Edwards.txt

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emm64
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147875
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Edwards.txt
Updated:
2012-04-16 01:14:11
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Systems S2 Edwards
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Systems 2 S2 Edwards
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  1. ´╗┐LPL
    • Lipoprotein Lipase
    • endothelial cells lining blood vessels of adipose(storage) and muscle(beta oxidation)
    • STIMULATED BY INSULIN
    • ApoCII is cofactor (surface of TG rich chylomicrons and VLDL)
  2. LPL deficiency
    • Hyperchylomicronemia and/or hypertriglyceridemia
    • Type I diabetics->acute pancreatitis & eruptive xanthomata from loss of LPL activity
  3. Liver Lipid metabolism
    • Endocytes chylomicron remnants
    • repackages & secretes VLDL(triglycerides and CE) or further to LDL (cholesterol ester-rich)
    • LDL cleared by liver (endocytosis after LDLR bound)
  4. Statins
    • indirectly upregulate hepatic LDL receptor through HMG-CoA Recductase inhibition
    • increase SREBP2 (transcription factor) processing and hepatic LDL rector expression
    • lowers plasma LDL 25-50%
    • DO NOT WORK FOR familial hypercholestrolaemia(receptors don't bind LDL) homozygotes
  5. How long does it take for chylomicrons (TG-rich) to clear from blood and fasting?
    12 Hours
  6. Plasma HDL
    • secreted into blood from liver (75%) and intestine (25%)
    • Niacin & exercise increase HDL
    • High HDL-reduced MI/athersclerosis risk
  7. LDL vs HDL
    • LDL in intima is oxidized and taken into macrophage depositing lipid CE into cells = FOAM CELLS
    • FOAM CELLS die and release nipid->becomes placque
    • HDL prevents LDL oxidation (ANTIOXIDANT) & removes excess toxic choleserol from foam cells
    • Lower LDL=diet, statins
    • Raise HDL=exercise, niacin (low compliance), limit alcohol
  8. Beta Oxidation
    • Mitochondrial matrix
    • increased, fasting, starvation, TYpe 1, some Type 2
    • produce ketone bodies
    • require carnitine, CPTI,CPTII (transerases for each membrane in mitochondria)
    • blocked by malonyl CoA
    • High Beta-ox->excess acetyl CoA->ketone bodies (only in liver)
  9. Keto acidosis
    • problem in fasting and TYpe 1 diabetes
    • acidify blood->coma death
    • breath contains acetone-sweet smelling
    • ketonuria-ketone bodies in urine
    • associated with acute pancreatitis,eruptive xanthomata, severe hypertriglyceridemia
  10. Portahepatis
    • hepatic artery (30%) systemic circ
    • portal vein (70%) from GI and spleen (largest)
    • bile duct
    • Travel along TRACTS (other vessel is Central Vein)
  11. Liver anatomy
    • Hepatocytes with bile (brown) canuliculs between them (store glycogen PAS stain)
    • Sinusoids lined with endothelial cells
    • Kupffer cell-macrophages inside sinusoids
    • stellate cells between endothelium and hepatocytes store VITAMIN A
  12. Stellate cells
    Btwn endotheliumand hepatocytes->store Vitamin A
  13. hepatocyte pathology
    • swelling when injured
    • inflammatory infiltrate (deep blue)
    • steatosis
    • apoptosis (deep pink)
  14. hepatocellular plates
    usually onecell thick, widened in regeneration and neoplasia
  15. cirrhosis
    large bands of (blue)fibrosis surrounding nodules of hepatocytes
  16. Steatosis
    fatty accumulation in hepatocytes
  17. hepatitis
    • infection
    • autoimmune
    • drugs
    • steatohepatits-fatty liver disease
  18. viral hepatitis
    • systemic-herpes, adeno, CMV, Rubella
    • Epstein Barr- MONO
    • Hepatitis A-G= acute (somechronic (> 6 months)
  19. Hepatitis A
    • fecal oral
    • day care, military water, seafood
    • most self limiting
    • no chronic
    • vaccine
  20. Hepatitis B
    • most (90%) self limited
    • ubiquitous body fluid
    • vertical, STD
    • most kids get chronic
    • Vaccine available
  21. Hep C
    • blood borne-transfusions, needless
    • CHRONIC INFECTION-80-90%
    • no vaccine
  22. Acute viral hepatitis
    • lobular inflammation
    • hepatocye injury-apaptosis, necrosis, swelling
    • NO FIBROSIS
    • hepatic failure when 80-90 % of hepatocytes necrose
  23. Chronic Viral hepatitis
    • inflammation in portal areas extended beyond in parenchyma
    • Regeneration evidence
    • fibrosis (scarring) -beginning in portal areas, periportal septa->BRIDGING FIBROSIS
    • cirrhosis(end stage liver disease)
  24. Bridging fibrosis
    • fibrosis connecting portal tracts->CIRRHOSIS
    • Transplant only option
    • cobblestone, nodular gross appearance
  25. Steatohepatitis
    • injury due to necroinflammatory activity and fat deposition->Mallory bodies (cytoplasmic inclusions)
    • lobular/pericentral fibrosis, chicken wire fibrosis
    • chronic hepatitis
    • alcohol or non-alcohol (NASH)
    • METABOLIC SYNDROME => NASH = insulin resistance, type 2 diabetes, obesity, hyperlipidemia
    • or caused by drugs
  26. Cirrhosis
    • Portal HTN
    • esophogeal varicies, caput medusae(musclesout at belly button
    • ascites-fluid accumulationinabdomen
    • hepatic encephalopathy (no detoxification)
    • coagulopathy
    • hepatocellular carcinoma
  27. Gall bladder
    columnar villiform structures similar to small intestine
  28. Gall stones
    • alteration from stasis or infection
    • composed of cholesterol
    • bilirubin, bile salts(Calcium) (Pigment stones) less than 50% cholesterol
    • females, obese,industrial, old, tribes
  29. cholecystitis
    • gall inflammation-> 90% have gall stones
    • yet only 25% of pts w stones develop clinically evident cholecystitis
    • acute=calculous 90%, trauma burns etc remainder
    • chronic-no history of acute, biliary colic, right upper quadrant pain, fibrotic(thick walls)
  30. Pancreas
    • acinar-exocrine
    • islets-endocrine, insulin, glucagon (rich vascularity)
  31. pancreatitis
    • gallsones & alcohol
    • AUTODIGESTION
    • enzymatic necrosis and inflammation
    • hemorrhage, edema and necrosis of fat or parenchyma
    • looks like soap
    • leads to fibrosis, scaring leaving just islets & fat
  32. Sulfonylureas
    • -amide (1st generation, cardiotoxicity)
    • gli-ide (2nd generation, no cardiotoxicity) (1-3 onset, 10,12-24 duration)
    • Glimepiride best protection against MI
    • A. Insulin Release
    • 1. inhibits ATP K+ channels
    • 2. depolarize islet Beta cells
    • 3. Ca2+ influx and induced insulin secretion
    • B. Depress glucogon
    • C. Enhance insulin activity
    • Side effects: weight gain, teratogenic, impaired liver kidney
    • Increase effect-H2 antagonist, Mg salt, oral anticogulants, salicylates, Beta blockers
    • Decrease effect-estrogen, thiazide diuretics, thyroid hormones
  33. Meglitinides
    • 1. bind to KATP channel on beta cell on different binding site than sulfonylureas
    • 2. depolarize
    • 3. Ca2+ influx -> release insulin
  34. Nateglinide
    • D-phenylalanine
    • more rapid less sustained
  35. Repaglinide
    benzoic acid derivative
  36. Biguanides
    • phenformin & metformin (glucophage)
    • 1. Activates AMP(K) -inhibit hepatic gluconeogenesis
    • 2. Increase insulin sensitivity, peripheral uptake
    • 3. Decrease glucose GI absorption
    • metformin used in combo
    • Contraindication - Iodinated radiographic contrast dye impairs kidney function
    • Adverse-GI upset, lactic acidosis, increased homocystein levels and B12 maleabsorption
  37. Thiazolidindiones
    • TZDs Rosiglatazone Avandia (increase CHD)
    • pioglitazone (no inc CHD)
    • 1. insulin-sensitizing through peroxisome proliferator- activated receptor gamma, PPARr -> nucleus production of glucose and lipid homeostasis
    • 2. Decrease hepatic gluconeogenesis
    • 3. Increase insulin dependent glucose uptake in muscle and fat
    • Adverse-risk of hepatitis (monitor liver)
    • Fluid retention, edema, weight gain,
  38. alpha-Glucosidase Inhibitors
    • competitive brush border enzyme->less glucose absorption
    • acarbose (precose) inhibits alpha amylase
    • miglitol (glyset) monosaccharide
  39. Aborption of glucose drugs
    • Alph-glucosidase inhibitors
    • biguanides
  40. Biosynthesis (hepatic gluconeogenesis) drugs
    • biguanides
    • thiazolidine diones
  41. Insulin uptake, effect enhancers
    • biguanides
    • thiazolidine diones
  42. Pancreas secretion
    • slufonylureas
    • Meglitinides
  43. H2 receptor antagonists
    • Histamine receptor
    • -TIDINES
  44. Proton Pump Inhibitors
    • -PRAZOLES
    • cytoprotective
  45. Antiemetic Agents
    • D2 Antagonists (dopamine
    • H1 Antagonists (histamine 1)
    • Muscarinic Antagonists
    • 5HT3 Antagonists (seratonin)
    • Corticosteroids
    • Cannibinoids

    • Emetic Agents
    • Syrop of Ipecac
    • Apomorphine
  46. Domperidone
    • Antiemetic and Laxative
    • does not cross blood brain barrier unlike other D2 antagonists

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