Pharm > Coagulation Disorders > Flashcards

Coagulation Disorders Flashcards

Test 4 (98 cards)

Study These Flashcards
1
Q

What does hemostasis mean?

A

The ability of the body to stop itself and bleeding out

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

Coagulation causes ______

A

hemostasis

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

What causes injury?

A

A break in the epithelial or endothelial layers

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

What activates the clotting cascade?

A

Exposed collagen & vWF from injury to the endothelial layer

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

vWF =

A

Von Williebrand Factor

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

What does a red thrombus consist of vs a white thrombus?

A

Red: lots of RBC trapped in a vein

White: fibrin & platelets in an artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is an embolism?

A

When a thrombi breaks off & moves through vessels

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

What does thrombogenesis mean?

A

Formation of a thrombi

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

Describe how thrombogensis works

A

A brick & mortar structure that will clog a bleeding area

Bricks = platelets
Mortar (glue) = fibrin

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

Damage to blood vessels cause ________

A

Vasoconstriction

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

What does serotonin do in ther peripheral vascular?

A

increases vascular tone

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

T/F: Thrombocytes are cells

A

F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are Thrombocytes?

A

Components that are broken off of megakaryocytes

they allow for platelet aggregation by degranulation to activate other platelets in the are

this allows platelts to stick together by fibrin & form a clot

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

Define coagulation

A

Forming a clot

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

Define Fibrinolysis

A

dissolving an existing clot (lyse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the 4 platelet phases

A
  1. exposure of collagen & vWF -> causes platelets to ADHERE to surface
  2. adhesion to the surface causes platelet AGGREGATION
  3. platelets SECRETE substances: serotonin (primary) ADP, TXA2
  4. The secretion encourages CROSS-LINKING OF ADJACENT PLATELETS which allows a clot to form (coagulation)

AASC

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

A megakaryocyte is a _______ cell

A

bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What do endothelial cells produce? What does this do?

A

PGI2 - prostacyclin (part of AA cascade)

Inhibits platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does prostacyclin (PGI2) do?

A

Inhibit platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the platelet aggregation pathway

A
  1. Cell wall damage d/t injury to the epithelial and endothelial cells; This releases collagen & vWF
  2. Collagen binds to GP1a receptor & vWF binds to GP1b receptor which causes a signaling in the platelet & activates the release of Serotonin, ADP, & TXA2 (Thromboxane A2)
  3. Once released, these bind to their respective receptors on other platelets which causes degranulation.
  4. A positive feedback system is activated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

T/F: both platelet aggregation and coagulation cascade are required in order to form a staple clot

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 2 clotting cascade pathways called?

A

Intrinsic (Inside): damage to endothelial

extrinsic (outside): exposes tissue factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the common pathway in the clotting cascade? What does this mean?

A

Xa

Both pathways meet here

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

What does factor Xa do?

A

Converts Prothrombin to Thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the active form of Prothrombin?
Thrombin
26
What general effects does Thrombin have?
-Converts Fibrinogen to Fibrin -Activates platelets -Increases production of more thrombin
27
What is the active form of fibrinogen?
Fibrin
28
When you get to ________ you are in the common pathway
factor Xa
29
Describe the extrinsic pathway in the clotting cascade
1. Trauma activates factor VII 2. factor VII -> factor X 3. factor Xa --> converts prothombin to thrombin 4. thrombin -> activates platelets & converts fibrinogen to fibrin
30
What factors are involved in the extrinsic pathway in order?
7 10 2 1 13
31
Describe the intrinsic pathway in the clotting cascade
1. Trauma to the endothelial layer activates factor XII 2. factor XII -> XI 3. XI -> IX 4. IX -> X 5. factor Xa --> converts prothombin to thrombin 6. thrombin -> activates platelets & converts fibrinogen to fibrin
32
What is thrombin's MAIN effect?
convert fibrinongen to fibrin
33
What factors to thrombin effect? How?
-Activates factor XIII (13): allows for cross link -- V (5): assists factor Xa -- IIX (8): assists Xa but isnt needed -- XI (11): intrinsic cascade -- Protein C: C+S INHIBIT factor V & IIX
34
Active protein C inhibits which factors? What does this cause?
Factors V & IIX Prevents conversion of prothrombin to thrombin
35
What does antithrombin do?
Blocks thrombin & has effects on factor X
36
What factors are your thrombin activators?
5, 8, 11, 13, & Protein C
37
What factors are your thrombin inhibitors?
Protein C with 5 & 8 Antithrombin with 10
38
What factors are involved in the intrinsic pathway in order?
12 11 9 10
39
What factor is prothrombin/thrombin?
II 2
40
What is hemophilia?
Factor 8 deficiency
41
Where do DVTs form?
Large veins of lower limbs
42
DVT =
Deep vein thrombosis
43
Why are DVTs an emergency?
They are in the veins. They are break off go into the heart and into the pulm artery and cause a PE.
44
What type of thrombi is associated with DVTs?
Red Thrombi
45
What is Virchow's Triad? How is that related to DVTs?
1. Stasis: decreased skeletal muscle movement = decreased blood flow 2. Hypercoagulability: dt genetics or leaky veins esp varicose veins 3. Endothelial injury: exposes collagen **SHE** Increases the likelihood of developing DVTs
46
Describe a white thrombus
-platelets & fibrin crosslinked **occurs in high pressure arteries** -will get stuck in capillary beds downstream Caused by damage to endothelium; plaque
47
Describe a red thrombus
-RBC around a white thrombus (platelets & fibrin) **occurs in veins** --has a long tail d/t being built up for awhile d/t low pressure area **High Risk for PE**
48
What are DVT risk factors?
Genetics: Antithrombin III deficiency, Protien C deficiency, Protein S deficiency, Sickle cell anemia, Activated protein C resistance Lifestyle: Bedridden, surgery, trauma, obesity, estrogen, use, malignancies, chronic venous, insufficiency
49
How does sickle cell anemia contribute to DVT risks?
RBC become trap and damage endothelium cells
50
How often should you stretch her legs when flying for a long time?
Every 2-3 hours
51
Why is it important to keep coagulation localized?
unregulated coagulation can cause DIC (microclots everywhere)
52
Describe DIC
Disseminated coagulation Microclots everywhere Uses up all platelets & clotting factors Increases risks of bleeding out **medical emergency** High mortality Causes: Trauma; gram neg. bacterial infection/sepsis, cancer, abruptio placentae
53
What is the Tx for DIC?
Plasma/Platelet transfusion Tx underlying cause
54
What are 2 ways to prevent over coagulation?
Fibrin inhibition Fibrinolysis
55
What are the 3 proteins that break down active clotting factors?
A1-antiprotease A2-macroglobulin A2-antiplasmin
56
What 4 things rapidly inactivate coagulation proteins?
A1-antiprotease A2-macroglobulin A2-antiplasmin antithrombin
57
What does plasminogen convert to? what does it do?
plasmin -Regulation of coagulation by breaking down & limiting fibrin/fibrinogen into split products - remodels & limits extension of thrombus
58
Describe endogenous tPA
Tissue plasminogen activator Released from injured cells **Converts plasminogen to plasmin**
59
What 3 things permit conversion of plasminogen to plasmin?
tPA Urokinase Streptokinase
60
What 2 things protect clots from lysis and stop conversion of prothombin to thrombin?
Aminocaproic acid TXA
61
What are the 4 classes of coagulation modifiers?
1. Anticoahulants: prevent clot formation 2. Antiplatelets: inhibit platelet aggregation 3. Thrombolytics/Fibrinolytic: breakdown existing clots 4. Hemostatics/Antifibrinolytics: promote blood coagulation
62
Where are coagulation factors produced?
Liver
63
What is the antiplatelet prototype?
ASA
64
What is the anticoagulant oral prototype?
Warfarin
65
What is the anticoagulant IV prototype?
Heparin
66
What is the thrombolytic prototype?
Streptokinase
67
Drugs: Heparin Please list and compare all 3
Class: Indirect Thrombin inhibitor MOA: Binds & activates antithrombin (conformational change) enhance AT activity 1000x -> inactivates factor Xa -> inhibits thrombin 1. Unfractioned Heparin -MW 5,000-30,000 -unpurified -made from pig intestine/cow lung 2. LMW Heparin -More specific for factor Xa -> less effect on thrombin -> less effect on coagulation -**-parin** 3. Fondaparinux -Pentasaccharide -synthetic -Selective for factor X --> least effective --> least bleedind risk -no interaction with thrombin
68
What lab is used for heparin?
aPTT PT
69
Which heparin is useful for HIT?
Fondaparinux
70
What is the suffix for LMW heparin?
-parin
71
Describe HIT
Heparin Induced Thrombocytopenia - heparin recognized by immune system, and making antibodies against it - antibodies target are thrombocytes which deplete our platelets - **occurs 7-10 days after given heparin**
72
Differentiate between PT, PTT and INR
PT/PTT -- Heparin -- Time to clot INR -- Warfarin --Time to clot compared to control
73
What labs use for warfarin?
INR
74
What are normal INR ranges?
Normal: 0.8 - 1.2 While taking warfarin: 2 - 3
75
What is the normal values for aPTT? what have to be added to this lab?
35-45 phospholipids
76
Drugs: Protamine Sulfate
**Heparin Antidote** MOA: (+) charged drug; Heparin is (-) -> they bind and inactivate each other Only want to give enough to counter heparin **EXCESS CAUSES ANTICOAGULANT** Most effect on unfractioned No effect on fondaparinux
77
What are heparins contraindications related to?
Bleeding **Advanced hepatic disease related to clotting factors**
78
Drugs: Lepirudin (Hirudin)
Class: Direct Thrombin inhibitors **Comes from leech saliva** Some surgeons still use leeches MOA: Bind to both active & substrate recognition sites of thrombin
79
Drugs: Argatroban; Dabigatran (Pradaxa)
Class: Direct Thrombin Inhibitors MOA: Bind only to thrombin active sites
80
Drugs: Warfarin
Class: Coumarin Anticoagulant PO **MOA: Blocks gamma-carboxylation of glutamate residues on cloting factors 2, 7, 9, & 10. - Prevents recyclin of vitamin K by inhibiting Vitamin K reductase** Discovered by University of Wisconsin Originally was a rat poision 100% PO bioavailability **99% protein binding** 36 hours half life
81
When is warfarin taking?
When weaning off heparin
82
What clotting factors does heparin effect?
2 7 9 10
83
T/F: You can take warfarin while pregnant
F
84
Warfarin reduces prothrombin activity to ____ of normal
25%
85
T/F: warfarin is metabolize differently in different people, so everyone will need a different does
T
86
Drug: Vitamin K
**Warfarin ANTIDOTE** Confers activity on: Factors VII, IX, X, and prothrombin Good sources come from green leafy vegetables & gut bateria
87
How do you reverse warfarin?
Stop drug Vit K FFP Factor IX concentrates
88
Drugs: Rivaroxaban; Apixaban
Class: Indirect Thrombin inhibitors MOA: Factor Xa inhibitors -> less specific for thrombin -> clotting cascade more closely controlled **No reversal**
89
Drugs: tPA, Streptokinase, Urokinase
Class: Fibrinolytics MOA: Lyse thrombi; catalyze formation of plasmin
90
Drugs: Aspirin
Class: Antiplatelets MOA: Blocks COX1 which also inhibits Thromboxane A2 synthesis -> increases bleeding time
91
When should you stop taking aspirin before Sx?
A week beforehand
92
How many half life's before a drug is out of your system?
4
93
Drugs: Clopidogrel (Plavix)
Class: Antiplatelet MOA: Irreversibly inhibit ADP receptor on platelets -8.7% reduction in ischemic events in comparison to aspirin
94
Drugs: Abiciximab
Class: Monoclonal antibody/antiplatelet MOA: Block IIb & IIIa receptors on platelets preventing degranulation and aggregation
95
What are plasma fractions?
Isolations in plasma blood where we can get specific factors that we need Ex) we can isolate and give a patient plasma with factor 8 in hemophilia
96
Drugs: FFP
Plasma is what our clotting factors are in girl!!!!!!!!!!!
97
Drugs: Desmopressin
Class: ?? MOA: Increases Factor VIII activity Tx: Mild hemophilia A; Von WIlliebrand disease
98
Drugs: Aminocaproic acid; Tranexamic acid
Class: Fibrinolytic inhibitor MOA: competitively inhibits plasminogen conversion to plasmin -stabilizes clot & prevents breakdown Aminocaproic acid Uses: Post surgical, bleeding, intracranial, aneurysm, bleeding from tPA, hemophilia therapy Tranexamic acid uses: decrease risk of death in major bleeding in: trauma, postpartum, epistaxis, heavy menstrual bleeding
Pharm
flashcards
Decks in class (30)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions