Lecture 3: Hemodynamics Flashcards

1
Q

Artery or vein

A

artery

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2
Q

Artery or vein

A

vein

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3
Q

What is edema

A

Abnormal accumulation of fluid in the interstitium and body cavities

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4
Q

What are the 4 causes of edema

A
  1. Increased microvascular permeability
  2. Increased vascular hydrostatic pressure
  3. Decreased intravascular oncotic pressure
  4. Decreased lymphatic drainage
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5
Q

What are some causes of increase microvascular permeability

A

Inflammation, neovascularization, anaphylaxis, toxin, clotting abnormalities

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6
Q

What are some causes for increased vascular hydrostatic pressure

A

Portal hypertension, pulmonary hypertension, localized venous obstruction

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7
Q

What are some causes of decreased intravascular osmotic pressure

A

Hypoalbumemia, excessive albumin loss

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8
Q

What are some causes for decreased lymphatic drainage

A

Lymphatic obstruction or compression, lymphatic aphasia or hypoplasia, interstitial lymphangiectasia, lymphangitis, spirotrichosis

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9
Q

What are 2 major causes of non-inflammatory edema and transudate

A
  1. Hepatic disease- hypoalbumemia, portal hypertension—> increase hydrostatic pressure
  2. Heart failure- LHF- pulmonary edema, RHF- ascites—> increase hydrostatic presure
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10
Q

How does the body attempt to compensate for hepatic failure and heart failure resulting in decreased CO

A

Activate RAAS system—> increase Na+ and H20 retention, AII activates anti-diuretic hormone- retain water

Ends up increasing hydrostatic pressure

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11
Q

What is hyperemia and what are some reasons why

A

Ateriolar dilation (erythema in skin) due to inflammation, physical activity, increase BF to GI after meal, physiological mechanism of dissipate heat

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12
Q

What is congestion (BF and perfusion) and some reasons why

A

Impaired/decreased outflow due to CHF, local venous obstruction, displacement of organ

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13
Q

What is hemostasis

A

Physiological response to vascular damage and stop bleeding- normal to prevent blood loss

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14
Q

What is thrombosis

A

Inappropriate activation of hemostatic processes in blood vessels, occurs without trauma

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15
Q

What is Virchow’s Triad

A

3 factors that contribute to hemostasis and thrombosis
1. Endothelial injury
2. Alterations in blood flow
3. Blood hypercoaguability

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16
Q

What are the steps in the hemostatic process

A
  1. Primary hemostasis- vasoconstriction and platelet aggregation to form platelet plug at site of damage- uses von willebrand factor to help adhere platelets to endothelium
  2. Secondary hemostasis- coagulation to form a mesh work of fibrin- uses tissue factor because once activated upon endothelial injury activates extrinsic coagulation pathway
  3. Fibrinolysis
  4. Tissue/vascular repair
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17
Q

Describe the intrinsic and extrinsic coagulation pathway

A

Intrinsic: Factor XII—> Factor XI—> Factor IX—> Factor VIII— Factor X—> Factor II (thrombin)—> Factor I (fibrin)—> clot

Extrinsic: Factor III (tissue factor)—>factor VII—> Factor X—> Factor II (thrombin)—Factor I (fibrin)—> clot

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18
Q

What are the vitamin K dependent coagulation factors

A

Factor II, VII, IX, X

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19
Q

What is the purpose of fibrinolysis

A

Prevents blood clots forming pathogenic condition

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20
Q

What is the purpose of plasmin

A

Digest fibrin clots and releases fibrin degradation products and inhibits additional fibrin formation

21
Q

What do FDP’s do

A

Inhibit thrombin and interfere with fibrin polymerization and coat platelet membranes to inhibit platelet agggregation

22
Q

What is the most clinically significant and most potent coagulation inhibitor

A

Antithrombin III

23
Q

What produces Anti-thrombin III

A

Hepatocytes and endothelium

24
Q

What is hemorrhage

A

Extravasated blood caused by abnormal function or integrity of one or more of the major factors of Virchows triad

25
What are the 3 descriptive terms to describe hemorrhage
1. Petechiae 2. Ecchymosis 3. Suffusive
26
What is petechia hemorrhage
1-2mm, pinpoint, associated with minimal vascular a damage
27
What is ecchmosis hemorrhage
2-3cm in diameter, more extensive vascular damage
28
What is suffusive hemorrhage
Larger, continuous areas of tissue, paintbrush
29
What type of hemorrhage
Suffusive hemorrhage
30
What type of hemorrhage
Petechia
31
What type of hemorrhage
petechia and ecchymosis
32
What type of hemorrhage
Ecchymosis
33
What is the pathogensis of hemopericardium causing cardiac tamponade
1. Right auricular hemangiosarcoma ruptured—> compression on heart—> decreased diastolic filling—> decreased CO—> death
34
What % of blood needs to be lost to die from exsanguination
40%
35
What is thrombosis
Aggregate of platelets, fibrin and other blood elements in injured blood vessel
36
What is physiological thrombus
Part of normal hemostasis
37
What is persistent inappropriate thrombus
Forms on the wall of injured blood or lymphatic vessel or heart (mural thrombosis) or free in a vessel human (thromboembolism)
38
What is mural thrombosis
Thrombosis in the wall of blood vessel, lymphatic vessel, or heart
39
What is thromboembolism thrombus
Forms free in the vessel lumen
40
What are the major determinants of thrombosis
Virchows triad, specifically endothelial damage which results in increase production of pro-coagulant substances and decreases anticoagulants
41
How are small thrombi resolved
Thrombolysis and blood vessel returns to normal structure and function
42
How are large thrombi resolved
Removal or thrombotic debris by phagocytes with subsequent granulation tissue formation and fibrosis with regrowth of endothelium over sure to incorporate the affected area into vessel wall
43
How are large mural or occlusive thrombi resolved
Invasion and growth of endothelial lined blood channels through fibrotic area—> recanalization Causes permanent vascular narrowing- leading to more turbulent flow
44
What does this show
thrombus resolution- recanalization Fibrous tissue surrounding, but multiple smaller areas of blood flow
45
What does an acute infarct look like
Red, swollen and slightly raised due to hemorrhage
46
What does a subacute infarct look like
Pale, necrotic, swelling, still surrounded by hyperemia areas
47
What does a chronic infarct look like
Paleo, shrunken, firm, fibrosis
48
Identify the different types of infarcts
Red: acute infarct Yellow: subacute infarct Green: chronic infarct
49
What is the pathogensis of DIC
1. Activation of intravascular coagulation 2. Platelet consumption (decrease platelets), coagulation factor consumption (increase PT and aPTT, increase D-Dimer)—> impaired coagulation and bleeding Endothelial damage—> microvascular thrombosis—> multi organ ischemia or failure Summary: initially overactive coagulation system—> exhaust coagulation system—> excessive bleeding—> death