Exam 2 (Lecture 10) - Hemorrhage and Thrombosis Flashcards

1
Q

Arrest of Hemorrhage

A

1) Formation of a clot (hemostasis)

2) Pressure of surrounding tissue (internal hemorrhage)

3) If massive trauma/blood loss: decreased BP
- decreased BP > blood flow slows > stasis > death

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2
Q

Describe the methods of disposal for escaped blood.

A

1) Small hemorrhages (serum absorbed)
- this is when we start seeing the cholesterol crystals/bruising
patterns

2) Large hemorrhages
clot > contraction > fluid to lymphatics
- macrophages
- fibroblasts (make collagen)

3) Large hematoma
- All of the above PLUS seromas (RBCs and serum)
- bacteria love seromas!

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3
Q

What is thrombosis?

A

Excessive or inappropriate intravascular blood coagulation in the living animal.

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4
Q

What are the three main factors of pathogenesis that leads to thrombosis?

A

1) Endothelial injury

2) Blood turbulence or stasis

3) Hypercoagulability

**AKA Virchow’s Triad

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5
Q

What is the significance of thrombosis?

A

1) Ischemia (blocking blood flow to that location):
- depends on location and collateral circulation

2) Embolism:
- free mass (or air) in circulation

3) Infarction:
- the outcome is ischemic necrosis (coagulative necrosis)

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6
Q

What are the fates of thrombi?

A

1) Propagation
- Ex: toward the heart

2) Embolism
- Ex: pulmonary embolism

3) Fibrinolysis
- Via plasmin
- Results in resolution (clot dissolution)

4) Organization or recanalization
- Ex: organized and incorporated into blood vessel wall
- Ex: recanalized so that blood can flow through other areas

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7
Q

Describe an arterial thrombus.

A

1) Initiated at areas of endothelial damage.

2) Downstream growth (away from site of attachment)

3) “Tail” not attached; can break off
- thromboemboli

4) Prevents oxygenated blood from entering site

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8
Q

Describe venus thrombi.

A

1) Areas of stasis

2) Often occlusive

3) Upstream growth (toward attachment)

4) Prevents deoxygenated blood from leaving site

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9
Q

Describe a venous infarct. What are some examples of venous infarct?

A

Occurs when there is pressure on a vessel.

Veins are more at risk of compression due to less muscle in the vessel.

Examples:
- a strangulating lipoma that has cut off blood supply to the SI
- twisted colon resulting in stasis of deoxygenated blood
- inguinal hernia with intestinal entrapment

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10
Q

Compare the gross appearance of a venous infarct and an arterial infarct.

A

Venous infarct:
- will appear dark red/purple

Arterial infarct:
- will appear pale due to lack of blood flow
- zones of hyperemia around the pale areas (will undergo
coagulative necrosis)

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11
Q

Are “chicken fat” clots normal post mortem?

A

Yes, they are seen in animals that are in high stress situations.

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12
Q

What are some types of emboli?

A

1) Blood (thromboemboli)
2) Bacteria
3) Fat
4) Air (from IV injections/catheterization)
5) Parasites
6) Cartilage

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13
Q

What is hemorrhage? What causes it?

A

The escape of blood from the blood vascular system.

Hemorrhage by rupture:
- Causes:
- Trauma
- Vessel wall necrosis (burns, insects, etc)
- Vessel wall invasion by a neoplasm
- Primary vascular disease
- Atherosclerosis:
*Brain: stroke
* Coronary arteries: occlusion > MI

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14
Q

What does the clinical significance of a hemorrhage depend on?

A

Amount
Rate
Site (how easy will it be to stop the hemorrhage?)
Duration
Hypovolemic shock
Fluid redistribution
Anatomic consequences
Acute
Chronic

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15
Q

What are the 2 main types of hemorrhage?

A

1) Regional
- diffuse
- hematoma

2) Surface
- petechiae
- ecchymosis
- purpura
- paint brush/suffusive

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16
Q

What is hemorrhage by diapedesis and how does it occur?

A

Passage of RBCs through an intact vascular wall.

Site: lung and GI tract

Situation: left heart failure

Problem: increased intravascular pressure in pulmonary capillaries

17
Q

What are the major mechanisms of hemorrhage?

A

1) Endothelial/vessel injury

2) Platelet dysfunction or thrombocytopenia

3) Coagulation disorders
- Acquired:
- hepatic dysfunction
- vitamin K antagonism (II, VII, IX, X)
- disseminated intravascular coagulation
- Inherited:
- hemophilia

18
Q

Describe the pathogenesis of DIC.

A

1) Primary disease (like septicemia or neoplasia)
- toxins, vascular damage, viral infections, etc

2) Endothelial damage (widespread)

3) Microthrombi formation
- ischemic injury (leads to multiple organ failure)
- tissues not getting blood
- consumption of platelets and coagulation factors (spontaneous)
- activation of fibrinolysis (fibrin degradation products)
** Last 2 bullet points lead to hemorrhagic diathesis

19
Q

How do you diagnose consumption coagulopathy?

A

Thrombocytopenia (less than 50,000) - at risk for hemorrhage

Increased fibrin degradation products (FDPs): D-dimers

Increased clotting time
- PT (extrinsic)
- PTT (intrinsic)
* ways to measure arms of clotting cascade

20
Q

What are the two major consequences of DIC?

A

1) Hemorrhage
- consumptive coagulopathy (continual hemorrhage)

2) Multiple organ failure due to ischemia
- microthrombi in microvasculature
- hypovolemic shock possible (blood volume leaving vascular
space)