Brainscape's Knowledge GenomeTM

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


See full index

PHARMACOLOGY > Homeostasis and Treatment of Coagulation Disorders > Flashcards

Homeostasis and Treatment of Coagulation Disorders Flashcards

1
Q

hemostasis

A

normal (regulated) activation of blood coagulation system in response to vascular damage (stop blood flow)

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

coagulation

A

blood clot

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

problems with hemostatic defects

A
  1. thrombosis - blockage of vein/artery resulting from inappropriately activated/persistent blood clot
  2. hemorrhage - loss of blood from arteries/veins due to injury or aneurysm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hemostatic systems

A
  1. coagulation factors: plasma proteins (serine proteases) - involved in blood clot formation after injury
  2. platelets: cell fragments form primary plug - involved in blood clot formation + release mitogenic factors - aid in repairing damaged blood vessels
  3. fibrinolytic system: plasma proteases: remove fibrin clots once repair to damaged blood vessel occurs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

heparin

A

natural compound = inhibit blood clot (inhibits cleavage of factors)

a form = active form

inactive form = zymogen
activated by cleavage

more selective for 2a than 5a

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

clotting pathways

A

extrinsic pathway = activated in response to tissue injury
V11a (7) tissue factor + phospholipid (PL) + Ca2+
convert X >Xa (10)

intrinsic pathway: glass surface activates XII (12)
activating XII (12), XI (11), IX(9)
IXa + VIIIa + PL + Ca2+ = activate X

common pathway: Xa (Va + PL + Ca2+)
convert prothrombin (II) > prothrombin (IIa)
= converts fibrogen > firbrin monomers
= XIIIa converts > fribin polymer

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

functional assessment of coagulation

A

prothrombin time (PT)

  • tests extrinsic + common pathways
  • addition of tissue factor, calcium, and PL
  • 10-13 secs

activated partial thromboplastin time (aPPT)

  • tests intrinsic + common pathways
  • addition of activating surface, Ca2+, and PL
  • 35-55 secs

(reproducible - store blood for future use)

whole blood clotting time

  • whole blood drawn into glass tube (activating surface)
  • tests for disorders in any aspect of coagulation
  • 2-3 minutes (done there and then)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

inherited disorders of coagulation

A

hemophilia A - deficiency/defect factor VIII (8)

hemophilia B - deficiency factor IX (9)

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

treatment for hemophilias

A

plasma factor concentrates factor 8+9

  • purified from pooled human plasma donors
  • risk of transmission of infectious disease (HIV/Hepatitis)

hemophilia a = RECOMBINATE

  • recombinant form of factor 8
  • produced in CHO cells

hemophilia b = BENEFIX

  • recombinant production of factor 9
  • produced in CHO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

anticoagulants

A

used to prevent occurrence/progression of deep vein thrombosis/pulmonary embolism

carefully monitored to avoid overdose with hemorrhage

effects may be increased with liver disease + antiplatelet drugs

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

intravenous anticoagulants

A

HEPARIN

  • activate antithrombin III
  • extracted from animal tissues
  • direct inhibitor of serine protease of intrinsic/common pathway factors
  • rapid onset of action - monitored by aPPT
  • low molecular weight = more reproducible
  • rare se: osteoporosis/hypoaldosteronism/elevated K+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

oral anticoagulants

A

WARFARIN

  • inhibitor of intrinsic/common pathways
  • vitamin K antagonist
  • interferes with activation of 9,10,7,2
  • used for long-term anticoagulant therapy
  • teratogenic
  • monitored with PT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PT measurements are normalized

A

. PT - measured in tandem with patient sample
. patient PT converted to International Normalized Ratio (INR) (dividing patient clotting time by standard clotting time)
. dose of warfarin adjusted to give INR between 2-4

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

side effects of warfarin

A

risk of intracranial bleeding with INR>4
skin necrosis associated with genetic protein C/S deficiency
teratogenic - first trimester

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

drugs that interact with warfarin metabolism by mixed-function oxidase (cytochrome P450)

A

disulfiram
fluoxetine
clopidogrel
bile acid resins

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

roles of platelets in hemostasis

A
  • platelets are activated by contact between glycoprotein receptors on platelet surface + collagen exposed during cell wall injury
  • platelets adhere to damaged site + provide PL for the formation of 10a + 11a
  • aggregation of platelets further stimulated by thromboxane + ADP
  • platelets form nucleus for clot formation
  • clot = cluster of platelets cross-linked by fibrin
17
Q

platelet aggregation + activation

A

adhesion of platelets to damaged surface

release of ADP

synthesis of thromboxane

expression of aggregation receptors: glycoprotein 2b/3a

crosslinking of platelets by binding of firbin to glycoproteins receptors

18
Q

antiplatelet aggregation agents

A

ASPIRIN = inhibits Cox 1 blocking synthesis of thromboxane
long-term effect = platelets cannot synthesize new cox-1

prevent atherosclerotic plaques, pulmonary embolism, strokes

contraindicated if patient is being treated with anticoagulants/liver disease

//others: TXA2 R antagonists
GP IIB/IIIa expression inhibitors/receptor antagonists
19
Q

CLOPIDOGREL

A

competes with ADP for binding to ADP receptor on platelets = prevents expression of glycoprotein R for fibrin

inactive when administered, requires metabolism by cytochrome P450

fewer problems with GI irritation than aspirin

20
Q

Optical Aggregometry

A

measures the quantity of light passing through a sample of platelet-rich plasma (PRP) using platelet-poor plasma as a reference

Addition of a platelet agonist to PRP causes
platelets to aggregate & fall out of solution producing an increase in % transmittance of the sample

21
Q

Impedance Aggregometry

A

Measures the electrical current passing between
two electrodes placed in whole blood.

Addition of a platelet agonist causes platelets to
aggregate on the electrode surface resulting in a decrease in current between the electrodes

22
Q

Quantitative Platelet Disorders

A

• Thrombocytosis*: (>700,000 platelets/µL), can
be caused by malignancies of the megakaryocyte lineage, splenectomy, anemia or rebound from thrombocytopenia

• Thrombocytopenia: (<50,000/µL), can be caused by autoimmune diseases, transfusion reactions, radiation, chemotherapies, extracorporeal circulation, and heparin

23
Q

Treatment of Platelet Disorders

A

• Thrombocytosis:
HYRDOXYUREA + APIRIN + APLHA INTERFERON
(side effect: nausea, diarrhea, seizures)

• Thrombocytopenia:
CORTICOSTEROIDS / PLATELET RICH PLASMA

24
Q

The Fibrinolytic System

A
  • Initiated after coagulation occurs
  • Active agent is plasmin, a serine protease = degrades fibrin and factors II, V, and VIII
  • Plasminogen is inactive precursor of plasmin
  • Endogenous plasminogen activators include tissue plasminogen activator (tPA) and kallikrein
25
Q

Fibrinolytic Drugs

A

• Activate plasminogen to form plasmin

STEPTOKINASE

• Used primarily to treat acute myocardial infarct (MI) and prevent a 2nd heart attack (must be used within 12 hrs of original MI to be effective)

PHARMACOLOGY (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions