Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

tPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is primary hemostasis? Secondary hemostasis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the coagulation cascade?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does heparin, and LMWH look like?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

able to interact with both antithrombin III and thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the dosing of heparin?

A
  • IV or subcutaneously (SC)
  • IV: given as bolus plus continuous IV infusion (short half-life)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the adverse effects of heparin?

A
  • Bleeding
  • Osteoporosis – long-term therapy
  • Heparin induced thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

HIT – alternative treatments
* What do you give more critcally ill patients?
* What do you give stable patients?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
A

Discontinue heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Warfarin
* What is the moa?

A
  • Factors II, VII, IX and X dependent on vitamin K for synthesis
  • Warfarin inhibits vitamin K recycling and synthesis
  • Not available for factor production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Warfarin
* What are the indications? (2)

A
  • DVT, atrial fibrillation, prosthetics valves
  • Only oral anticoagulant indicated for patients with mechanical heart valves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Warfarin-Pharmacokinetics:
* What is half life? What is onset?
* Requires what?
* How is metabolized?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CYP2C9 inducers and inhibors? What do they cause to the levels of warfarin?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the diet issues with warfarin?

A

Vit K needs to be stabilized with txt
* for example: winter vs summer months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Warfarin
* What are the SE? (3)
* What is CI (1)?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Warfarin overdose:
* Txt based on what?

A

Treatment depends on INR level and if patient is bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Warfarin overdose:
* What do you with a patient who is not bleeding? (3)

A
  • Hold warfarin
  • Give vitamin K (1 to 5 mg PO)
  • Resume warfarin at lower dose once INR is 2 to 3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Warfarin overdose:
* What do you with a patient who is bleeding? (2)

A
  • 4-factor prothrombin complex concentrate [PCC (Kcentra)] plus vitamin K -> PCC will not work without vit k

OR
* Fresh frozen plasma (FFP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q
A

Fresh frozen plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Direct inhibitors
* What are the two types and their MOA?

A

Factor Xa inhibitors
* Directly bind factor Xa
* Prevent conversion of prothrombin to thrombin

Thrombin inhibitors
* Bind to and inhibit thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Direct oral anticoagulants (DOACS)
* First oral agent since what?
* What is dadigratran?
* What are the types of oral factor Xa inhibitors (4)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Direct oral anticoagulants (DOACS)
* What are the benefits over warfarin?

A
  • 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
Q

Direct oral anticoagulants (DOACS)-Indications
* Reduce risk of what?
* What does it treat?
* Prophylaxis if what?
* Not recommened as alternative when?
* Contraindicated when? ⭐️

A
  • 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
42
Q

DOACs – drug interactions
* What does P-glycoprotein mediate?
* Inhibits do what? Examples
* Inducers do what? Exampes?

43
Q

DOACs – drug interactions
* What does CYP3A4 mediate?
* Inhibits do what? Examples
* Inducers do what? Exampes?

44
Q

Fill in for DOACS

46
Q

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?

47
Q

Fill in for Venous Thromboembolism treatment

48
Q

ANTICOAGULATION TRANSITIONS
* What is complex?
* What exist?
* What is recommended?

49
Q

Anticoagulation bleeding
* Anticoag are CI with what?
* What is major bleeding?

A

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

50
Q

Anticoagulation bleeding
* What is minor bleeding?

51
Q

CONTRAINDICATIONS TO ANTICOAGULATION
* What are absolute?

52
Q

CONTRAINDICATIONS TO ANTICOAGULATION
* What are relative?

53
Q

Treatment of severe vte: Life-threatening pulmonary embolism with hemodynamically unstable patient
* What is first line and second line?

A
  • First-line: IV thrombolytic therapy
  • Second-line: Catheter-directed thrombolytic therapy
54
Q

Massive proximal lower extremity thrombosis or ilio-femoral thrombosis associated with severe symptoms (< 14 days duration)
* What is first line?

A

First-line: Catheter-directed thrombolytic therapy

55
Q

Treatment of severe vte
* What is last line?

A

Embolectomy

56
Q

Tissue plasminogen activator (tpa)
* What is the MOA?
* What is the half-life?
* How do you dose it?

A

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
Q

Tissue plasminogen activator (tpa)
* What are the adverse effects?

A

Bleeding
* Increased risk with recent hemorrhage, trauma, surgery; uncontrolled hypertension or advanced age

58
Q

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?

59
Q

Von Willebrand disease:
* Deficiency in what?
* VW stored where?
* VW released when?
* vWF attaches to what?
* vWf also carries what?

A
  • 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
Q

Von Willebrand disease
* What is prolonged?

A

Bleeding time may be prolonged; aPTT may be mildly elevated

61
Q

Von Willebrand disease
Inherited subtypes: Type 1
* What type of disease?
* What are the sx?

A

Type 1 (75%)
* Autosomal dominant; quantity low, function normal
* Mild disease – bruising, bleeding gums, epistaxis, menstrual bleeding

62
Q

Von Willebrand disease
Inherited subtypes: Type 2
* What type of disease?
* What are the sx?

A

Type 2 (20%)
* Autosomal dominant
* Variable severity; quantity good, function not good

63
Q

d disease
Inherited subtypes: Type 3
* What type of disease?
* What are the sx?

A

Type 3 (5%)
* Autosomal recessive; no vWF and factor VIII deficiency
* Severe disease – joint, muscle, GI bleeding

64
Q

vWD treatments
* What is first line for type 1 and 2?
* What is the MOA?
* How long do you use it for?

A

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
Q

Desmopressin (DDAVP)
* What is the dosing?
* What route is recommended and what is the dose?

A

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
Q

Vwd type3 treatments
* What is the first line txt?
* What are examples?

67
Q

vWF /antihemophilic factor & complexes vWF and factor VIII replacement
* What is the dose and goal?

A
  • Dose: variable; dependent on disease and bleeding severity
  • Goal: VWF: RCo activity > 50%
68
Q
A

D. Bleeding time platelets / platelet aggregometry

69
Q
70
Q

Hemophilia
* What type of disease?
* What is type A and B?
* What are the sxs?

A
  • 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
Q

Hemophilia
* What are the labs?
* What is the txt?

A
  • 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
73
Q

Hemophilia treatment-Prophylaxis:
* Prevent what? (2)
* Geneally how many transfusions a week?
* Dependent on what?
* Given where?

A

sereve patients

74
Q

Hemophilia treatment
* _ episode
* Stop what?
* Doses?
* Where is initial txt?

A
  • 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
Q

Hemophilia treatments-inhibitors
* Most common with who?
* What targets Factor VIII
* What happens?
* What needs to be used instead?

76
Q

Hemophilia treatments
* What is the gene therapy?

A
  • valoctocogene roxaparvovec gene therapy for severe hemophilia A
77
Q
A

C. FactorVIII

78
Q

What are the most common types of leukemia? Who does it occur in?

79
Q

Acute lymphoblastic leukemia (ALL)
* MC what?
* What is the general txt?

80
Q

Acute myelogenous leukemia (AML)
* MC in who?
* What is the general txt?

82
Q

Chronic lymphoblastic leukemia (CLL)
* Malignancy of what?
* What is avg onset?
* What are the sxs?
* What is on smear?

A
  • Malignancy of mature lymphoid cells
  • Average onset 70 years with mean WBC >20,000 - predominantly lymphocytes
  • Indolent, lymphadenopathy, HSM
  • Smudge cells
83
Q

Chronic lymphoblastic leukemia (CLL)
* What is the txt (3)?

A
  • Observation vs Bruton’s TKIs (ie ibrutinib)
  • Monoclonal antibodies
  • Chemotherapy (purine analogs, alkylating agents
84
Q

Chronic myelogenous leukemia (CML)
* Malignancy of what?
* Onset when?
* What are the sxs?
* Caused by what? ⭐️
* What is the txt? ⭐️

85
Q

CML - Tyrosine kinase inhibitors
* Inhibts what? Explain the MOA?
* What does it induce?

A
  • 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
Q
  • CML treatment with TKIs improved what?
  • Initial treatment of choice depends on what?
A
  • 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
87
Q

Tyrosine kinase inhibitors
* Resistance MC with what?
* Second generation agents are what?
* What is key?
* Txt is how long?
* Studies show what?

A
  • 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
88
Q

Tyrosine kinase inhibitors
* All metabolized by what?

91
Q

CLL Treatment
* What type of inhibitors?
* What are the 3 drugs?

A

Bruton’s tyrosine kinase (BTK) inhibitors
* Ibrutinib
* Acalabrutinib
* Zanubrutinib

92
Q

CLL txt

Bruton’s tyrosine kinase (BTK) inhibitors
* Binds to what?
* Organizes what? Lymphocyte count within what?
* What occurs?

A
  • 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
Q

CLL treatment
* What is the efficacy?
* What are the SE?

94
Q

Hodgkin’s Lymphoma
* What type of lymphoma?
* Age?
* gender?
* Presents with what?
* What is the txt?
* What happens if relapse?

95
Q

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?

96
Q

Hodgkin’s Lymphoma
* What is the txt drugs?
* What is the doses?
* How many cycles?

97
Q

Non-Hodgkin’s Lymphoma
* What is the txt drugs?
* What is the doses?
* How many cycles?

98
Q

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?

99
Q

What is the first line txt of multiple myeloma?

100
Q

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions