ episode * Stop what? * Doses? * Where is initial txt?
* Bleeding episode * Stop bleeding ASAP; prevent long-term sequela * Doses variable and dependent on severity of disease and patient activity * Initial treatment in hospital
75
Hemophilia treatments-inhibitors * Most common with who? * What targets Factor VIII * What happens? * What needs to be used instead?
76
Hemophilia treatments * What is the gene therapy?
* valoctocogene roxaparvovec gene therapy for severe hemophilia A
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C. FactorVIII
78
What are the most common types of leukemia? Who does it occur in?
79
Acute lymphoblastic leukemia (ALL) * MC what? * What is the general txt?
80
Acute myelogenous leukemia (AML) * MC in who? * What is the general txt?
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Chronic lymphoblastic leukemia (CLL) * Malignancy of what? * What is avg onset? * What are the sxs? * What is on smear?
* Malignancy of mature lymphoid cells * Average onset 70 years with mean WBC >20,000 - predominantly lymphocytes * Indolent, lymphadenopathy, HSM * Smudge cells
83
Chronic lymphoblastic leukemia (CLL) * What is the txt (3)?
* Observation vs Bruton’s TKIs (ie ibrutinib) * Monoclonal antibodies * Chemotherapy (purine analogs, alkylating agents
84
Chronic myelogenous leukemia (CML) * Malignancy of what? * Onset when? * What are the sxs? * Caused by what? ⭐️ * What is the txt? ⭐️
85
CML - Tyrosine kinase inhibitors * Inhibts what? Explain the MOA? * What does it induce?
* Inhibits BCR-ABL tyrosine kinase * Blocks BCR-ABL’s ATP binding site; inhibiting enzyme activity and halts down stream cellular processes that lead to carcinogenic transformation * Induces cell apoptosis
86
* CML treatment with TKIs improved what? * Initial treatment of choice depends on what?
* CML treatment with TKIs improved disease outcomes with near normal lifespans * Initial treatment of choice depends on disease mutations, patient specific factors, TKI side effect profiles
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Tyrosine kinase inhibitors * Resistance MC with what? * Second generation agents are what? * What is key? * Txt is how long? * Studies show what?
* Resistance MC with imatinib * Second generation agents higher binding affinity and selectivity for BCR-ABL kinase binding site * Compliance key to prevention of resistance * Treatment generally life long * Studies have evaluated discontinuation for patients with complete genetic remission
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Tyrosine kinase inhibitors * All metabolized by what?
CYP3A4
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CLL Treatment * What type of inhibitors? * What are the 3 drugs?
Bruton’s tyrosine kinase (BTK) inhibitors * Ibrutinib * Acalabrutinib * Zanubrutinib
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# CLL txt Bruton’s tyrosine kinase (BTK) inhibitors * Binds to what? * Organizes what? Lymphocyte count within what? * What occurs?
* Bind to BTK receptors within the leukemia cell and inhibit protein kinase cell signaling important for cell replication and proliferation * Organizes B-cell migration from tissues into peripheral blood * Lymphocyte count within blood * stream increases temporarily Cells death occurs
93
CLL treatment * What is the efficacy? * What are the SE?
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Hodgkin's Lymphoma * What type of lymphoma? * Age? * gender? * Presents with what? * What is the txt? * What happens if relapse?
95
Non-Hodgkin’s Lymphoma * Common or rare? * What types? * Common inital therapies include what? * What is txt in some cases? * What is primary staging system? * What are examples?
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Hodgkin's Lymphoma * What is the txt drugs? * What is the doses? * How many cycles?
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Non-Hodgkin's Lymphoma * What is the txt drugs? * What is the doses? * How many cycles?
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Multiple Myeloma * Malignacy of what? * What is the median age? * What is present? * What is elevated and formed? * What type of staging? * What is it txt with?
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What is the first line txt of multiple myeloma?
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Granulocyte colony stimulating factor (GCSF) * Stimulates what? * prevent or reduce what? (2) * Stimulate what? * How do you give it? * What is the MC SE? How do you tx this? ⭐️

Pharmacology (14 decks)

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