Overview Hemostasis & Thrombosis (Pb&t)

Front 1

Most common cause of systemic edema

Back 1

Congestive Heart Failure

Front 2

Edema in CHF is mainly caused by which mechanism?

A. Increased venous hydrostatic pressure
B. Increased arterial hydrotatic pressure
C. Increased venous oncotic pressure
D. Increased arterial oncotic pressure

Back 2

A.

Front 3

Albumin loss will cause edema through (increased or decreased) (hydrostatic or oncotic pressure)

Back 3

Albumin loss will casue edema through DECREASED ONCOTIC pressure

Front 4

Pulmonary edema is typical in (left/right) ventricular failure but is also seen in renal failure, ARDS, infx, and hypersensitivity reactions.

Back 4

LEFT

Front 5

How do hyperemic tissues appear?

Back 5

Hypermia is increased volume of blood to a particular site (active process) so tissues will appear redder and more engorged.

Front 6

Order the following in terms of size of hemorrhage:

Purpura
Ecchymoses
Petechia
Hemothorax

Back 6

In terms of size, PETECHIA < PURPURA < ECCHYMOSES < HEMOTHORAX

Front 7

(T/F) Thrombosis represents a physiologic state.

Back 7

FALSE - Thrombosis is pathologic (according to Robbins, however the notes say that thrombosis can be appropriate following vessel injury)

Front 8

Von Willebrand factor mediates adhesion between platelets and what?

In general, what type of disorder characterizes von Willebrand disease?

Bonus: What exactly does von Willebrand factor bind to on platelets?

Back 8

Mediates adhesion to sub-endothelium by binding to platelet and exposed sub-endothelial collagen.
Von Willebrand disease is a bleeding disorder

Bonus: VWF binds to GPIB on platelets.

Front 9

Platelet aggregation creates the (primary or secondary) homeostatic plug which is (reversible or irreversible)

Back 9

Aggregation creates the PRIMARY plug, which is reversible

Front 10

The intrinsic pathway of coagulation is initiated by activation of _____ factor, while the extrinsic pathway is activated by ____ factor.

Back 10

Intrinsic pathway = Hageman factor (XII)
Extrinsic = Tissue factor

Front 11

Receptors are clipped by thrombin to yield _______ ________ that bind to another site on the receptor causing changes that activate associated G proteins. This autocatalytic activity explains the impressive potency of even relatively small amts of thrombin

Back 11

clipped to yield TETHERED PEPTIDES

Front 12

(T/F) factor activatin can only occur at sites of exposed phospholipids.

Back 12

TRUE

Front 13

What does plasmin do to fibrin?

Back 13

Cleaves it

Front 14

Where is plasminogen found? What is the name of the enzyme that turns it into plasmin?

Back 14

Plasminogen circulates in the blood stream. Enzyme t-PA turns it into plasmin.

Front 15

What is the term for inappropriate activation of blood clotting in uninjured vasculature or occlusion of a vessel after minor injury.

Back 15

Thrombosis

Front 16

What are the three primary influenzes in thrombus formation (Virchow's triad)?

Back 16

Endothelial injury
Alterations in normal blood flow
Heritable hypercoagulable states

Front 17

Aortic thrombi tend to be (nonocclusive or occlusive) while venous thrombi tend to be (nonocclusive or occlusive).

Back 17

Aotrtic thrombi tend to be nonocclusive while venous thrombi tend to be occlusive

Front 18

If you hear a thrombus described as red-blue, and containing a relatively large number of erythrocytes among sparse fibrin strands, are you thinking arterial or venous?

Back 18

Arterial

Front 19

What is a phlebothrombosis and where specifically does it occur?

Back 19

Phlebothrombosis = venous thrombosis and it affects the superficial or deep veins in the lower extremity (90% of the time).

Front 20

In infective endocarditis, organisms form large infected masses (vegetations) on which part of the heart?

Back 20

Heart valves

Front 21

Name (and describe) the four outcomes that can happen if a patient survives the immediate ischemic effects of a thrombus.

Back 21

Propagation (complete vessel obstruction)
Embolization (clot travels to another site)
Dissolution by fibrinolytic activity
Organization and recanalization (reestablish flow by ingrowth of endothelial cells creating vascular channels).

Note that patients usually experience a combination of the four outcomes.

Front 22

Which are more prone to embolize, superficial or deep vein thrombosis?

Back 22

Deep Vein Thrombosis are more likely to embolize.

Front 23

Approximately what percent of patients are asymptomatic when it comes to deep vein thromboses? How is a deep vein thrombosis usually found in asymptomatic patients?

Back 23

50% of patients are asymptomatic. In these cases, DVT is often recognized following an embolism.

Front 24

Give five clinical settings in which a deep venous thrombosis can occur:

Back 24

Diminished milking action of lower leg muscles due to age, bedrest, or immobilization
CHF
Trauma/surgery/ burns
Amniotic fluid embolization
Tumor associated procoagulant release

Front 25

(T/F) Artherosclerosis is a major cause of arterial thromboses.

Back 25

True

Front 26

In general, what is more important when considering venous thromboses - their ability to embolize or their ability to cause congestion? What about for arterial thromboses?

Back 26

The most dire consequence of venous thrombosis is the propensity to embolize, while the most dire consequence of arterial thrombosis is obstruction.

Front 27

How can disseminated intravascular coagulation lead to uncontrollable bleeding?

Back 27

Through consumption of platelets and coagulation factors with fibrinolytic pathway activation.

Front 28

"List six ""other"" forms of embolism besides thromboembolism."

Back 28

Fat
Gas bubbles
Atherosclerotic debris
Tumor fragments
Bone marrow
Foreign bodies (like bullets)

Front 29

Greater than 95% of pulmonary emboli originate from where?

A. Superficial leg venous thrombosis
B. Deep leg venous thrombosis
C. Coronary artery thrombosis
D. From a small vein in the lung.

Back 29

B. Deep leg venous thrombosis

Front 30

(T/F) Most (60-80%) pulmonary embolisms obstruct medium-sized arteries which may result in pulmonary hemorrhage but do not cause pulmonary infarction because of collateral bronchial artery flow.

Back 30

False - Most pulmonary embolisms are small and clinically silent.

Front 31

What is systemic thromboembolism? Where do they mostly arrise from?

Back 31

Term refers to emboli in the arterial circulation.

In 80% of the time they arrise from intracardiac mural thrombi; 2/3 are secondary to MI and 25% arise within dilated left atria.

Front 32

(T/F) Most fat emboli come from excessive triglycerides circulated in the body.

Back 32

False - Most fat emboli come from fractures of long bones or in rare cases after burns or soft tissue trauma.

Front 33

What is decompression sickness?

Back 33

Decompression sickness is a type of air-embolism formed during sudden decreases in atmospheric pressure (as in divers rapidly ascending to the surface). Depressurization allows the dissoleved gases to expand and bubble out of solution.

Bubbles in joints and muscles causes painful 'bends', while 'chokes' are bubbles in the lungs.

Front 34

What causes amniotic fluid embolism? What are the signs/symptoms?

Back 34

Caused by amniotic fluid infusion into maternal circulation. Findings include fetal squamous cells, mucin, lanugo hair, and vernix caseosa fat in the maternal pulmonary microcirculation.
Leads to severe dyspnea, cyanosis, hypotensive shock, seizures, and coma.

Front 35

(T/F) Amniotic fluid embolism is very serious but luckily very rare.

Back 35

True

Front 36

The vast majority of infarction is caused by occlusions of (arterial supply or venous supply).

Back 36

Vast majority = arterial occlusions

Front 37

Infarctions may be classified as ____ (hemorrhagic) or ______ (pale, anemic) and may be either _____ or ______.

Back 37

Infarctions may be classified as RED or WHITE and may be either SEPTIC or BLAND.

Front 38

Name 5 places where red infarctions may occur:

Back 38

Venous occlusions
Loose tissues
Tissues w/ dual circulation
Tissues previously congested because of sluggish outflow
Sites of previous occlusion and necrosis when flow is reestablsihed.

Front 39

Where do white infarctions tend to occur?

Back 39

White infarcts tend to occur in solid organs (like heart/spleen/kidney) with end-arterial circulations (few collaterals)

Front 40

What is the dominant histologic characteristic of infarction? What is the exception?

Back 40

Dominant characteristic is ischemic coagulative necrosis.
Exception in the brain which undergoes liquefactive necrosis

Front 41

For each of the following factors, which states tend to lead to infarction?

Anatomic pattern of vascular supply (many vs few anastomoses)
Rate of developing of occlusion (slow vs fast)
Vulnerability to hypoxia (low vs high)
Oxygen content of blood (low vs high)

Back 41

Anatomic pattern: Fewer anastomoses leads to ischemia
Rate of development of occlusion: Faster rate more often causes infarction
Hypoxia volunerability: More vulnerable cells like neurons and heart cells will undergo infarction quicker than less vulnerable cells like fibroblasts
If blood has a lower O2 content, infarction is more likely

Front 42

What are the three major types of shock?

Back 42

Cardiogenic, Hypovolemic, Septic

Front 43

More than 70% of cases of septic shock result from infection by which type of bacteria?

Back 43

Gram negative bacilli expressing endotoxin

Front 44

Myocardial infarction may cause which type of shock?

Back 44

Cardiogenic

Front 45

In hypovolemic and cardiogenic shock, what is the typical presention you would see in terms of the following signs:

Pulse
Respiratory rate
Skin

Back 45

Pulse = rapid and weak
Respiratory rate is fast (tachypnea)
Skin is cyanotic and clammy (compare to septic shock in which the skin may be warm initially).

Front 46

Hemorrhage or fluid loss can lead to which type of shock?

Back 46

Hypovolemic shock

Front 47

What are the four steps in the sequence of normal homeostasis?

Back 47

1. Vasoconstriction
2. Primary hemostasis (platelet plug)
3. Secondary hemostasis (fibrin deposition on platelet plug)
4. Thrombus formation and antithrombotic events

Front 48

List four ways that endothelial cells prevent coagulation

Back 48

Intact endothelium prevents platelets and coag factors from contacting ECM
Endothelial cells make hepain-like molecules on cell membranes which inactivate Xa and others
Endothelial cell makes thrombomodulin which converts thrombin into anticoagulant that activates protein C (inhibits clotting by proteolysis)
endothelial cells synthesize t-PA which clear fibrin deposits

Front 49

List three ways that endothelial activation cause procolagulant effects:

Back 49

Von Willebrand factor (for platelet adhesion)
Tissue factor III (thromboplastin ->activates extrinsic pathway via Factor VII)
Inhibitors of plasminogen activator (stop plasmin from doing its job)

Front 50

List four platelet products critical for hemostasis:

Back 50

ADP
Thromboxane A2
Calcium
Histamine, serotonin, epinephrine (dense)

Front 51

What does thromboxane A2 (TXA2) do? What enzyme makes it?

Back 51

TXA2 stimulates recruitment/aggregation of platelets leading to primary plug. (ADP does this too).

TXA2 is a product of cyclooxygenase-1 in mature platelets.

Front 52

Which lab test evaluates the integrity of the extrinsic pathway for coagulation. What about intrinsic? What about for the common pathway?

Back 52

Prothrombin Time & INR measure extrinsic and common.

Partial Thromboplastin Time measures intrinsic and common pathways.

Thus, both measure common pathways.

Front 53

What is the dominant mechanism fo rpathologic thrombosis within arterial circulation?

Back 53

Endothelial injury

Front 54

How do TxA2 & ADP release trigger positive feedback thus accelerating aggregation?

Back 54

TxA2 release triggures upregulation of TxA2 receptors. ADP release triggers ADP receptors.

Front 55

What does the ADP post-receptor cascade do to the amount of cAMP and what does this mean for platelet activation?

Back 55

ADP cascade DECREASES cAMP PROMOTES clotting. (Increases in cAMP decrease platelet activation)