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Pathology I > Lecture 3: Hemodynamics > Flashcards

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
Q

What are the 3 descriptive terms to describe hemorrhage

A
  1. Petechiae
  2. Ecchymosis
  3. Suffusive
26
Q

What is petechia hemorrhage

A

1-2mm, pinpoint, associated with minimal vascular a damage

27
Q

What is ecchmosis hemorrhage

A

2-3cm in diameter, more extensive vascular damage

28
Q

What is suffusive hemorrhage

A

Larger, continuous areas of tissue, paintbrush

29
Q

What type of hemorrhage

A

Suffusive hemorrhage

30
Q

What type of hemorrhage

A

Petechia

31
Q

What type of hemorrhage

A

petechia and ecchymosis

32
Q

What type of hemorrhage

A

Ecchymosis

33
Q

What is the pathogensis of hemopericardium causing cardiac tamponade

A
  1. Right auricular hemangiosarcoma ruptured—> compression on heart—> decreased diastolic filling—> decreased CO—> death
34
Q

What % of blood needs to be lost to die from exsanguination

A

40%

35
Q

What is thrombosis

A

Aggregate of platelets, fibrin and other blood elements in injured blood vessel

36
Q

What is physiological thrombus

A

Part of normal hemostasis

37
Q

What is persistent inappropriate thrombus

A

Forms on the wall of injured blood or lymphatic vessel or heart (mural thrombosis) or free in a vessel human (thromboembolism)

38
Q

What is mural thrombosis

A

Thrombosis in the wall of blood vessel, lymphatic vessel, or heart

39
Q

What is thromboembolism thrombus

A

Forms free in the vessel lumen

40
Q

What are the major determinants of thrombosis

A

Virchows triad, specifically endothelial damage which results in increase production of pro-coagulant substances and decreases anticoagulants

41
Q

How are small thrombi resolved

A

Thrombolysis and blood vessel returns to normal structure and function

42
Q

How are large thrombi resolved

A

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
Q

How are large mural or occlusive thrombi resolved

A

Invasion and growth of endothelial lined blood channels through fibrotic area—> recanalization

Causes permanent vascular narrowing- leading to more turbulent flow

44
Q

What does this show

A

thrombus resolution- recanalization

Fibrous tissue surrounding, but multiple smaller areas of blood flow

45
Q

What does an acute infarct look like

A

Red, swollen and slightly raised due to hemorrhage

46
Q

What does a subacute infarct look like

A

Pale, necrotic, swelling, still surrounded by hyperemia areas

47
Q

What does a chronic infarct look like

A

Paleo, shrunken, firm, fibrosis

48
Q

Identify the different types of infarcts

A

Red: acute infarct
Yellow: subacute infarct
Green: chronic infarct

49
Q

What is the pathogensis of DIC

A
  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

Pathology I (11 decks)

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