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71 Cards in this Set

  • Front
  • Back
• Acetaminophen (Tylenol
be toxic, Uses CYP2E1, inducable by EtOH
• adhesion step
GPIa, and GPIb bind to collagen and vWF, respectivly
• ADP
- ADP granules released during recrutment, potent platelet activator.
• Aflatoxin B1
Aspergilus flavus, grows on peanuts, hepatocarcinogenisis in humans, 8,9epoxide is activated by 2 dif. isozymes of cytp450, modifies DNA(G>T mutation)
• alanine
produced by most tissues, alaninetransferase elevated is sign of liver damage
• Albumin
made by liver, 50-60% protein pool of plasma, important osmoregulator(70-80%), bind to many things, including Long chain FA's, many drugs, decreasing dose, but lengthning it too, Ca, Co, steroids, Zn, bilirubin.
• AMP In muscle glycogen degradation
allosteric activation of glycogen phosphoylase b, normally low concentration, increases many times with ATP decrease, activates PFK-1,
• anaerobic catabolism of glucose
important at initiation of exercise, during strenuous exercise, and in Fast twitch glycolitic muscle with low oxidative capacity
• antibodies
complex with antigens, classical interaction, activation of complement
• BCAA carbon skeletons
most can be oxidized to CO2 in liver, muscle can handle alanine, aspartate, glutamate, valine, leucine and isoleucine, but not others, glutamine synthesis from them after 5 steps
• BCAA oxidation
fuel for gut and skeletal muscle, lucine, isolucine and valine, increased metabolism (20% max) during rest(in muscle) if glucose and and AA's are elevated
• brain
net producer of glutamine
• Branched-chain amino acids
valine, leucine, isoleucine
• Calcium
reqired for coagulation if factors, muscle activation,
• cAMP
adenylate cyclase activates it, it activates protein kinase, part of glycogen degradation pathway
• Chylomicrons-
too big to get through endothelial cells of the liver
• collagen
when exposed, glycoprotiens bind (GPIa),
• complement proteins
activation in immune responce, MAC
• components is unique to the extrinsic pathway
VII to VIIa, tissue factor III
• Cori cycle
lactate turned to glucose
• CYP2EI
EtoH and acetaminophen
• CYP3A4
most common Ctyochrome p450 isozyme
• cytochrome P450
uses NADPH to detox, found in smooth ER
• Factor VIII
activated by thrombin (IIa), activates X
• Factor X
activated by VIIIa, Tissue Factor III/VIIa
• fibrinogen
turned by thrombin into a soft clot (fibrin)
• glutamine
major carrier of NH4+ to kidney
• glutathione
interacts with NAPQI forms mercaptopuric acid>>kidney>>urine
• glycogen phosphorylase kinase
fully activates glycogen phosphorylase b, activated by Ca as well,
• glycogen synthase
activated by insulin after high carb meal
• glycoproteins IIb and IIIa (GPIIb/IIIa)-
come available after GPIb binds vWF
• hippurate
secondary product salicylic acid secretion
• HMWK
high molecular weight kininogen
• immunoglobulins
antibodies
• Kallikrein
begins life as prekallikrein, activted by XIIa (intrinsic pathway), assembled with HMWK, XI and XII on a surface, unknown importance in coagulation.
• kidney-
excretes waste products like murcaptopuric acid (NAPQI), salicyluric acid (asprin), etc
• lactate
enters the Kori cycle, increases in muscle in anaerobic conditions, esp. Fast twich glycolytic fibers.
• metabolism of aspirin
glycine added and excreated as salicylurate(primary) and hippoate
• N-acetyl-p benzoquinoneimine (NAPQI)
Toxic Byproduct to Acetaminophen breakdown,excreted after conjugation with glutathione
• N-acetyl cysteine
administered for Tylonol poisoning
• NADH
produced to help reduce methemoglobin back to ferrus and
• NADPH
used by p450 to detox
• NO
vasodialator and_________
• nonthrombogenic surface
endothelial surfaces
oxidation of ethanol and acetaldehyde
CYP2E1
• Plasmin
active clot degradation
• Plasminogen
- inactive form of Plasmin, activated by plasminogen activators
• platelet activation
activation, aggragation, secretion
• platelet-subendothelial interaction
vWF, and glycoproteins, binding of GPIb exposes GPIIb/GPIIIa to fibinogen and vWF
• prostaglandin I2 (PGI2)-
Activated Protien C stimulates endothelial cell to secrete to reduce aggregation.
• Protein C and protein S
suppress coagulation cascade, S binds C to clot with -carboxyglutamate/Ca, destroy VIIIa and Va. anticoagulant, decreasing thrombin
• protein kinase
activated by cAMP, activates phosphorylase kinase, >>glycogen degradation
• prothrombin
factor II, activated by IIa, Va, Xa
• Thrombin
factor IIa, activated by Xa and Va, activates V, VIII, XI, XIII, binds to thrombomodulin to inhibit cascade.
• Tissue factor III-
extrinsic factor, activates X to Xa
• valine, isoleucine, and leucine
BCAA's- used as fuel in most tissues
• Vitamin K
esential for production of -carboxyglutamic acid residues
• VLDL
Uses NADPH to be made, impared in liver disease
• von Wille-brand factor (vWF)-
contained in alpha granules
• -carboxyglutamic acid residues
made with Vitamin K cofactor, found on factors VII, IX, X and prothrombin, that bind Ca which is attracted to negative charged platelet surface,
 Cysteine
Blank
 Elastin
fibrous structural protein, hyrophobic strechyness
 Hyaluronic acid
glucuronic acid bound to N acetyl-glucosamine (glycosaminoglycan), cell migration in Embryogenisis, Morphogenisis and Wound Healing!!
 Hydroxylation reactions
see below
 hydroxylysine
lysine residue, posttranslational, requires vit C,- attachment site dissacarite moieties and crosslinks
 hydroxyproline
proline residue, posttranslational, req. vit C, H bond stabilize triple helix, scurvy
 Laminin
adhesion protein, alpha helix, 3 subunits, Disorder causes JEB (blisters)
 the major components of connective tissue
?
 Type I collagen
most abundant,skin bone, tendon, cornea. 3 strands, 1/3 is glycine
 Vitamin C (ascorbic acid
required to form hydoxylysine, scurvy
• glycogen phosphorylase b
-AMP activates, does not need phosphorilation like liver isozyme,