Thromboembolism and shock

Question 1

(clot in original position):

Precedent of everything formation of inappropriate blood clot

Answer 1

Thrombosis

Question 2

(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

Answer 2

Embolism

Question 3

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

Answer 3

Shock

Question 4

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

Answer 4

Thrombosis

Question 5

If there is embolism in the lungs particularly in the

pulmonary vein, there will be________

Answer 5

pulmonary infarction.

Question 6

Virchow’s triad: Endothelial Injury can cause ____

Answer 6

abnormal

blood flow and hypercoagulability

Question 7

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

cause _____

Answer 7

endothelial injury and

hypercoagulability

Question 8

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

Answer 8

T

Question 9

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

Answer 9

Platelet activation

Question 10

When there is endothelial injury, it exposes the

endothelium to _________ which leads to platelet activation.

Answer 10

Von Willebrand factor and tissue

factor

Question 11

Causes of Endothelial injury

Answer 11

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

Question 12

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

Answer 12

prothrombotic.

Question 13

The 2 Prothrombotic Alterations

Answer 13

o Procoagulant changes

o Antifibrinolytic effects

Question 14

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

Answer 14

Protein C and TFPI

Question 15

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

Answer 15

plasminogen activator

inhibitors (PAIs)

Question 16

normal flow of blood in the

vessels is known as

Answer 16

laminar flow

Question 17

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.

Answer 17

T

Question 18

Blood flow can be altered in 2 ways:

Answer 18

Turbulence

Stasis

Question 19

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

Answer 19

Turbulence

Question 20

▪ Allows development of venous thrombi

Answer 20

Stasis

Question 21

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

Answer 21

HYPERCOAGULABILITY

Question 22

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

Answer 22

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

Question 23

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

Answer 23

fivefold; 50-fold

Question 24

▪ Single nucleotide change (G20210A) in 3’-

untranslated region of prothrombin gene

Answer 24

Prothrombin gene mutation (1-2%)

Question 25

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

Answer 25

threefold

Question 26

▪ 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.

Answer 26

Others: Deficiencies of anticoagulants (antithrombin III, | protein C or protein S)

Question 27

Homocystenemia can be caused by inherited deficiency of ______

Answer 27

cystathione β-synthetase

Question 28

Homocystenemia can also be acquired, causes include deficiency of vitamin

Answer 28

B6, B12, and folic acid.

Question 29

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

Answer 29

endothelial PGI2

Question 30

Life-threatening disorder that occurs following | administration of unfractionated heparin

Answer 30

HEPARIN INDUCED THROMBOCYTOPENIA (HIT) | SYNDROME

Question 31

(HIT) | SYNDROME: Most common presentation:

Answer 31

Thrombocytopenia

Question 32

(HIT) | SYNDROME: Most serious complication:

Answer 32

Thrombosis

Question 33

(HIT) | SYNDROME: Sequelae

Answer 33

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

Question 34

(HIT) | SYNDROME: diagnosis

Answer 34

requires the demonstration of anti– | PF4-heparin antibodies

Question 35

``` ▪ 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. ```

Answer 35

ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS)

Question 36

manifests only hypercoagulable state in the absence of other autoimmune disorders

Answer 36

ANTIPHOSPHOLIPID ANTIBODY SYNDROME (APS): PRIMARY

Question 37

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

Answer 37

Secondary

Question 38

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

Answer 38

``` 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 ```

Question 39

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

Answer 39

ARTERIAL THROMBI

Question 40

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

Answer 40

ARTERIAL THROMBI

Question 41

Red-blue; contain more enmeshed | red cells

Answer 41

VENOUS THROMBI

Question 42

Arterial thrombi grows in a _____ manner

Answer 42

retrograde

Question 43

Venous thrombi grows in the ___________

Answer 43

direction of blood | flow

Question 44

1. How do you distinguish an antemortem from a post | mortem clot?

Answer 44

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.

Question 45

Thrombi on heart valves are called?

Answer 45

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).

Question 46

Thrombi accumulate | additional platelets and fibrin.

Answer 46

Propagation

Question 47

Thrombi dislodge and travel | to other sites in the vasculature.

Answer 47

Embolization

Question 48

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.

Answer 48

Dissolution

Question 49

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

Answer 49

Organization and recanalization.

Question 50

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

Answer 50

DISSEMINATED INTRAVASCULAR COAGULATION

Question 51

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.

Answer 51

T

Question 52

Causes of DIC

Answer 52

o Obstetric complication o Cancers o Severe Traumas o Sepsis

Question 53

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

Answer 53

EMBOLISM

Question 54

▪ Originate from DVT and the most common form | of thromboembolic disease.

Answer 54

PULMONARY EMBOLISM

Question 55

when the embolus straddles | the pulmonary artery bifurcation

Answer 55

Saddle embolus

Question 56

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

Answer 56

Paradoxical embolism:

Question 57

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

Answer 57

F ** but usually does not cause pulmonary infarction.

Question 58

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

Answer 58

T