Robbins Ch 4: Hemodynamic Disorders, Thrombosis And Shock

Front 1

Definition of "edema"

Back 1

the accumulation of abnormal amounts of fluid in the intercellular tissue spaces or body cavities; two main types are inflammatory edema (an exudate) and noninflammatory (hemodynamic) edema (a transudate)

Front 2

Definition of "anasarca"

Back 2

severe generalized edema, producing marked swelling of subcutaneous tissues

Front 3

Conditions under which noninflammatory edema may occur (4)

Back 3

1. increase in intravascular hydrostatic pressure
2. decrease in colloid osmotic pressure of plasma
3. impairment of lymph flow
4. renal retention of salt and water

Front 4

Reasons for increase in intravascular hydrostatic pressure

Back 4

Local increases:
--impaired venous outflow, e.g from thrombosis
General increases:
--congestive heart failure affecting right ventricular function
--constrictive pericarditis
--cirrhosis of liver
--arteriolar dilatation

Front 5

Reasons for reduced plasma oncotic pressure

Back 5

1. Loss of albumin (i.e., nephrotic syndrome)
2. Reduced synthesis of serum proteins (e.g., cirrhosis of liver or malnutrition)

Front 6

Reasons for lymphatic obstruction

Back 6

(usually localized)
--inflammatory (e.g. from rxn to parasite)
--neoplasm or cancer metastasis
--postsurgical/postirradiation

Front 7

Reasons for renal retention of salt and water

Back 7

--acute renal failure
--post-streptococcal glomerulonephritis
--secondary aldosteronism due to decreased blood volume

Front 8

Definition of "dependent edema"

Back 8

subcutaneous edema of the lower extremities due to right heart failure, called "dependent" because of the effects of gravity

Front 9

Definition of "pitting edema"

Back 9

generalized edema (anasarca) caused by renal dysfunction where finger pressure squeezes edemetous fluid out of subcutaneous tissues, leaving depressions

Front 10

Morphological appearance of brain edema

Back 10

In generalized edema: brain heavier than normal; swollen and flattened gyri, narrowed sulci; gelatinous white matter; perivascular spaces are widened into halos around vessels

Front 11

Definition of "hyperemia"

Back 11

AKA "active hyperemia," when arterial and arteriolar dilatation, caused by sympathetic neurogenic mechanisms, produce an increased flow into capillary beds with opening of inactive capillaries; causes redness (e.g., blushing)

Front 12

Definition of "congestion"

Back 12

AKA "passive hyperemia," results from impaired venous drainage and causes a blue-red coloration because of the increase in deoxygenated hemoglobin in the dammed blood. It can be localized, as in portal hypertension secondary to cirrhosis, or systemic, with either lungs affected (left heart failure) or the entire body except the lungs (right heart failure)

Front 13

These 3 organs develop the most obvious signs of chronic passive congestion

Back 13

lungs, liver and spleen

Front 14

Definition of "heart-failure cells"

Back 14

Chronic passive congestion of the lungs causes alveolar capillaries to be engorged with blood. When one ruptures, blood hemorrhages into the alveolar space and is cleaned up by macrophages. The breakdown of the hemoglobin fills the macrophages with the brown-yellow pigment hemosiderin, which is indigestible. This happens most often because of left heart failure.

Front 15

Definition of "nutmeg liver"

Back 15

Red-blue speckled appearance of liver with chronic passive congestion due to the distension of the central vein and surrounding sinusoids with blood; the peripheral hepatocytes develop fatty change.

Front 16

Definition of "ecchymosis"

Back 16

A large (greater than 2cm) subcutaneous hematoma, e.g., a bruise

Front 17

Definition of "thrombosis"

Back 17

A pathologic process in which a clotted mass of blood forms within the non-interrupted vascular system

Front 18

Overview of sequence of events in formation of normal hemostatic plug (4 steps)

Back 18

1. Brief period of vasoconstriction
2. Platelet activation and aggregation (primary hemostasis)
3. Formation of thrombin and fibrin (secondary hemostasis)
4. Polymerized fibrin and aggregated platelets form solid mass

Front 19

Agonists released by activated platelets

Back 19

--adenosine diphosphate (ADP)
--thromboxane A2
--serotonin

Front 20

Anti-platelet effects of endothelium

Back 20

--insulation from collagen
--surface prostacyclin (PGI2) and nitric oxide (NO) that vasodilate and inhibit platelet aggregation

Front 21

Anticoagulant properties of endothelium

Back 21

--membrane-associated heparin-like molecules that catalyze the inactivation of thrombin and other factors via antithrombin III
--membrane-associated thrombomodulin that binds thrombin, turning it into an anticoagulant and activating Protein C, which inhibits clotting
--Produces Protein S, which is a cofactor for Protein C activity

Front 22

Fibrinolytic properties of endothelium

Back 22

--synthesis of tissue-type plasminogen activators (t-PA) that promote fibrinolytic activity and help clear fibrin deposits

Front 23

Prothrombotic properties of endothelium

Back 23

--synthesize and secrete von Willebrand factor (vWF) which is essential for platelet adhesion
--can be induced to make tissue factor, which activates the intrinsic clotting pathway
--express binding sites for activated factors IX and X
--secrete t-PA inhibitor

Front 24

alpha granules

Back 24

Granules in platelets that contain fibrinogen, fibronectin, factors V and VIII, platelet factor 4 and growth factors. Their membranes also contain P-selectin.

Front 25

electron-dense bodies

Back 25

Granules in platelets that store nonmetabolic ATP and ADP, ionized calcium, histamine, serotonin, and epinephrine.

Front 26

3 reactions of platelet activation

Back 26

1. adhesion/shape change
2. secretion/release reaction
3. aggregation

Front 27

What happens during platelet adhesion?

Back 27

Platelets attach to exposed collagen via pseudopods and vWF, then spread out and adhere tightly.

Front 28

What occurs during the secretion (release reaction) of platelets?

Back 28

After adhesion, agonists bind to platelet surface receptors and activate phospholipase C and signal transduction pathways mediated by protein kinase A and C, which allow the alpha granules and electron-dense bodies (delta granules) to secrete their contents.