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Fall 2024 > Pharm Test 4 > Flashcards

Pharm Test 4 Flashcards

1
Q

What is thrombogenesis

A

formation of thrombi

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2
Q

What is hemostasis?

A

The ability of the body to stop itself from bleeding out

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3
Q

Part of hemostasis is _____________

A

thrombogenesis

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4
Q

what is fibrin?

A

a net that traps the platelet plugs and traps red blood cells at site of injury “glue”/”morter”

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5
Q

What happens when we have a larger injury in the vessels?(pharm)

A

it can expose collagen and (von Willebrand factor) vWF.
When these are exposed they act with glycoproteins that are on platelet cell surfaces and this sets up platelet coagulation or thrombogenesis
Eventually this will lead to clotting cascade

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6
Q

what is a red thrombus and where do they occur?

A

A lot of fibrin with a long tail and with RBC’s trapped in it that occurs in slow moving vessels like veins

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7
Q

what is a white thrombus?

A

a thrombus with more fibrinogen or platelets in it that occurs in high pressure arteries d/t damaged or plaque buildup in the endothelium

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8
Q

What is a thromboembolism?

A

a thrombus that has broken off of the vessel it was made it and is now moving through the body

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9
Q

what happens in response to damage of Blood vessels

A
  • vasoconstriction d/t serotonin
  • formation of platelet plugs
  • degranulation of platelet aggregation which leads to the activation of more platelets
  • That forms a fibrin clot
  • tight regulation of coagulation and fibrinolysis
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10
Q

what are the phases of platelets?

A

Adhesion
Aggregation
Secretion
Cross-linking of adjacent platelets

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11
Q

what causes adhesion?

A

Exposure of collagen and von willebrand factor cause platelets to adhere to surface

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12
Q

what is the secretion related to platelets?

A

They secrete substances,
primarily serotonin,
adenosine diphosphate,
and thromboxane A2
and they encourage additional cross linking of platelets

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13
Q

what is cross-linking?

A

formation this cross linked platelet clot or thrombocyte clot

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14
Q

Where does PGI2 aka prostacyclin come from?

A

The blood vessel lining is made up of endothelial cells which normally produce prostaglandin I2 or PGI2 (aka prostacyclin)

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15
Q

what does PGI2/prostacyclin do?

A

it inhibits platelet aggregation

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16
Q

When is PGI2 activated?

A

During the normal state of endothelial cell, if there’s no damage, is to inhibit platelet aggregation because we don’t want clots forming when there shouldn’t be clots forming

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17
Q

Why is there a black box warning for CV events on NSAIDs?

A

NSAIDs inhibit prostaglandin synthesis, so they are actually “proclot”

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18
Q

How does aspirin work?

A

aspirin targets specifically the platelets themselves by inhibiting thromboxane A2

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19
Q

what receptor does collagen bind to?

A

glycoprotein 1-A receptor.

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20
Q

what receptor does Von Willebrand factor bind to?

A

glycoprotein 1-B

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21
Q

what results in the activation and release of soluble mediators

A

Collagen binding to platelets at the glycoprotein 1-A receptor.
Von willebrand factor binding to platelets at the glycoprotein 1-B.

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22
Q

which soluble mediators are released d/t the binding of Collagen and vWF to platelets?

A
  1. adenosine (ADP)
  2. thromboxane A-2
  3. serotonin (5 HT)
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23
Q

What are the steps to platelet aggregation?

A
  1. Damage exposes collagen and von willebrand factor
  2. Collagen binds to platelets specifically at the glycoprotein 1-A receptor.
    Von willebrand factor binds to platelets at the glycoprotein 1-B receptor.
  3. adenosine(ADP), thromboxane A-2, and serotonin(5 HT) is released
  4. Serotonin causes vasoconstriction of smooth muscle on vessels and it binds to serotonin receptors on other platelets which activates those platelets.
    ADP and thromboxane A2 also bind to additional receptors on other platelets that are going to activate more platelets
  5. Once the second platelet is activated it degranulates and releases additional ADP, thromboxane A2 and 5 HT.

It’s a positive feedback mechanism where multiple platelets are going to join together to be cross linked into this network

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24
Q

what does fibrinogen do and where is it produced?

A

Fibrinogen turns into fibrin which holds platelets together! Fibrinogen is produced through the coagulation cascade.

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25
what is required in order to form a stable clot that's going to prevent us from bleeding out?
both platelet aggregation and coagulation cascade
26
what is the common pathway?
Where the intrinsic and extrinsic pathways meet in the coagulation cascade
27
What are the steps in the common pathway?
1. Factor 10 is activated. 2. Factor 10 activates the inactive form of thrombin (aka prothrombin) to its active form called thrombin. 3. Thrombin increases the release of more thrombin, it activates platelets, and it converts the inactive form of fibrinogen into the active form of fibrin. 4. Fibrin helps platelets aggregate together and it forms a mesh network to trap platelets.
28
What are the steps in the intrinsic pathway?
Damage to the surface activates factor XII(12) XII activates factor XI(11) XI activates factor IX(9) IX + VIII(8) activates factor X(10) this starts the common pathway
29
What are the steps in the extrinsic pathway?
Trauma activates factor VII(7) VII activates factor X(10) this starts the common pathway
30
what is another name for the intrinsic pathway?
contact activation
31
what is another name for the extrinsic pathway?
Tissue factor
32
What all does thrombin do when activated?
1. It increases the release of more thrombin 2. It activates platelets 3. It converts the inactive form of fibrinogen into the active form of fibrin.
33
Which number is the contact factor?
XII (12)
34
which number is the tissue factor?
VII(7)
35
What is Virchow's triad?
stasis endothelial injury hypercoagulability
36
What causes DVTs and PEs most often?
Red thrombi
37
What are the inherited risk factors for DVTs?
Antithrombin III deficiency Protein C deficiency Protein S deficiency Sickle cell anemia Activated protein C resistance
38
What are the aquired risk factors for DVTs?
Bedridden Surgery/trauma Obesity Estrogen use Malignancies Chronic venous insufficiency
39
What is DIC?
Over stimulation of the blood clotting mechanism and risk of impaired blood flow Clots are formed all over the body. Using up all of the platelets and clotting factors which leads to spontaneous bleeding
40
what is the mortality rate of DIC?
10% to 50%
41
What causes DIC?
* Massive tissue injury * Malignancy (cancers) * Bacterial sepsis / bacterial infection - usually gram negative bacteria b/c of endotoxins it produces * Abruptio placentae
42
What are the treatments for DIC?
Plasma transfusions or transfusion of clotting factors Treat the underlying cause
43
What is HIT?
thrombocytopenia due to HMW heparin admin
44
what causes HIT?
Heparin induced thrombocytopenia (HIT) is a clinicopathological syndrome that occurs when heparin dependent IgG antibodies bind to heparin/platelet factor 4 complexes to activate platelets and produce a hypercoagulable state. Heparin is being recognized by our immune system and we are making antibodies that target thrombocytes and get rid of our platelets
45
How long does it take for HIT to occur?
7-10 days after heparin administration
46
Treatment for HIT?
Stop heparin monitor PT PTT, INR and platelets
47
What is the pathway for fibrinolysis?
Plasminogen → plasmin (active form) → breaks down fibrin into FSP and fibrinogen into degradation products ○ tPA activates plasminogen into plasmin (active form) ○ Urokinase and streptokinase also do this ^^
48
What is TTP?
Thrombotic thrombocytopenic purpura You dont have enough of the ADAMTS13 enzyme, and since insufficient, body makes blood clots. Results in low platelets Heparin can cause TTP
49
Treatment for TTP
steroids, plasma exchange, immune lowering meds
50
What are the 2 main regulation systems of coagulation?
Fibrin inhibition Fibrinolysis
51
What are the proteases made by the liver that rapidly inactivate the coagulation proteins?
alpha1-antiprotease alpha2-macroglobulin alpha2-antiplasmin antithrombin
52
After the clot is formed, how do we break it down? (fibrinolytic system)
plasminogen is activated into plasmin by TPA (tissue plasminogen activator) urokinase streptokinase+ activator=anistreplase to break down fibrin
53
what are the 2 main functions of plasmin?
Breaks down fibrin into split products (picked up by D-Dimer) Breaks down fibrinogen locally.
54
What can we use to keep a clot from breaking down? how does it work?
Aminocaproic acid transischemic acid (TXA) inhibits the breakdown of plasminogen to plasmin
55
List the four classes of coagulation modifier drugs, how they work, and examples of each.
Anticoagulant- **Parenteral: heparin Oral: Warfarin** Inhibit the action or formation of clotting factors Prevent clot formation Antiplatelet drugs- **Aspirin** Inhibit platelet aggregation Prevent platelet plugs Thrombolytic drugs (Fibrinolytic)-**Streptokinase** Lyse (break down) existing clots Hemostatic or Antifibrinolytic drugs Promote blood coagulation
56
How does an indirect thrombin inhibitor work? Examples of this type of drug?
Enhances antithrombin activity Inactivates factor Xa Unfractionated heparin LMW heparin Fondaparinux (Arixtra)
57
What is the difference in the different types of heparin?
How purified they are: Unfractionated heparin Less purified but more effective LMW heparin More purified but less effective Fondaparinux (Arixtra) → pentasaccharide complex – 5 carbs stuck together Less effective than molecular weight or unfractionated heparin
58
How does a direct thrombin inhibitor work? Examples of this type of drug?
they directly inhibit thrombin by binding to active sites on thrombin Bind to both active and substrate recognition sites of thrombin: * Hirudin (Lepirudin is recombinant form) from leeches - saliva from leeches prevents clotting from occurring * Bivalirudin (Angiomax) Bind only to thrombin active sites - * Argatroban * Melagatran * Dabigatran (Pradaxa)
59
Explain the difference between HMW, LMW, and Fondaparinux heparins, and the use of each.
They all have a Pentasaccharide sequence. Heparin: Binds and activates AT Enhances activity (1000x) Has a High molecular weight fractions (Unfractionated) Extracted from porcine intestinal mucosa and bovine lung LMW Heparin More purified form of heparin More specific for factor Xa Less effect on thrombin Less effective on coagulation in general Examples (-parin) Fondaparinux (Arixtra) Synthetic Not as effective (selective for factor X) Less bleeding risks Useful for HIT
60
What are the toxicities and contraindications for HMW heparin?
Bleeding Transient thrombocytopenia Heparin induced thrombocytopenia (HIT) Hemophilia Thrombocytopenia Severe hypertension Intracranial hemorrhage Infective endocarditis Active TB GI ulcers Advanced hepatic disease
61
What is the reversal for heparin? How does it work?
protamine sulfate- made from salmon sperm now synthetic It is highly positive so binds to the highly negatively charged heparin thereby inactivating it
62
What is the normal INR? What is the warfarin target?
0.8-1.2 2-3
63
What is Prothrombin time?
The time it takes to clot
64
what is the normal aPTT?
35-45 seconds
65
List the oral anticoagulants
warfarin (coumadin) Factor X inhibitors
66
MOA of heparin
Blocks the γ-carboxylation of several glutamate residues (vitamin K dependent) Targets 2,7,9,10 Binds and activates antithrombin
67
Where was warfarin discovered and what was it initially used for?
Discovered by University of Wisconsin as cause for cattle hemorrhagic disease Wisconsin Alumni Research Foundation -arin originally meant as rat poison
68
Pharmacokinetics of warfarin
100% oral availability Protein binding = 99% Long half-life = 36 hours
69
What are the fibrinolytic drugs?
Streptokinase urokinase t-PA - alteplase
70
What are the targets for aspirin?
COX-1 Selective - platelet TXA2 causes platelets to change shape, Granule release, and Aggregation Inhibition of TXA2 synthesis increases bleeding time
71
MOA of Clopidogrel (plavix) and ticlopidine (Ticlid)
Irreversibly inhibits ADP receptor on platelets causing reduction in platelet aggregation
72
MOA of Abciximab
IIb/IIIa receptor blocker found in the common pathway Inhibits platelet aggregation
73
How can bleeding disorders be treated with Vitamin K?
Necessary for efficient blood coagulation Fat soluble vitamin Comes from: Leafy green vegetables Gut bacteria Confers activity on: Prothrombin (primarily affect this) Factors VII, IX, and X
74
How can bleeding disorders be treated with plasma fractions?
We can give plasma to treat bleeding disorders; replaces clotting factors. Whatever they are missing, we can isolate that factor and give to patient
75
How can bleeding disorders be treated with desmopressin acetate?
Desmopressin Increases factor VIII activity Good for Mild hemophilia A Also good for von Willebrand disease
76
How can bleeding disorders be treated with aminocaproic acid(fibrolytic inhibitor)
Competitively inhibits plasminogen activation Stabilizes clot; prevents clot breakdown Use Adjunctive hemophilia therapy Bleeding from fibrinolytic therapy Intracranial aneurysms Post surgical bleeding
77
How can bleeding disorders be treated with Tranexamic acid (TXA)
Helps to stabilize clot and prevent clot breakdown→helps blood to clot to stop bleeding Decreased risk of death in major bleeding Used for: Trauma, heavy menstrual bleeding, postpartum, epistaxis So used for more massive bleeds MOA Antifibrinolytic Inhibits plasminogen->plasmin

Fall 2024 (86 decks)

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