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Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

What does exudate contain that transudate does not

A

Inflammatory cells

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2
Q

Examples of Localized Increased hydrostatic pressure

A

Venous stasis

Ascites

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3
Q

Examples of Generalized Increased hydrostatic pressure

A

Cardiac Failure

Renal Failure

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4
Q

What infiltrate is indicative of liquefactive necrosis

A

Neutrophils

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5
Q

What are the reasons a transudate can form?

A 
Increased Hydrostatic Pressure
Loss of Plasma Colloid
Increased Vascular Permeability
Impaired Lymphatic Drainage
Salt and Water Retention
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6
Q

What is the difference b/w hyperemia and congestion?

A

Hyperemia = Active process due to increased blood inflow

Congestion = Passive process due to impaired venous outflow

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7
Q

Why would Renal Failure patients have non-gravity dependent edema?

A

Because their edema is due to a loss of colloid pressure, not hydrostatic pressure

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8
Q

Why is ventricular hypertrophy such a threat to induce heart failure?

A

Because there is no angiogenesis in the heart tissue. The heart muscle gets bigger without a corresponding increase in bloodflow to support it

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9
Q

Clinical symptom of left ventricular failure

A

Pulmonary Edema

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10
Q

Clinical symptom of right ventricular failure

A

Pitting edema. Blood accumulates in lower extremities because it cannot return to heart effectively

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11
Q

Clinical symptom of congested liver

A

Ascites

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12
Q

what happens to the architecture of the lungs after long-term heart failure?

A

Septa become very thickened.

Macrophages ingest RBC and form HFC’s to retain iron

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13
Q

What is amyloidosis

A

Amyloid is a misfolded protein that can accumulate in blood vessels

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14
Q

What can pericardial hemorrhage lead to

A

Tamponade

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15
Q

What is the state of normal hemostasis?

A

Conditions that allow for the fluidity of the blood to be maintained as well as allow for the formation of a solid plug to close a vascular defect

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16
Q

What are the three factors that determine hemostasis and thrombosis

A

Vascular endothelium
Platelets
Coag System

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17
Q

Endothelial cell anti-thrombotic properties

A

Antiplatelet effects
Anticoag properties
Fibrinolytic properties

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18
Q

Endothelial cell

PRO-thrombotic properties

A

Adhesion of platelets
Make vWF
Make TF

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19
Q

What is the first thing that happens after a vascular injury?

A

Transient arteriorlar vasoconstriction (reflex pathway)

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20
Q

What is exposed after a vascular injury that facilitates platelet adherence and activation?

A

Highly pro-throbotic subendothelial ECM

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21
Q

What is factor 3?

A

Tissue factor, made by endothelial cells

22
Q

What factor does factor 3/TF mix with to help start the coag cascade?

A

Factor 7

23
Q

What is the main goal of the cascade?

A

Activate Thrombin

24
Q

What does activated Thrombin do?

A

It cleaves fibrinogen to create the insoluble fibrin

It also recruits more platelets to the clot

25
Q

What happens after the clot has controlled the bleeding?

A

Fibrinolysis occurs to help smooth out the clot and limit its size so it doesn’t disrupt laminar blood flow

26
Q

What is the fibrinolysis molecule released by Endo Cells?

A

t-PA

27
Q

What does thrombomodulin do?

A

Blocks additional coagulation cascade activity

28
Q

What can “trick” endothelial cells into forming clots without injury to the vessels?

A

Microbes
Inflammatory mediators
hemodynamic forces

29
Q

What does heparin do?

A

It binds to thrombin and causes a modification so that it cleaves Protein C instead of Fibrinogen

Protein C is an anticoagulant

30
Q

What factors does Protein C cleave?

A

5a and 8a

31
Q

What does t-PA stand for?

A

Tissue type plasminogen activator, which cleaves plasminogen into plasmin

32
Q

What does plasmin do

A

Cleaves insoluble fibrin to bust up clots

33
Q

What makes vWF?

A

EC’s

34
Q

What does vWF do?

A

It binds to both platelets and sub-endothelial ECM

35
Q

What secretes PAI? (Plasminogen activator inhibitors)

A

EC’s

36
Q

What do PAIs do?

A

Favor thrombosis by limiting plasminogen activity

37
Q

What makes platelets

A

Megakaryocytes in bone marrow

38
Q

What 2 things do platelets need to do to work?

A

Have a contractile cytoskeleton

Secrete 2 Cytoplasmic granules

39
Q

What are the 2 Granules

A

Alpha granules

Dense bodies

40
Q

What do Alpha granules have inside?

A

P-selectin (adhesion)
Fibrinogen (fibrin precursor)
Fibronectin
Factors 5 and 8

41
Q

What do dense bodies have?

A

ADP/ATP
Ca++
Histamine
Epi

42
Q

What bleeding disorders are caused by missing or defective vWF

A

Von Willebrands’

Bernard Soulier

43
Q

What happens when a Platelet has adhered (via vWF and ECM Collagen)

A

It changes shape and releases its granules and expresses binding sites for fibrinogen

44
Q

In normal vessels what two mediators are constantly keeping hemostasis in balance

A

EC: PGI2 (vasodilator)

Platelet: TxA2 (Thromboxane) Promotes platelet aggregation

45
Q

What does Aspirin do?

A

Permanently blocks TxA2. It also blocks PGI2 but the ECs can remake their own Cyclooxygenase to make more PGI2

46
Q

What works in a similar manner to Aspirin?

A

NO Nitric Oxide

47
Q

What factor does heparin inhibit?

A

10a

48
Q

What is virchow’s triad

A

Edothelial Injury
Changes to normal blood flow
Blood Stasis

49
Q

What are lines of zahn

A

Show there is still laminar blood flow and the RBC and platelets are forming in layers

50
Q

What organs will have Red Infarcts instead of Pale?

A

Those with dual blood supply like the lungs or the GI tract

Pathology (12 decks)

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