Brainscape's Knowledge GenomeTM

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


See full index

NUR 612 Advanced Pathophysiology > Module 2.7 Hemostasis > Flashcards

Module 2.7 Hemostasis Flashcards

1
Q

Heparin reversal agent

A

Protamine Sulfate

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

Where does heparin act in the coagulation path

A

Inhibits Factor X to produce fibrin formation.

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

Which pathway does PTT measure?

A

Intrinsic (Play Table Tennis Inside)

Used to measure heparin effect

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

Which pathway does PT measure

A

Extrinsic (Play tennis outside)

Used to measure Warfarin effect.

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

How is platelet function measured

A

Bleeding time test.

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

3 phases of restoring hemostasis

A
  1. Vessel Spasm
  2. Formation of platelet plug.
  3. Blood Coagulation or development of an insoluble fibrin clot.

(Spazz, plug, clot)

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

Vessel spasm in hemostatic restoration

A

Spasm is transient (minutes-hours)

Mechanically slows blood flow to the area.

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

What initiates vessel spasm

A

cytokines

Prostaglandins (Thromboxane A2, Prostacyclin)

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

Thromboxane A2

A

causes constriction

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

Prostacyclin

A

Causes dilation, inhibits platelet aggregation in normal uninjured vessels

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

Half life of platelets

A

8-12 days

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

What produces platelets

A

megakaryocytes

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

Listen at 7:30

A

Listen at 7:30

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

Vitamin K is soluble in

A

fat only

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

Requirements for clotting

A

Platelets
Von Willebrand Factor
Clotting Factors

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

Where is Von Willebrand factor generated

A

by the vessel endothelium

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

Where are clotting factors synthesized

A

in the Liver using Vitamin K

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

Antithrombin III

A

Contains naturally occurring heparin

Protects against uncontrolled thrombus formation

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

Protein C

A

Plasma protein

Acts as anticoagulant by inactivating factors V and VIII

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

Intrinsic Pathway

A

Slow

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

Extrinsic Pathway

A

Fast

Trauma response

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

Where do the intrinsic and extrinsic pathways become the same

A

Activation of Factor X

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

Describe the activation of the coagulation pathway after factor X

A

Xa activates prothrombin to thrombin

Thrombin activates fibrinogen to fibrin

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

Listen to 13:50 Mark)

A

Listen to 13:50 Mark)

25
Q

Listen to khan academy vid on clotting

A

Listen to Khan Academy vid on clotting

26
Q

Protein S

A

Accelerates the action of protein C

27
Q

Negative feedback systems in clotting cascade

A

Proteins S and C
Plasminogen > Plasmin breaks down fibrin mesh into fibrin degradation products
Thrombin stimulates anti-thrombin production

28
Q

Anti-thrombin action

A

inhibits conversion of prothrombin to thrombin

By inhibiting activation of factor X (which is the common pathway!!)

29
Q

Warfarin MoA

A

Affects vitamin K and therefore dependent factors

NOT IMMEDIATELY REVERSABLE

30
Q

Heparin MOA

A

Affects factor X without other clotting factors

IMMEDIATELY REVERSIBLE

31
Q

Heparin is measured with

A

PTT

32
Q

Warfarin (Coumadin) is measured with

A

PT

33
Q

What may also decrease vitamin K levels other than Coumadin

A

Antibiotics (kills bacteria needed for absorption)

Clofibrate

34
Q

Conditions that cause increased platelet function

A 
Atherosclerosis 
Diabetes
Smoking
HLD and high cholesterol
Pregnancy (estrogen increases coagulation)
Protein S and C deficiency
35
Q

Leiden mutation

A

Factor V mutation
Decreased Protein C effect
Hypercoagulability

36
Q

Virchow’s Triad

A

Vessel Injury
Stasis
Hypercoagulable state

37
Q

Antiphospholipid syndrome

A

IgG antibodies directed against phospholipids

Recurrent venous and ARTERIAL thrombi

DVT’s, arterial thrombosis in coronary, renal and peripheral arteries

Recurrent pregnancy loss

TIA’s

38
Q

Risk factors for hypercoagulability states

A 
Pregnancy and puerperium
Oral contraceptives (estrogen)
Post-surgical state
Virchow's Triad/immobility
Congestive Heart Failure
Malignant diseases
39
Q

Thrombocytosis

A

> 1,000,000 platelets/uL

Due to increased thrombopoietin production

40
Q

Primary thrombocytosis

A

bone marrow disorders - increased platelet production.

Often dysfunctional platelets.

41
Q

Secondary Thrombocytosis

A

Disease states causing more platelet production

Post-op
Infection
cancer
CHRONIC INFLAMMATORY CONDITIONS
Myeloproliferative disorders.
42
Q

Arterial thrombi are associated with

A

turbulent blood flow.

43
Q

Venous thrombi are associated with

A

stasis

44
Q

Thrombocytopenia

A

<150,000 platelets/uL

clinical issues really start at <100k though.

45
Q

Causes of thrombocytopenia

A

Decreased platelet production secondary to decreased thrombopoietin.
Increased sequestration of platelets in spleen.
Decreased Platelet survival
Impaired platelets function

46
Q

Types of thrombocytopenia

A

Drug induced
Immune thrombocytopenia purpura (ITP)
Thrombotic hrombocytopenia purpura

47
Q

Immune thrombocytopenia purpura (ITP)

A

autoimmune
increased platelet antibody formation
usually follows viral infections in children
DOESN’T INVOLVE CLOTTING FACTORS

48
Q

Manifestations of thrombocytopenia

A

Bleeding (nose, mouth, GI
Petechiae - pinpoint purple-red spots
Purpura - PURPLE areas
Splenic enlargement in ITP due to sequestration. Possible Splenectomy.

49
Q

Vitamin K deficiencies

A

Antibiotics - kill bacteria needed for absorption

Impaired fat absorption (bile salts!)

50
Q

Hemophilia A

A

Factor VIII deficiency (30% of new cases are new mutations!!!)
X-linked recessive

ayyyy 8

51
Q

Hemophilia B

A

Factor IX deficiency

X-Linked Recessive

52
Q

Von Willibrand Disease

A

Autosomal Dominant (type 1 and 2)
Autosomal recessive for type 3 (rare)
Normal platelet count
Increased bleeding time

53
Q

Hemorrhagic Telangiectasia

A

Autosomal Dominant

thin walled vessels, dilated capillaries and arterioles

54
Q

Cushing Diseases

A

protein wasting and loss of vessel tissue support due to increased cortisol

55
Q

Vit. C Deficiency

A

Scurvy

Poor collagen synthesis and failure of endothelial cells to cement together

56
Q

Senile Purpura

A

old person bruising

57
Q

Disseminated Intrvascular Coagulation (DIC)

A

Consumptive process. System wide clotting cascades via INTRINSIC system.

All components of cascade wiped out. Severe Hemorrhage occurs.

Caused by some other disease or injury.

58
Q

Causes of DIC

A 
Gram negative sepsis
Obstetric complications
Any trauma
Hypoxia
Shock 
Hypotension

NUR 612 Advanced Pathophysiology (21 decks)

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