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Pathology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

Movement of fluid into/out of tissues is dependent on the ________ pressure on the arterial end and the _______ _______ _______ pressure on the venous end of the capillary.

A

hydrostatic pressure on arterial end

plasma colloid oncotic pressure on venous end

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2
Q

Fluid that remains in the tissues is drained by the ________ system.

A

lymphatic

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3
Q

The dude that first said that the passage of fluid through the capillary wall is dependent on the balance between hydrostatic pressure and osmotic pressure was named _______.

A

Starling

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4
Q

Define edema.

A

Increased fluid in interstitial spaces.

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5
Q

What is anasarca?

A

Severe systemic edema.

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6
Q

Edema in a body cavity is called _______.

A

ascites

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7
Q

Protein-poor edema is called ________ and protein-rich edema is called ________.

A

transudate is protein poor

exudate is protein rich

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8
Q

Can edema be either inflammatory or non-inflammatory in origin?

A

Yeah

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9
Q

Name the five general causes of edema.

A
  1. Increased hydrostatic pressure.
  2. Decreased colloid osmotic pressure.
  3. Lymphatic obstruction.
  4. Primary renal sodium retention with associated H2O retention.
  5. Increased vascular permeability.
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10
Q

Name one disease that causes a generalized increase in hydrostatic pressure and one disease that results in a regional increase in hydrostatic pressure.

A

Generalized: congestive heart failure
Regional: DVT

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11
Q

Hyperemia and congestion both cause __________, _________, and __________.

A

vasodilation, increased volume, and increased pressure

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12
Q

How can kidney disease result in a decrease in colloid osmotic pressure?

A

Proteinuria - loss of serum proteins lowers osmotic pressure.

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13
Q

What is hyperemia?

A

Increased inflow and engorgement of oxygenated blood, which causes erythema.

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14
Q

What is congestion?

A

Decreased outflow of blood, capillary bed swells with deoxygenated blood, called cyanosis.

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15
Q

Hemorrhagic centrilobar necrosis (aka nutmeg liver) was an example of what type of phenomenon as presented in lecture?

A

Congestion

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16
Q

The extravasation of blood from vessels into the extravascular space is called a _______.

A

hemorrhage

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17
Q

What is hemorrhagic diathesis?

A

Increased susceptibility to bleeding, often due to hypocoagulability.

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18
Q

What is a hematoma?

A

Localized hemorrhage that is confined in an organ or tissue.

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19
Q

___________ is characterized by 1-2mm hemorrhages on skin, mucous membranes, or serosal surfaces.

A

Petechiae

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20
Q

Name the four possible causes of petechiae/purpura. Note that purpura (3mm spots or larger) would also require additional trauma, vasculitis, or increased vascular fragility.

A
  1. Increased local intravascular pressure
  2. Low platelet count (thrombocytopenia)
  3. Defective platelet function (uremia)
  4. Loss in vascular wall support (vitamin C deficiency)
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21
Q

What is the fancy word for bruises?

A

Ecchymoses

22
Q

The blue-green color of a bruise is due to ________ and the gold-brown color is due to ________.

A

Blue-green caused by bilirubin, gold-brown caused by hemosiderin.

23
Q

A hemorrhage into a body cavity is called a _________.

A

hemothorax

24
Q

What are the three components of thrombosis?

A
  1. Endothelium
  2. Platelets
  3. Coagulation cascade
25
Q

Name the four events of primary hemostasis that occur following vascular injury.

A
  1. Vasocontriction (quick)
  2. Exposure of thrombogenic substances: ECM, vWF
  3. Platelet activation, adherence and aggregation
  4. Formation of a primary hemostatic plug
26
Q

Name the six events of secondary hemostasis that occur following vascular injury.

A
  1. Release of tissue factors (factor III/thromboplastin from endothelial cells) and phospholipids (from platelets).
  2. Coagulation cascade generates thrombin.
  3. Thrombin converts fibrinogen to fibrin.
  4. Fibrin meshwork consolidates the primary plug.
  5. Secondary hemostatic plug is formed from the polymerized fibrin, platelet aggregates, RBCs, and WBCs.
  6. Counter-regulatory mechanisms limit the plug to the local injury site.
27
Q

In platelet aggregation, injury to endothelial cells exposes __________, which binds to ___________ receptors on platelets. This allows platelets to stick to the subendothelium. Next, platelets stick to each other with their ___________ receptors, using ________ as cross-bridges between platelets.

A

Injury exposes von Willebrand Factor on the subendothelium which binds to glycoprotein 1b receptors on platelets. Platelets stick to each other using GpIIb-IIIa receptors with fibrinogen serving as the cross-bridge.

28
Q

Bernard-Soulier Syndrome is a congenital disease of __________.

A

clotting

29
Q

Glanzmann Thrombasthenia is a congenital disease of __________.

A

clotting

30
Q

What are thrombin’s five roles in hemostasis and cellular activation?

A
  1. Stimulates PDGF release
  2. Activates endothelial cells
  3. Aggregates platelets
  4. Activates lymphocytes
  5. Increases endothelial-neutrophil adhesion
31
Q

What is Virchow’s Triad in thrombosis?

A
  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoagulability
32
Q

In maintaining hemostasis, the _________ of the endothelium is the most important factor, especially in the heart and arteries.

A

integrity

33
Q

Does the endothelium need to be denuded or physically injured to contribute to the development of thrombosis?

A

Nope

34
Q

Turbulent blood flow is important in the development of ________ and _______ thrombosis.

A

arterial and cardiac

35
Q

Stasis is important in the development of ________ thrombi.

A

venous

36
Q

What are the two types of hypercoagulability?

A

Primary (genetic) and secondary (ex. prolonged bedrest, MI, cancer, Afib, heparin-induced thrombocytopenia).

37
Q

In which direction do thrombi grow?

A

Towards the heart

38
Q

What are Lines of Zahn?

A

Gross or microscopic morphological changes of a thrombus that include pale platelet/fibrin layers that alternate with dark RBC-rich areas.

39
Q

What are the three types of thrombi?

A
  1. Mural - happens in heart chambers or aortic lumen
  2. Arterial
  3. Venous (aka phlebothrombosis)
40
Q

What type of thrombi is characterized by a long red cast in the vessel lumen?

A

venous

41
Q

A gelatinous clot with a yellow supernatant region and a RBC-rich lower region is a _________ clot.

A

postmortem

42
Q

What are the four fates of a thrombi?

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and recanalization
43
Q

Is original lumen size retained after recanalization?

A

Nope it gets smaller

44
Q

When an emboli lodge in small blood vessels, downstream tissues can undergo _______ necrosis.

A

ischemic

45
Q

Are fat droplets, nitrogen bubbles, atherosclerotic debris, tumor fragments, bone marrow, or foreign bodies types of thrombi?

A

Yeah

46
Q

The lungs and liver are more likely to incur a ____ infarct because blood from the alternate supply can infiltrate the ischemic cells.

A

red

47
Q

Do red infarcts happen with venous, or arterial occlusions?

A

venous

48
Q

White infarcts happen in _____ organs and are often ______-shaped.

A

solid organs, wedge-shaped

49
Q

What are the three types of shock?

A

Cardiogenic, hypovolemic, septic

50
Q

What is the clinical triad of septic shock?

A
  1. Hypotension
  2. Disseminated intravascular coagulation (DIC)
  3. Metabolic disturbances
51
Q

What are the three stages of shock?

A
  1. Initial nonprogressive stage
  2. Progressive stage
  3. Irreversible stage

Pathology (6 decks)

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