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pandachowmein
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Asialoglycoprotein
- Protein tagged for Hepatocyte denaturing by removal of surface sialic acid by neuraminidase
- Kuffer cells recognize asialoglycoproteins and engulf to destroy
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Alpha 1- antiTrypsin
- Protease inhibitor (anti-coagulation, anti thrombin)
- low levels in ZZ-homo deficiency -- pulmonary emphysema resulting from overactive protease
- Low level also a sign of hepatic transport disorder due to liver damage (trypsin inhibitor overstorage)
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Alpha 1-Macroglobulin
- Protease inhibitor (anti-coagulation AND anti-clot breaker)
- -- inhibits both thrombin (clotting) and plasmin (fibrinolysis)
- Onocotic pressure keeper in nephrotic patients (replaces albulmin)
- Elevation indicaties renal failure or analbuminenia as proteins are peed out
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Beta 1 band on protein electrophorisis
- Apoprotein Transferrin - transport Ferric Iron (3+)
- Increase in transferrin (TIBC) - is a sign of iron deficiency
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Beta 2 band on protein eletrophorisis
- Fibrinogen clotting factor
- C3 compliment protein
- some reason has to with obstructive jaundice
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Albumin (most neg charged on electrophorisis)
- Unconjugated Bilirubin transport (from spleen to liver)
- Oncotic pressure
- drug transport (warfrin and penicillin)
- Decrease means nephotic syndrom, or tissue inflammation or blood loss (could be genetic as well)
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Thyroxine
Thyroid hormones T3/T4 transport
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Retinol binding protein
Vita A transport
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Haptoglobin
- Free hemoglobin transport
- Scavenges hemoglobin diners from blood
- Used for intravescular hemolysis indicator (DIC would cause decrease in Hpt)
- Destroyed along with heme it transports
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Hemopexin
- Heme that escapes spleen and liver degradation is scavenged by hemopexin
- decrease Hpx could also be hemolytic anemia
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Ceruloplasmin
- Copper transport
- absence results in wilson's disease and copper deposits in eye (kaiser fletcher ring)
- Transferrin
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Alpha fetoprotein
- increase in prego means neuro tube defect
- decrease in prego means down's syndrom
- increase in adult means liver cancer (cause the fuck are you doing producing a fetal protein liver...)
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C-reactive protein
acute infection
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Liver enzymes
- Liver makes a lot of enzymes
- --Choline esterases
- -- Transaminases (AST/ALT)
- -- Phosphotases (ALP/AP)
- -- GGT
- -- LDH
- -- CK
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Choline-esterase
- degrades choline (neurotransmittor)
- Decrease in choline esterase:
- --overdose of choline esterase inhibitor (Myathenia gravis therapy)
- --Organophosphate poisoning
- --Scoline apnea (succinylcholine esterase deficiency)
- --Liver failure (it no make)
- Increase in choline esterase:
- --nephrotic syndrom (i pee it out)
- -- liver tumor (it make too much)
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SuccinylCholine
- Anasthetic
- Genetic Scoline apnea has deficient coline esterase for succinlcholine
- Over activation of anasthetic effects
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AST
- Aspartate transaminase
- -- Increase ALONE - MI/skeleto cell damage or RBC lysis
- -- Increase WITH ALT - acute liver hepatitus
- Normal increase with neonatal hemolysis due to RBC turnover
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ALT
- Alanin transaminase
- --increase ALONE - liver cirrhosis/disease
- --Increase WITH AST - acute liver hepatitus
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ALP
- Alkaline Phosphotase- released by hypertrophied cartilage to lay down calcium
- --Increase in ADULT WITH GGT means bile duct damage
- --Increase in ADULT WITHOUT GGT means bone tumor or some shit
- --Increase in CHILDHOOD/Placenta/After meals normal due to increase in bone formation and bile duct normal function
- use gammaGT to follow up billiary duct damage
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gammaGT
- Billiary protein
- Increase means cholestatic liver Disease
- useful over AST < ALT < ALP (from least useful to most besides gamma GT)
- Also a sign of alcohol or drug abuse
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LDH
- Lactate dehydrogenase
- increase in LDH1 - myocardio infarction
- increase in LDH5 - acute hepatitus
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Creatine Kinase
- CK-BB for brain tumors
- CK-MB for Myocardio infarctions
- CK-MM for muscle dystrophies
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Amylase
- mainly in pancrease
- acute pancreatitus - you are going to get neutrophilia as well.... GOOO NEUTROPHILS
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Asprin as anti-clot
- COX-1 inhibitor
- Thromboxane inhibitor (prostacylin inhibitor too but thromboxane more preferential)
- Will increase bleeding time test
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Thromboxane
- clotting factor
- increase platelet aggregation and number
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von Willibrand Factor
- present on endothelium(bound to factor 8 to inactivate it), platelet surface, plasma soluble protein
- binds to GP1b receptors on other platelets, promote platelet aggregation
- Deficiency is von Wilibrand disease
- --increase bleeding time test
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Thrombin (2a)
- major clotting factor
- intrinsic and extrinsic final effector
- self promote by activating 8a(tenase complex) and 5a(Prothrombin complex) and 11a (christmas activator)
- fibrin formation by cutting fibrinogen into fibrin and 13a(fibrin crosslinker) activation
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9/9a
- Christmast factor - forms 10ase complex with 8a and Ca2+
- binds platelet with vita K carboxylation
- Hemophelia B missing
- can be activated by extrinsic 7a
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8/8a
- Bound to von Wilibrand when inactive
- forms 10ase complex to activate 10a
- hemophilia A when deficient
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10ase
- intrisinc
- 8a+9a---platelet
- with ca2+ turns 10agolden
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Extrinsic 10a
- 7a bound platelet and tissue factor 3
- this is tested in PT test (no intrinsic activation)
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Heprin
- AntiThrombin III activator
- kills 12a, 11a, 9a, 10a, 2a and probably 7a
- not degraded
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Warfrin
Anti-vita K, it no add COO- to factors 7, 9, 10, 2
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Vita K
- Adds COO- to 7, 9, 10, 2
- needed for blood clot
- babies sometimes have a deficiency
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12/12a
- first one of the intrinsic (don't need cause 2a can activate 11a too)
- pre-kallikren + HMWK+ collagen activates
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13/13a
- transglutamase
- cross links fibrin dimers
- activated by thrombin
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Fibrin
- Dimers from inactive Fibrinogen
- activated by Thrombin
- forms dimers when activated and linked by 13a
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Prothrombin Complex
- 10a+5a+2+Calcium
- 10a from tenase complex
- 5a is activated by 2a (or mechanical stress as shown by research paper)
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Plasmin
- Cuts fibrin (clot buster)
- activated by tissue plasminogen activator and urokinase
- deactivated by alpha2 antiplasmin and plasminogen activator type 1/2
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Urokinase/Tissue plasminogen activator
- plasmin activator
- bust a clot
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Serpin/alpha-2 antiplasmin/plasminogen activator 1/2
- anti-plasmin
- don't bust a clot
- alpha 2 macroglobulin also a anti plasmin
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Protein C/S
- Thrombinmodulin activated effector
- busts up 8a and 5a turning then back to 5/8
- effectivly bust up tenase and prothrombin complex respectivly
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Thrombinmodulin
- needs thrombin to work
- -- an example of self regulation, lots of thrombin activate thrombinmodulin
- activates protein C,S
- deactivate 5a and 8a
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Prothrombin time (PT)
- really checking for common pathway and extrinsic pathway
- Tissue factor 3 is added without collagenase, only extrinsic and common is activated
- Increased time in --vitamin K deficiency
- --factor 7 deficiency - over comsumption of substrates in DIC
- --warfrin therapy
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Partial Thromboplastin time (PTT)
- Add in kaolin to simulate collagen
- tests for intrinsic and common pathway, especially hemophilia A/B and von Wilibrand pathway (factor 8)
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Bleeding time
- adds nothing, tests for platelet number and functionality
- Increased time when taking asprin
- or when there is a decresae in von Wilibrand factor (reduced platelet to platelet adhesions)
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DMT1
- Transports ferrous iron into lumen cell
- controlled by hepcidin
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Ferritin
- Iron storage in cell, ferric iron
- forms hemosiderin during iron overload
- plasma levels correspond to bone marrow levels
- decreased plasma levels means iron deficiency
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Ferriportin
- transports ferrous iron out of cell and into plasma
- hepcidin controlled (IL-6 indrectly controled)
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Transferrin
- transports ferric iron within plasma from asportion to area of utilization
- High capacity and low saturation indicates anemia (due to iron deficiency)
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Iron overload
- thalassemia
- genetic hemochromatosis DMT1 upregulation
- Lead poisoning
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Colbalamine
B12 with cobolt co-factor
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B12 absoption
- ilium absorption requring intrinsic factor (from parietal cells)
- lack of absorption is pernicious anemia
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B12 reactions
- Methymalonyl CoA Mutase -- B12 only
- Homoysteine methyltransferase -- WITH folate
- if abscent --> methylmalonic acidimeia (conclusive for B12 def)
- increased homosytein could mean B12 deficiency but also could be folate deficiency
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B12 Def.
- Methymalonic acidimeia (definitive)
- all folate anemia signs PLUS neurological disorders
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Folate reactions
- makes purines and thymidine
- mythylation of DNA/RNA
- needed for cell replication
- which is why cells can't divid (they grow but can't divid) without folate
- and why pregos need more folatic acid
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B6 defi
- not really part of the lecture but B6 is ALAsynthase cofactor
- Ala synthase deficient means no Heme and produce sideroblast anemia
- no heme/hemoglobin == siderobplast, microcytic, iron overload anemia... pretty much
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Folate drugs
Leuvencore... i think, dude look at pharmaco
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RBC breakdown
- Heme-->biliverdin-->bilirubin (this is in spleen)
- bilirubin +albumin = unconjugated indirect bilirubin (this is in plasma right out of spleen)
- bilirubin -albumin + glucuronic acid = conjudated direct bilirubin-diglucuronide (this is in hepatocyte)
- direct bilirubin --> bile --> gut --> poop or reuptake
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NADPH nicotinamide cofactor
- strong anti-oxident and produce steroids
- pentose phosphate pathway made by G6PDH
- shortage of NADPH means excess H2O2
- this will be the way RBCs lyse and aqumulate heinz bodies (heme fragments) in G6PDH def
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G6PDH def.
- can't lead with reactive O2 because NADPH not made from the pentose phosphate pathway
- jaundice resulting from hemolysis
- Heniz body (oxidative stress) Hb degraded hemolytic anemia
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Methemoglobin
- Hemoglobin bound to ferric iron without oxygen
- none functional, results from oxidative compound poisoning
- Methemoglobin reductase to reverse
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Congenital Methemoglobin
Congenital His-Try mutation that favors oxidation of ferrous iron to ferric once bound to hemoglobin
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Fetal Hemoglobin
- alpha/gamma hemoglobin
- high affinity for O2 low affinity for BPG
- can't form salt group with BPG so decrease affinity for its negative allosteric regulator (BPG)
- His --> Ser
- Will take O2 from Hb (from mother) like Myoglobin
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CO poisoning
- CO high affinity for Hemoglobin 25k times
- Irreversible
- 0.1% CO is lethal
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Myoglobin
- High affinity for O2
- takes from Hemoglobin
- gives to cytochrome oxidase in ETC
- O2 storage in muscle
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Co-operative binidng
- Hemoglobin trait
- Each successive O2 addition increase affinity for next O2 and O2 is scavenged
- Each successive O2 subtraction decreases affinity and all O2 is completely released
- Low [O2] low affinity --> release all O2
- High [O2] high affinith --> bind all O2
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Negative allosteric regulators of hemoglobin
- neg allosterics help decrease O2 affinity thus release at site of need
- all are metabolic by products
- BPG>CO2>Low pH
- stablize T(deoxy state)
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CO2 transport
- Hemoglobin trasports small fraction in carbamate
- mostly as HCO3- (CO2+H2O-->H2CO3-->HCO3-) in tissue rich in CO2
- Hb will buffer extra H+
- Once at lung low CO2 drive reaction in reverse and HCO3- is turned back into CO2 and H2O
- Cl- used to balance ion concentration
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Carbonic Anhydrase
- Perfect enzyme, completely converts
- CO2+H2O --> H2CO3 and reverse
- depending on concetration
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