Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology Exam 3 > Coagulation Lectures > Flashcards

Coagulation Lectures Flashcards

1
Q

What is hemostasis

A

A process where an injured blood vessel triggers a series of reactions

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

How does hemostasis work

A

Formation of platelet fibrin to plug injury site to stop blood loss.

Clot will dissolve gradually as healing advances

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

What are the components of Hemostasis

A

Coagulation factors

Platelets

Endothelium - vessel wall

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

What is the role of platelets in coagulation?

A

Adherence to injury site where collagen is exposed

platelets activate by thrombin.

Release ADP, Vasoactive amine and form Thromboxane A2

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

What does Thromboxane do?

A

Contracts Smooth Muscle - Causes vasoconstriction - stops blood leakage

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

What are the steps of clot formation

A

Procoagulant proteins are activated by proteolytic cleave to form a clot

Goal is to product thrombin

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

How does thrombin work?

A

Convers fibrinogen to fibrin - makes fibrous network in clot

Promotes platelet aggregation to seal injury as well

Also activates cofactors (V and VIII) and factors to lyse clot

Activates protein C to prevent uncontrolled thrombosis

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

Describe control of Coagulation

A

Clotting cascades and platelets are inhibits by vascular endothelium and continuous blood flow

Natural anticoagulant proteins

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

What are some of the anticoagulant proteins?

A

Anti-Thrombin III - binds to heparin and thrombin to inactivate

Protein C - cleaves factors V and VIII

Protein S - cofactor to protein C

Tissue Factor Pathway Inhibitor - Inhibits Xa and VIIa-TF complex

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

What are physiologic Anticagulants

A

Antithrombin III

Protein C and S

Tissue Factor Pathway Inhibitor

Thrombomodulin

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

Describe Fibrinolysis

A

Fibrin is degraded by plasmin

Plasminogen is activated by TPA

Fribinolysis is inhibited by plasminogen activator inhibitors (PAIs) and Alpha 2-Antiplasmin

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

Role of Vitamin K in Coagulation

A

All serine proteases require post translational mods which require Vitamin K

Need vitamin K and adequately functioning liver

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

What is the most widely used anticoagulant drug?

A

Warfarin (Coumadin) interferes with Vitamin K Dependent reactions

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

What does Prothrombin Time measure?

A

PT measures procoagulant activity of factors VII, X, V, II and fibrinogen.

PT normal range is 9-12 seconds.

Results compared to an International Normalized Ratio = 1.0 = normal

Long PT = Deficiency of Vit. K factors

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

What does Activated Partial Thromboplastin Tim (APTT/PTT) measure?

A

Measures the procoagulant activity of entire pathway

Most sensitive to XI, VII, and IX. not effected by VII

Can be prolonged also by drugs like heparin.

25-32 seconds

Hemophiliacs = prolonged

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

Thrombin Time (TT) measurement

A

Measures platelet and vessel interaction, # and function of platelets

Performed by making cut on forearm

Tim to clotting is measured

2-9 minutes. Severe platelet decrease will prolong bleeding time

prolonged by Von Willebrand disease

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

PFA-100

A

New - Platelet Function Analyzer

Tests in vitro bleeding time

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

What is Hemophilia A and B a deficiency of?

A

Factors VIII and IX

X-Linked

Females are carriers

Prolonged PTT

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

Describe Hemophilia A

A

Factor VIII deficiency - Most common cause of severe bleeding tendency

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

Describe Hemophilia B

A

Christmas disease or Factor IX deficiency

10 times less common than A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Severe Hemophilia

A

<1%
Spontaneous hemorrhaging

Early Death before factor replacement therapy.

Can lead to severe arthritis

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

Moderate Hemophilia

A

2-5%

Takes some degree of trauma to cause bleeding

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

Mild Hemophilia

A

10%

Only bleed after trauma

Need specific factor therapy to resolve bleeding

Can have hematoma formation, wound breakdown, disability if not treated during surgery

Dinged after bad traumatic event or surgery

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

Carrier Females

A

30%-100%

Carriers can be mildly affected or normal

Carriers w/bleeding - symptomatic carrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Factor IX Deficiency
Congenital Disorder - autosomal recessive Spontaneous bleeding is rare Ashkenazi Jews in US and Middle East Post-Operative Hemorrhage Prolonged PTT
26
Von Willebrand Disease
Most common congenital - Autosomal dominant Large protein in plasma Adheres platelets to collagen = prolonged bleeding time Carries Factor VIII = decreased factor VIII prolongs PTT Nose bleeds/Mucosal bleeds
27
What are the two types of Von Willebrand disease?
Type 1 - Deficiency - Treat with DDAVP Type 2 - Abnormal Protein 2b - Abnormal clearance of platelets Type 3 - severe or total deficiency
28
6 Tests for Von Willebrand Disease
1. Bleeding Time - Platelet function 2. vWF Antigen - Amount of factor 3. VWF activity - function of factor to aggregate platelets 4. Factor VIII activity - ability to carry VIII 5. Multimeric Analysis - Loss of large forms 6. RIPA - hyperaggrebility to ristocetin to diagnose type 2b
29
Acquired bleeding disorders that cause prolonged PTT
``` Herpain in sample Hemophilia A and B Factor XI Deficiency Factor XII Deficiency - no bleeding Acquired Hemophilia Von Willebrand Disease Lupus Anticoagulant - No bleeding ```
30
Acquired bleeding disorders that cause prolonged Pro Time
1. Protime more prolonged than PTT = liver disease, Vit. K Deficiency, Warfarin/Rat Posion 2. PTT more prolonged = Disseminated Intravascular Coagulation (DIC)
31
How does Liver Disease affect Coagulation?
Can cause deficiencies in clotting factors. Severe liver disease = Low Fibrinogen = possible Thrombin prolonged Prolonged Protime Consumption of platelets by spleen Deficiencies in antithomrbin III and Protein C/S
32
How does Vitamin K Deficiency Affect Coagulation
Prolonged protime Occurs when patients do not intake Vit. K through diet Broad Spectrum Antibiotics can kill gut flora (makes Vit. K)
33
How does Long Acting Fat Soluble Rat Points affect coagulation?
Used in suicide attempts Extremely prolonged protime and PTT Intensive Vit. K therapy for months is required
34
Disseminated Intravascular Coagulation (DIC)
Can be caused byMassive Trauma, hemorrhagic, septic shock, amniotic fluid embolism, burns, acute leukemia Micro thrombi plug capillaries and causes tissue infarction Coagulation Factor deficiencies Low levels of fibrinogen and platelets Prolonged PTT due to fibrin split products
35
Abnormalities in DIC (6)
``` Prolonged PT Greatly Prolonged PTT Prolonged Thrombin Time Low platelet count Low fibrinogen level Increased fibrin split products ```
36
Define Thrombosis
Formation of clot within vasculature Occurs with stasis, inflammation and vessel wall injury
37
Virchow's Triad
1. Decreased blood flow (venous stasis) 2. Inflammation of or near the injured Blood vessel 3. Intrinsic alterations in nature of the blood
38
When do arterial thrombi occur?
Conditions of shear stress Composted of aggregated platelets (white thrombi)
39
What abnormalities can contribute to Arterial thrombi development?
hypertension & turbulent blood flow @ arterial branch points and sites of atherosclerosis
40
What blood vessel abnormalities contribute to Arterial thrombi (5)
intraluminal vascular endothelial cell injury atherosclerotic plaque rupture Hyperhomocysteinemia Aneurysm foramtion Vessel Dissection
41
When does Venous Thrombi occur?
Slow blood flow (low shear stress) Composted of large amounts of fibrin (red thrombi)
42
What factors contribute to venous thrombi? (7)
``` R. Side heart failure, Pre existing thrombosis Tumor compression Immobility Obesity Chronic venous insufficiency Increased Age ```
43
What are some Symptoms of Venous Thromboembolic Disease?
50% Asymptomatic Phlegmasia ceruleans dolens (swollen, blue, painful leg) Pain Pitting Edema Warm,Dusky,Reddish-blue discoloration on skin
44
Complications/Consequences of Extermity DVT
Postthombotic Syndrome - Chronic Swelling, cutaneous ulcers Pulmonary Embolus - Infarct
45
Classic Signs and Symptoms of PE (6)
``` Chest Pain Dyspnea Anxiety Cough Syncope Cyanosis ```
46
Diagnosis of DCT and PE
D-Dimer Assay - only occurs in clots Venous UltraSound - Measures blood flow/pressure 95% specificity to symptomatic DVT Spiral CT for PE and V/Q scans
47
Treat of Arterial Thrombosis
Acute: Heparin and Fibrinolytic agents (tPA) Prevention: Antiplatelet agents: aspirin, thienopyridines, ticlopidine, clopidogrel
48
Treatment of DVT and PE
Acute: Heparin - to activate antithrombin III Long term:Oral Anticoagulation with Warfarin: doesn't affect coagulation factors that are already released. Heparin therapy at least 5 days after starting
49
How long is anticoagulation therapy generally
Individual basis: must determine if DVT occurred due to transient risk factors or underlying disorder Location of clot influences
50
Hypercoagulable States
Exist when: chronic damage to vessel walls Excess of procoagulant factors deficiency of anticoagulant factors
51
What are 4 clues to underlying Hypercoagulable state
1. Thrombotic episode in absence of conditions 2. Recurrent episodes of thrombosis 3. Severe, life threatening thrombosis 4. Family History
52
What is Factor V Leiden Inherited Thrombotic Disorder?
Autosomal Dominant mutation of Factor V Gene Inactivation through proteolytic cleavage of protein C most common in northern european caucasian populations
53
What is Prothrombin G20210A Gene Mutation Inherited Thrombotic Disorder?
Second most common Elevated concentrations of plasma prothrombin
54
What is Protein C Deficiency Inherited Thrombotic Disorder?
Autosomal Dominant Heterozygotes more effected 31 fold increased risk Large Doses of Warfarin increase risk
55
What is Protein S Deficiency Inherited Thrombotic Disorder?
Autosomal Dominant Pts. present with VTE or Arterial Thrombosis including stroke
56
Antithrombin Deficiency
Autosomal Dominant Homozygous fatal in utero 40 fold thrombosis risk Can lead to heparin resistance
57
Hyperhomocyteinemia
Inherited or acquired Increased risk of thrombosis enhanced platelet activation due to endothelial cell injury
58
Increased Factor VIII Activity (>150%)
3-6 fold greater risk of VTE 11 fold @ >200%
59
Impaired Fibrinolysis
Plasminogen Deficiency, tPA deficiency Increased thrombosis risk
60
Oral Contraceptives
Increased thrombosis risk by altering coagulation factor levels
61
The Lupus Anticoagulant
Common Acquired Abnormality - Hypercoaguable State IgG Antibody Antiphopholipid Antibody Syndrome (APL) Prolongs PTT No bleeding tendency Thrombotic Syndrome

Pathology Exam 3 (4 decks)

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