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2013/2014 > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

How is the body’s 60% water allocated?

A

15% interstitial, 40% in the cell, 5% in vasculature

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2
Q

Osmolality

A

Concentration of particles in a solution. In plasma, mostly sodium.

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3
Q

Two things that osmosis requires?

A

Driving force and semi permeable membrane. This allows the movement of fluid.

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4
Q

How do small polar molecules move from vascular spaces into the interstitium?

A

Intercellular clefts between endothelium. However, these molecules can’t traverse the lipid bilayer.

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5
Q

How does osmolarity of intravascular, interstitial and intracellular spaces compare? How about concentration of small ions?

A

Osmolarity is the same across all three spaces. Concentration of small polar molecules is the same between vascular and interstitial space, but not in cells.

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6
Q

Outward Hydrostatic Pressure

A

The outward force exerted by moving blood on capillary walls.

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7
Q

What is absorption?

A

The inward hydrostatic pressure and the inward oncotic pressure.

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8
Q

Oncotic pressure

A

A type of osmotic pressure created by proteins.

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9
Q

Inward oncotic pressure

A

Proteins in the vasculature generate an inward oncotic pressure. Water wants to move in. Opposed by outward oncotic pressure, created by proteins in interstitium.

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10
Q

Net Filtration Pressure

A

(Pc + πi) - (πc + Pi). If negative, absorption is favored.

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11
Q

Starling’s Equation

A

Fluid movement (Jz) = Kf (hydraulic conductance) *(Pc + πi) - (πc + Pi)

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12
Q

Role of lymphatics in hemodynamics

A

Return excess filtered fluid and proteins to circulation.

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13
Q

Hypoalbuminemia

A

πc is too low, so net movement of water is out of vasculature. Usually due to loss of proteins in urine.

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14
Q

Difference in clinical presentation for left vs right sided heart failure?

A

Right sided? Peripheral edema. Left sided? Pulmonary edema.

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15
Q

What happens if Kf is increased?

A

Sepsis and inflammation occurs

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16
Q

What happens if lymphatic drainage is blocked?

A

Edema due to increased πi.

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17
Q

Edema

A

Too much interstitial fluid, not to be confused with hydropic change, which is increased intracellular fluid.

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18
Q

Effusion

A

Edema in a body cavity

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19
Q

Anasarca

A

Generalized edema

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20
Q

Transudates

A

Accumulations of mostly salt water. Low protein content, low specific gravity (<1.012). Result when hydrostatic pressure is higher than inward oncotic pressure, lymphatic obstruction, or excess body fluid due to sodium retention (renal failure).

21
Q

Transudate Histology

A

Filled cavities with a uniform pink, very acellular.

22
Q

Exudates

A

Protein rich accumulations with a higher specific gravity. Result from increased vascular permeability. Most commonly seen with inflammation.

23
Q

Thrombosis

A

Transformation of flowing blood to a semisolid containing platelets, fibrin, and other cellular elements, within the vascular system of a living organism.

24
Q

Extrinsic pathway of blood coagulation

A

Tissue Factor sits in extravascular space. Vessel ruptured, TF contacts plasma, binds factor VII, that complex activates factor X, which converts prothrombin into thrombin. Thrombin converts fibrinogen to fibrin. TF can also activate IX to amplify clotting via intrinsic pathway.

25
Q

Fibrinolysis

A

Cutting of fibrin clot to prevent overclotting. Controlled by plasmin.

26
Q

Role of platelets in thrombosis

A

When platelets aggregate, they release calcium, ADP, and Thromboxine A. This promotes fibrin, which weaves platelets together.

27
Q

Role of endothelial cells in thrombosis

A

In their resting state, endothelial cells are anti-thrombotic. Have heparin like molecules where antithrombin can bind, thrombomodulin, PGI and NO2.

28
Q

Virchow’s Triad

A

Endothelial Injury (arterial), Alteration in Flow, Hypercoagulable Blood.

Causes of thrombosis.

29
Q

Primary Vs Secondary Hypercoagulable Blood

A

Primary is defect in clotting factors, like increased factor 5. Secondary are things like oral contraceptives etc.

30
Q

Lines of Zahn

A

Alternating layers of fibrin/platelets and red cells. Indicative of thrombus in flowing blood.

31
Q

Clot

A

Clot is a solidified mass outside the vascular system, or in blood vessels in a dead person. Chicken fat (plasma) and currant jelly (RBCs).

32
Q

What can thrombi do?

A

Propagate (grow towards heart in veins, away from heart in arteries), lyse, organize (scar), recanalize, become infected, embolize.

33
Q

Embolus

A

Anything that travels through vessels that is not liquid blood.

34
Q

Thromboemboli

A

Most common in deep veins of legs, can also be arterial

35
Q

Paradoxical embolus

A

Embolus forms in venous circulation, passes through PFO and ends up in systemic circulation.

36
Q

Other emboli

A

Atheroemboli, air, fat (from marrow)

37
Q

Infarction

A

Area of irreversible tissue necrosis due to ischemia.

38
Q

White Infarct

A

Spleen, Kidney, Heart. Caused by arterial insufficiency, single blood supply, tissue not reperfused.

39
Q

Red Infarct

A

Testicle, Lungs, Intestines, Liver. Caused by venous insufficiency, or in tissues with dual blood supply.

40
Q

Infarct histology

A

Coagulative Necrosis. Thick, bright pink, no nuclei.

41
Q

Disseminated Intravascular Coagulation

A

Excessive secondary activation of coagulation where thrombi form in microvasculature, which depletes clotting factors. However, this causes bleeding elsewhere. Micro-infarction of organs occurs, hemmorhage, and shock! Also show schistocytes!!!!

42
Q

Shock

A

Circulatory collapse. Global hypotension and hypoperfusion. This causes acidosis and multi-system organ failure.

43
Q

3 Major causes of Shock

A

Cardiogenic (MI, arrythmia), hypovolemic (hemmorhage), Septic (infection).

44
Q

Septic Shock

A

Secondary to infection (most commonly bacteria). Bacterial products cause vasodilation and increased vascular permeability. Associated with proinflammatory cytokines like IL-1 and TNF

45
Q

Nonprogressive (compensated) shock

A

Blood pressure maintained, no urine output, tachycardia, vasoconstriction. Cold and clammy with rapid heart beat. Recovery possible.

46
Q

Progressive (decompensated) shock

A

Hypotension, tissue hypoperfusion and hypoxia, renal insufficiency

47
Q

Irreversible shock

A

BP down, pH down, organs die, death occurs

48
Q

Histology of shock in liver

A

Centrilobular necrosis of the liver so it kind of looks like cirrhosis without the rigidity of the nodules.

2013/2014 (23 decks)

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