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35 Cards in this Set

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What do hageman factors do?

They activate the clotting cascade and the Kinin cascade . It causes clotting and can work in the Kinin/bradykinin/ plasmin/ fibrin system

What does bradykinin cause?

Pain and vascular permeability

What does kalikrein cause?



Activates hangman factor. Chalkier cleaves plasminogen toplasmin which activates clot lysis by cleaving fiber. HF also create costs through fibrin

What is the complement cascade?

Protein cascade that leads to activation of C3

Describe the protein cascade?


What is the key step?

C3 splits to C3a and C3b and then C3a continues to go and split C5 to C5a and C5b and then C5b goes on to activate C5-9




The key step is activation of C3

What does C3a and C5b cause

vascular dilitation and permeability

What does C5-C9 cause

It induced microbial and cell necrosis

What are the mediators in the plasma clotting system>

Plasmin--> It celaves C3-C5 and activates HF


HF- triggers knin cascade and clotting cascade


Plasmin- Acts on fibrin to cleave and increase vascular permeability


Fibrin is formed---> Vascular occlusion which leads to ischemia and necrosis

What is the other name for HF

Factor XII

What does hangman activate

HF activates Kinin and clotting system and it is activated by kalikrien and plasmin

What does chalkier activate?

HF, Coplement system C3-C5 and fibrinolysis, **It is chemotactic

NAme a vasoactice amine, its action and where is it released from>

Histamine and it is released from last cells/ basophils and it constricts BV resulting in permeability

2 preformed cellular factors

Vasoactive amines and lysosomal constituents

Lysosomal constituents is released from what

Released from POLY and the actin tissue destruction

PAF derived from where?

Cell membrane along with prostaglandins

Nickname of PAF

Ultimate mediator

What does PAF do

Acts as a vasodilator, vascular permeability leading to edema, WBC activation and chemotaxis.




Promotes synth of other mediators

How do e get Arachidonic acid? 2 pathways

We get it from Phospholipase 2 and the two pathways are the lipooxygenase and the Cyclooxygenanse pathways

actions of the Cyclooxygen pathway and the Lipooxygenase pathways

Cyclooxygenase- Arachidonic to prostaglandin


Lipooxygenase- Arachidonic to Leukotrienes

PGD, PGE, PGF, cause what? PGI2?

D, E*, F cause fEver


I2- VasodIlation

leukotriences cause what CDE? B?

CDE- cause casoconstriction B- Chemotaxis

What do corticosteroids prevent?

Formation of arachidonic acid (Antiinflammatory)

What inhibits cyclooxygenase?

NSAIDS

What are cyclooxyrgenases made of?where are they found

They are made of Cox-1, Cox-2,


1- is found in all cell types while


2- is found mainly in WBC's during inflammation (induced)

PGI2 comes from where? PGE2

PGI- Endothelium (vasoconstriction)

PGE- macrophages (fever)



Leukotrienes are made by?

WBC's

5 lipooxygenase is enhanced by?

FLAP

LT CDE causes? CTB

CDE- vascular perm


B- chemostaxis



Cytokines come from? Two groups

They come from lymphocytes and macrophages . IL1/TNF & IL-6

What do the different 3 cytokines cause

Il-1/TN-A- fever weight loss and induce ELAM and VCAM. Il-6 Fever

Chemokines role

regulate chemotaxis of cells to site of injury

Two macrophages are produced by what, roles of each ?

eNOS- endothelium


iNOS- macrophages


eNOS- puts a break on inflammation


iNOS- vasodilation

Role of free radicals?

GEnerated in macrophages and they cause damage to tissue. aging/ alter DNA can incite apoptosis

What enzyme can limit free radicals?

Superoxide dimutase

What is th main neuropeptide, produces what.


What is purinergic signlaing

Substance P- produces pain and perm




purinergic signaling is the ADP/ATP released from Polys that result in clotting.