Hematology Flashcards

1
Q

Heparin - MOA

A

Cofactor for the activation of antithrombin

  • Decrease thrombin
  • Decrease Xa

Short half life
Rapid onset of action
Large anionic acidic polymer

New low molecular weight heparins (Enoxaparin) act more on Xa, have better bioavaiability and 2-4 times longer half life, and can be administered sub Q without laboratory monitoring. They are not easily reversible

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

Heparin - Clinical Use

A

Immediate anticoagulation for:

  • PE
  • Stroke
  • Acute coronary syndrome
  • MI
  • DVT

Used in pregnancy - does not cross placenta

Follow PTT

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

Heparin - Toxicities

A
  • Bleeding
  • Osteoperosis
  • Drug-drug interactions
  • Heparin induced thrombocytopenia (HIT) - Heparin binds to platelet factor IV, causing antibody production that binds to and activates platelets leading to their clearance and resulting in thrombocytopenic, hypercoagulable state.

Protamine Sulfate is the antidote for Heparin toxicity - A positively charges molecule that binds negatively charged Heparin

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

Protamine Sulfate - MOA

A

Positively charged molecule that binds negatively charged Heparin

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

Protamine Sulfate - Clinical Use

A

Heparin toxicity

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

Lepirudin - MOA

A

Directly inhibit thrombin

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

Lepirudin - Clinical Use

A

Alternative to Heparin for anticoagulating patients with HIT.

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

Bivalirudin - MOA

A

Directly inhibit thrombin

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

Bivalirudin - Clinical Use

A

Alternative to Heparin for anticoagulating patients with HIT.

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

Direct Thrombin Inhibitors - Available Drugs

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

Warfarin / Coumadin - MOA

A

Interferes with normal synthesis and gamma-carboxylation of vitamin K dependent clotting factors (II, VII, IX, X) and proteins C, S
Acts within the liver
Slow onst of action - limited by the half lives of clotting factors and C,S
Taken PO
Small lipid soluble molecule (cross placenta)

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

Warfarin / Coumadin - Clinical Use

A

Chronic anticoagulation:

  • Post-STEMI
  • Venous thromboembolism prophylaxis

In laboratory assay, has an effect on extrinsic pathway
Follow PT/INR

“WEPT - Warfarin, Extrinsic, PT”

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

Warfarin / Coumadin - Toxicities

A
  • Bleeding
  • Teratogenic
  • Skin and tissure necrosis
  • Drug interactions - is metabolized by p450

Reversal of warfarin overdose is Vitamin K
For rapid reversal of severe overdose give fresh frozen plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Thrombolytics - Available Drugs

A
  • Streptokinase
  • Urokinase
  • tPA (alteplase)
  • APSAC (anistreplase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Thrombolytics - MOA

A

Directly or indirerectly aid in the conversion of plasminogen to plasmin

  • Cleave thrombin and fibrin clots
  • Increase PT and PTT
  • No change in platelet count

[Streptokinase, Urokinase, tPA (alteplase), APSAC (anistreplase)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Thrombolytics - Clinical Use

A
  • Early MI
  • Early ischemic stroke

[Streptokinase, Urokinase, tPA (alteplase), APSAC (anistreplase)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thrombolytics - Toxicities

A
  • Bleeding - CI in patients with active bleeding, hx of intracranial bleed, recent surgery, known bleeding diatheses, severe hypertension
    • Treat toxicity with aminocaproic acid - a fibrinolysis inhibitor

[Streptokinase, Urokinase, tPA (alteplase), APSAC (anistreplase)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aminocaproic Acid - MOA

A

Inhibit fibrinolysis

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

Aminocaproic Acid - Clinical Use

A

Treat thrombolytic toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Aspirin (ASA) - MOA

A

Acetylates and irreversibly inhibits cyclooxygenase (COX-1 and COX-2)

  • Prevent conversion of arachadonic acid to thromboxane A2 (TXA2)
  • Low dose therapy does not inhibit endothelial cell PGI production
  • Increased bleeding time
  • No effect on PT or PTT
13
Q

Aspirin (ASA) - Clinical Use

A
  • Antipyretic
  • Analgesic
  • Anti-inflammatory
  • Antiplatelet drug
14
Q

Aspirin (ASA) - Toxicities

A
  • Gastric ulcer
  • Bleeding
  • Hyperventilation
  • Reye’s syndrome
  • Tinnitus (CN VIII)
15
Q

ADP Receptor Blockers - Available Drugs

A
  • Clopidogrel
  • Ticlopidine
16
Q

Clopidogrel - MOA

A

Irreversibly block ADP receptors

  • Prevent expression of IIb/IIIa receptors on platelet surface
  • Prevent IIb/IIIa from binding fibrinogen
  • Prevent platelet aggregation
17
Q

Clopidogrel - Clinical Use

A
  • Acute coronary syndrome - Coronary stenting
  • Decrease incidence or recurrence of thrombotic stroke
18
Q

Clopidogrel - Toxicities

A

Neutropenia (more with Ticlopidine)

19
Q

Ticlopidine - MOA

A

Irreversibly block ADP receptors

  • Prevent expression of IIb/IIIa receptors on platelet surface
  • Prevent IIb/IIIa from binding fibrinogen
  • Prevent platelet aggregation
20
Q

Ticlopidine - Clinical Use

A
  • Acute coronary syndrome - Coronary stenting
  • Decrease incidence or recurrence of thrombotic stroke
21
Q

Ticlopidine - Toxicities

A

Neutropenia (more with Ticlopidine)

22
Q

Phosphodiesterase III Inhibitors - Available Drugs

A
  • Cilostazol
  • Dipyridamole
23
Q

Cilostazol - MOA

A

Inhibit phosphodiesterase III

  • Increase cAMP in platelets –> Inhibit platelet aggragation
  • Vasodilation
24
Q

Cilostazol - Clinical Use

A
  • Intermittent claudication
  • Coronary vasodilation
  • Prevention of stroke or TIA’s (in combination w/ Aspirin)
  • Angina prophylaxis
25
Q

Cilostazol - Toxicities

A
  • Nausea, headache, facial flushing
  • Hypotension
  • Abdominal pain
26
Q

Dipyridamole - MOA

A

Inhibit phosphodiesterase III

  • Increase cAMP in platelets –> Inhibit platelet aggragation
  • Vasodilation
27
Q

Dipyridamole - Clinical Use

A
  • Intermittent claudication
  • Coronary vasodilation
  • Prevention of stroke or TIA’s (in combination w/ Aspirin)
  • Angina prophylaxis
28
Q

Dipyridamole - Toxicities

A
  • Nausea, headache, facial flushing
  • Hypotension
  • Abdominal pain
29
Q

Abciximab - MOA

A

Monoclonal antibody to glycoprotein receptor IIb/IIIa

  • Prevent platelet aggregation
30
Q

Abciximab - Clinical Use

A
  • Acute coronary syndromes
  • Percutaneous transluminal coronary angioplasty
31
Q

Abciximab - Toxicities

A
  • Bleeding
  • Thrombocytopenia
32
Q

Packed RBC’s - MOA

A

Increase Hb and O2 carrying capacity

33
Q

Packed RBC’s - Clinical Use

A
  • Acute blood loss
  • Severe anemia
33
Q

Platelets - MOA

A

Increase platelet count

  • Usually given in a 6-pack for therapeutic effect.
34
Q

Platelets - Clinical Use

A

Stop significant bleeding

  • Thrombocytopenia
  • Qualitative platelet defects
35
Q

Fresh Frozen Plasma - MOA

A

Increase coagulation factor levels by about 20%

36
Q

Fresh Frozen Plasma - Clinical Use

A
  • DIC
  • Cirrhosis
  • Warfarin over-anticoagulation
37
Q

Cryoprecipitate - MOA

A

Contains fibrinogen, factor VIII, factor XIII, and vWF

  • Replace deficient coagulation factors
38
Q

Cryoprecipitate - Clinical Use

A

Treat coagulation factor deficiencies involving fibrinogen and factor VIII.

39
Q

Blood Transfusion Therapies - Toxicities

A
  • Infection (low risk)
  • Transfusion rxn
  • Fe overload
  • Hypocalcemia (Citrate is a Ca chelator)
  • Hyperkalemia (RBC’s may lyse in older blood units)