Hemodynamics Flashcards

(50 cards)

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?

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
What happens after the clot has controlled the bleeding?
Fibrinolysis occurs to help smooth out the clot and limit its size so it doesn't disrupt laminar blood flow
26
What is the fibrinolysis molecule released by Endo Cells?
t-PA
27
What does thrombomodulin do?
Blocks additional coagulation cascade activity
28
What can "trick" endothelial cells into forming clots without injury to the vessels?
Microbes Inflammatory mediators hemodynamic forces
29
What does heparin do?
It binds to thrombin and causes a modification so that it cleaves Protein C instead of Fibrinogen Protein C is an anticoagulant
30
What factors does Protein C cleave?
5a and 8a
31
What does t-PA stand for?
Tissue type plasminogen activator, which cleaves plasminogen into plasmin
32
What does plasmin do
Cleaves insoluble fibrin to bust up clots
33
What makes vWF?
EC's
34
What does vWF do?
It binds to both platelets and sub-endothelial ECM
35
What secretes PAI? (Plasminogen activator inhibitors)
EC's
36
What do PAIs do?
Favor thrombosis by limiting plasminogen activity
37
What makes platelets
Megakaryocytes in bone marrow
38
What 2 things do platelets need to do to work?
Have a contractile cytoskeleton Secrete 2 Cytoplasmic granules
39
What are the 2 Granules
Alpha granules Dense bodies
40
What do Alpha granules have inside?
P-selectin (adhesion) Fibrinogen (fibrin precursor) Fibronectin Factors 5 and 8
41
What do dense bodies have?
ADP/ATP Ca++ Histamine Epi
42
What bleeding disorders are caused by missing or defective vWF
Von Willebrands' Bernard Soulier
43
What happens when a Platelet has adhered (via vWF and ECM Collagen)
It changes shape and releases its granules and expresses binding sites for fibrinogen
44
In normal vessels what two mediators are constantly keeping hemostasis in balance
EC: PGI2 (vasodilator) Platelet: TxA2 (Thromboxane) Promotes platelet aggregation
45
What does Aspirin do?
Permanently blocks TxA2. It also blocks PGI2 but the ECs can remake their own Cyclooxygenase to make more PGI2
46
What works in a similar manner to Aspirin?
NO Nitric Oxide
47
What factor does heparin inhibit?
10a
48
What is virchow's triad
Edothelial Injury Changes to normal blood flow Blood Stasis
49
What are lines of zahn
Show there is still laminar blood flow and the RBC and platelets are forming in layers
50
What organs will have Red Infarcts instead of Pale?
Those with dual blood supply like the lungs or the GI tract