Thromboembolism and shock Flashcards

1
Q

(clot in original position):

Precedent of everything formation of inappropriate blood clot

A

Thrombosis

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2
Q

(clot in circulation): Can obstruct a
vessel where it will lodge can cause ischemia
to the surrounding tissue being supplied by
that vessel leading to infarction

A

Embolism

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3
Q

Circulatory failure part of
hemodynamic disorder with unique
characteristics but sometimes overlaps with
symptoms of thromboembolic disease

A

Shock

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4
Q

is one of the scourges of modern
man, because it underlies the most serious and
common forms of cardiovascular disease.

A

Thrombosis

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5
Q

If there is embolism in the lungs particularly in the

pulmonary vein, there will be________

A

pulmonary infarction.

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6
Q

Virchow’s triad: Endothelial Injury can cause ____

A

abnormal

blood flow and hypercoagulability

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7
Q

Virchow’s triad: Abnormal Blood Flow can lead to or

cause _____

A

endothelial injury and

hypercoagulability

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8
Q

T or F
Hypercoagulability does NOT cause
either endothelial injury or abnormal
blood flow

A

T

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9
Q

Injury to the endothelium leads to ______ (inhibited by aspirin)

A

Platelet activation

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10
Q

When there is endothelial injury, it exposes the

endothelium to _________ which leads to platelet activation.

A

Von Willebrand factor and tissue

factor

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11
Q

Causes of Endothelial injury

A
o Physical Injury
o Infection
o Abnormal Blood Flow
o Inflammatory mediators
o Metabolic Abnormalities
o Toxins from cigarette smoke
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12
Q

This triggers Endothelial activation or dysfunction
that shifts the pattern of gene expression in
endothelium to _______

A

prothrombotic.

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13
Q

The 2 Prothrombotic Alterations

A

o Procoagulant changes

o Antifibrinolytic effects

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14
Q

In procoagulant changes, there is downregulation of thrombomodulin, as well as _________ and _____

A

Protein C and TFPI

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15
Q

In antifibrinolytic effects, Activated endothelial cells
secretes _________which
downregulates t-PA and limits
fibrinolysis

A

plasminogen activator

inhibitors (PAIs)

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16
Q

normal flow of blood in the

vessels is known as

A

laminar flow

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17
Q

T or F
Laminar flow
allows the red cells to travel centrally in the blood
vessels and plasma in the outer portion to prevent
the red cells from having contact with the
endothelium.

A

T

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18
Q

Blood flow can be altered in 2 ways:

A

Turbulence

Stasis

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19
Q

▪ Contributes to arterial and
cardiac thrombosis by causing endothelial injury
▪ Also forming little pockets of countercurrents that contribute to stasis

A

Turbulence

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20
Q

▪ Allows development of venous thrombi

A

Stasis

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21
Q

-Refers to an abnormally high tendency of the
blood to clot, typically caused by alterations in
coagulation factors
- important in venous thrombosis

A

HYPERCOAGULABILITY

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22
Q

▪ also called Leiden mutation
▪ Arg to Gln substitution in amino acid residue 506
▪ 60% in patients with recurrent DVT

A

Factor V mutation (autosomal dominant) (2-15%)

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23
Q

In factor V mutation, Heterozygotes have a ____ increased relative
risk of venous thrombosis, and homozygotes
have a ____increase

A

fivefold; 50-fold

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24
Q

▪ Single nucleotide change (G20210A) in 3’-

untranslated region of prothrombin gene

A

Prothrombin gene mutation (1-2%)

25
Q

In prothrombin gene mutation, there is Increased prothrombin that leads to a
procoagulant state and an almost _____
increased risk of venous thrombosis

A

threefold

26
Q

▪ predisposes a patient to develop DVT in
adolescence and early adulthood
▪ Affected individuals typically present with venous
thrombosis and recurrent thromboembolism
beginning in adolescence or early adulthood.

A

Others: Deficiencies of anticoagulants (antithrombin III,

protein C or protein S)

27
Q

Homocystenemia can be caused by inherited deficiency of ______

A

cystathione β-synthetase

28
Q

Homocystenemia
can also be
acquired, causes include deficiency of vitamin

A

B6, B12, and folic acid.

29
Q

Hypercoagulability seen with advancing age may
be due to reduced ______(promotes
platelets aggregation) production which leads to
thrombosis

A

endothelial PGI2

30
Q

Life-threatening disorder that occurs following

administration of unfractionated heparin

A

HEPARIN INDUCED THROMBOCYTOPENIA (HIT)

SYNDROME

31
Q

(HIT)

SYNDROME: Most common presentation:

A

Thrombocytopenia

32
Q

(HIT)

SYNDROME: Most serious complication:

A

Thrombosis

33
Q

(HIT)

SYNDROME: Sequelae

A

o necrosis of the skin
o gangrene of the limbs
o stroke
o myocardial infarction

34
Q

(HIT)

SYNDROME: diagnosis

A

requires the demonstration of anti–

PF4-heparin antibodies

35
Q
▪ Autoimmune disorder characterized by:
o Presence of one or more 
antiphospholipid (aPL) autoantibodies
o Venous or arterial thromboses, or 
pregnancy complications such as 
recurrent miscarriages, unexplained fetal 
death, and premature birth.
A

ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS)

36
Q

manifests only hypercoagulable
state in the absence of other autoimmune
disorders

A

ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS): PRIMARY

37
Q
  • individuals with a well-defined
    autoimmune disease, such as systemic lupus
    erythematosus (lupus anticoagulant syndrome)
    this brings about the development of APS
A

Secondary

38
Q

ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS): Clinical presentations can include:

A
o pulmonary embolism (following lower
o extremity venous thrombosis),
o pulmonary hypertension (from recurrent 
subclinical pulmonary emboli),
o valvular heart disease
o stroke
o bowel infarction
o renovascular hypertension
39
Q

Usually mural, frequently
occlusive -> sequelae; coronary,
cerebral femoral occlusion

A

ARTERIAL THROMBI

40
Q

Grey-white; friable meshwork of
platelets admixed with fibrin, red
cells and degenerating leukocytes

A

ARTERIAL THROMBI

41
Q

Red-blue; contain more enmeshed

red cells

A

VENOUS THROMBI

42
Q

Arterial thrombi grows in a _____ manner

A

retrograde

43
Q

Venous thrombi grows in the ___________

A

direction of blood

flow

44
Q
  1. How do you distinguish an antemortem from a post

mortem clot?

A

Antemortem thrombosis contain lines of Zahn,
features that help distinguish them from postmortem clots.
Postmortem clots are gelatinous and have a dark-red
dependent portion where red cells have settled by gravity
and a yellow “chicken fat” upper portion, and are usually
not attached to the underlying vessel wall.

45
Q

Thrombi on heart valves are called?

A

Ans: Vegetations (can be sterile or infected as in infective
endocarditis). There are vegetations or thrombi that are
formed on valves especially in SLE patients and they are
called libman sacks. (Endocarditis associated with SLE is
k/s libman sacks endocarditis).

46
Q

Thrombi accumulate

additional platelets and fibrin.

A

Propagation

47
Q

Thrombi dislodge and travel

to other sites in the vasculature.

A

Embolization

48
Q

is the result of
fibrinolysis. Which can lead to the rapid
shrinkage and total disappearance of recent
thrombi. In contrast, the extensive fibrin
deposition and cross-linking in older thrombi
render them more resistant to lysis. This
distinction explains why therapeutic
administration of fibrinolytic agents such as tPA.

A

Dissolution

49
Q
Older
thrombi become organized by the in growth 
of
o endothelial cells
o smooth muscle cells
o fibroblasts.
A

Organization and recanalization.

50
Q

▪ WIDESPREAD THROMBOSIS within the
microcirculation that may be of sudden or
insidious onset.

A

DISSEMINATED INTRAVASCULAR COAGULATION

51
Q

T or F
DISSEMINATED INTRAVASCULAR COAGULATION
-It is not a specific disease but rather a
complication of a large number of conditions
associated with systemic activation of thrombin.

A

T

52
Q

Causes of DIC

A

o Obstetric complication
o Cancers
o Severe Traumas
o Sepsis

53
Q

Detached intravascular solid, liquid or gaseous
mass that is carried by the blood from its point of
origin to a distant site, where it causes tissue
dysfunction or infarction

A

EMBOLISM

54
Q

▪ Originate from DVT and the most common form

of thromboembolic disease.

A

PULMONARY EMBOLISM

55
Q

when the embolus straddles

the pulmonary artery bifurcation

A

Saddle embolus

56
Q

a venous embolus
passes through an interatrial or interventricular
defect and gains access to the systemic
circulation

A

Paradoxical embolism:

57
Q

T or F
Embolic obstruction of medium arteries with
subsequent vascular rupture can result in
pulmonary hemorrhage and usually cause pulmonary infarction.

A

F
** but usually does not
cause pulmonary infarction.

58
Q

T or F
Multiple emboli overtime may cause pulmonary
hypertension and right ventricular failure.

A

T