Intro To Pathology Lecture 4

Front 1

Ascites

Back 1

Hydroperitoneum, fluid in the peritoneum

Front 2

Anasarca

Back 2

Severe and generalized edema with widespread subcutaneous swelling

Front 3

Review the causes of edema that produce transudate.

Back 3

Increased hydrostatic pressure can be caused by cardiac failure, renal failure(through activation of renin-angiotensin which increases blood volume by retaining Na+) and reduced osmotic pressure which is caused by nephrotic syndrome(leaks albumin), hepatic failure(doesn't make albumin), malnutrition

Front 4

exudate appears in what type of edema?

Back 4

inflammatory edema

Front 5

Congestion vs hyperemia

Back 5

Congestion = lack of sufficient outflow. Filled with DEOXYGENATED blood.
hyperemia = increased inflow due to excercise or inflammation. Filled with OXYGENATED blood.

Front 6

List the range and size of hematomas

Back 6

petechiae(1-2mm), purpura(>3 mm), ecchymoses(>1-2 cm)

Front 7

List the change in color of bruises and what pigmentous endogenous substance causes them

Back 7

Hemoglobin is reddish-blue and is degraded to bilirubin which is blue-green and turns into hemosiderin which is gold-brown

Front 8

endothelin

Back 8

a potent endothelial derived vasoconstrictor responsible for immediate constriction of arterial vessel following injury

Front 9

Describe primary hemostasis

Back 9

"Primary hemostasis is the activation of platelets into flat discs that secrete their granules to recruit more platelets forming the initial hemostatic plug.

Front 10

Describe secondary hemostasis

Back 10

Secondary hemostasis involves the membrane bound pro-coagulant Tissue Factor(Factor III or thromboplastin) that acts with factor VII to activate the coagulation cascade which results in thrombin production. Thrombin cleaves fibrinogen into the insoluble fibrin and also recruits more platelets to solidify the initial plug.

Front 11

describe what tissue plasminogen activator(t-PA) does.

Back 11

t-PA along with thrombomodulin serves to inhibit the coagulation pathway once a clot has formed to confine the hemostatic process to the site of injury.

Front 12

What cytokines cause leakiness in inflamed blood vessels?

Back 12

"Histamine, Bradykinin, Leukotrienes

Front 13

Describe how thrombomodulin works

Back 13

Thrombomodulin activates protein C which turns Thrombin from a pro-coagulant into an anti-coagulant.

Front 14

Describe Virchows Triad

Back 14

Endothelial injury and turbulent flow are reciprocative while both can lead to hypercoagulability. All three eventually cause thrombosis

Front 15

What is the Leiden Mutation?

Back 15

A substitution in factor V gene causing it to be resistant to cleavage by protein C(what anti-coagulative pathway is this?). This leads to a much higher rate of Deep Vein Thrombosis. The mutation is highly prevalent in the caucasion population.

Front 16

Heparin Induced Thrombocytopenia and Thrombosis

Back 16

Antibody response to heparin treatment that creates factor 4+heparin immune complexes thereby reducing platelet count.

Front 17

Describe causes of red infarcts

Back 17

Occur with venous occlusions(testis, ovaries), lungs(loose tissues), and tissue with dual circulation(lungs, intestines). It is also present in tissue that was previously obstructed with poor venous outflow and also when arterial supply is repaired to normal after ischemic damage(such as after angioplasty).

Front 18

Describe causes of white infarcts

Back 18

Happens in arterial occlusions in solid organs with end-arterial supply(heart, kidney, spleen) and where tissue is dense to prevent seepage of blood into necrotic area

Front 19

Describe time scale of necrosis.

Back 19

Acute vascular occlusion difficult to detect if it happens right before death. Tissue takes 4-12 hours to show necrosis with inflammation defining the borders within 1-2 days

Front 20

Describe how you distinguish a post-mortem infarct from an in vivo infarct.

Back 20

post mortem clot is gelatinous with dark red dependent zone where red cells settle by gravity and yellow clotted plasma supernatant. (current jelly and chicken fat). Post mortem clots are also not attached to vessel wall.

Thrombi are attached(atleast at the head) and have lines of Zahn which arise from forming in flowing blood.

Front 21

Describe the anti-coagulant pathways

Back 21

1.) Protein C activation via thrombomodulin-thrombin complex
2.) Antithrombin binding to heparin like molecules which cleave thrombin and cascade proteins
3.) t-plasminogen activator leads to plasmin production which cleaves fibrin.
4.) Tissue Factor Pathway Inhibitor

Front 22

What does aspirin do?

Back 22

Aspirin inhibits cyclooxygenase permanently thereby preventing platelets from synthesizing Thromboxane A2, which is a vasoconstrictor important for clotting. Aspirin also inhibits the production of the vasodilator Prostoglandin, but the epithelial cells that secrete PG can resynthesize cyclooxygenase.