Extras from LOs

Question 1

What are 3 factors that are inhibiting platelet effects due to the presence of a normal endothelium

Answer 1

Prostacyclin (PGI2)
NO
adenosine diphosphatase

Question 2

Regurgitate the whole Clotting cascade

Answer 2

Intrinsic = need calcium and negative surface –> 12, 11, 9, 8, 10

Extrinsic = need tissue factor –> 7 –> 10

From 10 –> add 5 and you form thrombin from prothrombin.

thrombin changes fibrinogen to fibrin

Question 3

what three markers are found in individuals with an MI?

Answer 3

troponin

CK-MB

Myoglobin

Question 4

What are D-Dimers?

Answer 4

fibrin-derived. useful markers of several thrombotic states

Question 5

What’s the difference between fibrinoid necrosis and fibrinous inflammation?

Answer 5

fibrinoid necrosis –> antigens and antibodies are deposited in the walls of arteries –> these end up leaking out with FIBRIN and make a BRIGHT pink and amorphous appearance.. called “fibrinoid” or “fibrin like”

fibrinous exudate develops when the vascular leaks are large. characteristic of inflammation in the LINING OF body cavities (like meninges, pericardium, pleura)

Question 6

Antithrombin 3 deficiency is what kind of mutation?

Answer 6

primary hypercoaguable disorder

this is similar to protein C or S deficiencies –> presents with venous thrombosis and recurrent thromboembolism beginning in adolescence or early adulthood.

Question 7

macrophages of the central nervous system?

liver?

spleen and lymph nodes?

Answer 7

microglial cells

kupffer cells

sinus histiocytes

Question 8

What is a2-antiplasmin?

Answer 8

a plasma protein that binds and rapidly inhibits free plasmin.

Question 9

What is MCAD?

what is the problem?

what can’t you process?

what happens?

Answer 9

medium chain acyl-cow dehydrogenase mutation

can’t process medium-chain fatty acids –> sudden death from hypoglycemia after the child eats nothing for a few hours

Question 10

what are the 4 patterns of inflammation?

Answer 10

serous inflammation –> cell poor fluid.. created by cell injury or into body cavities lined by peritoneum, pleura, or pericardium

fibrinous –> vascular leaks are large.. characteristic of lining of body cavities

purulent –> production of pus, exudate with neutrophils, \liquefactive debris of necrotic cells, edema fluid (abscesses are associated with purulent inflammatory tissue)

ulcer –> shedding of inflamed necrotic tissue. (can only occur when necrosis and resultant inflammation exist on or near a surface)

Question 11

what is DIC?

what is it a complication of?

what’s going to happen?

so symptoms initially what can turn into what?

Answer 11

Disseminated Intravascular Coagulation

complication of a large # of conditions associated with SYSTEMIC activation of thrombin.

pretty much it leads to widespread formation of thrombi in the microcirculation, which uses up platelets and often activates fibrinolytic mechanisms.

thrombosis can turn into a bleeding catastrophe

Question 12

What is the function of Heparin or heparin like molecules? (what is it binding and what does it do)

Answer 12

they bind and activate antithrombin III, which then inhibits thrombin and a bunch of factors (IXa, Xa, XIa, XIIa) so you don’t clot.