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51 Cards in this Set
- Front
- Back
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Gal Stones Blocking the gal bladder.
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stop bile from being secreted into intestines, causes indigestion of fats (cannot emulsify fats)
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Gal Stones Blocking the common duct.
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stops bile and pancreatic enzymes (lipases, amylases, proteases) from being secreted into intestines- will not digest TG and Disaccharides - can cause type I diabetes because pancreatitis
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Pancreatitis
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Caused by gall stones blocking release of pancreatic juices, including zymogens. Zymogens will eventually self activate and nom away at the pancreas. Can lead to type 1 diabetes. Also caused by alcoholism and will also lead to problems with digestion of proteins, fats and sugars
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Elevated serum amylase
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diagnostic test for pancreatitis
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High Fat Diet
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causes Steartorrhea. causes oxidative stress via peroxisome overactivity
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Orlistat
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inhibits pancrease lipase so fat can't be absorbed, high fat diet causes indigestion (Alli)
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Olestra
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Fake fat. tastes like fat, but but body can't absorb it.
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Cholesterol absorption inhibitors
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bind to cholesterol in gut so it can't be absorbed, high fiber diet will do same thing naturally
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Vitamin absorption
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inhibited fat soluble Vitamin (ADEK) absorption if taking fat absorption inhibitors
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Steatorrhea
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fat in stool
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Carnitine
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Used to transport fatty acids from intermembrane space to the matrix of the mitochondria
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CPTI and CPTII defects
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Can't transport fatty acids into the mitochondrial matrix. Cant burn fatty acids for energy?
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Hyperlipoproteinemia
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cause by Apo protein defects or LPL defects (fat stays in blood)
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apoCII defect
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ApoCII marker protein on Chylomicrons is used to label them. If defective, target cells will not be able to take up triglycerides from them. Resulting in hyperlipoproteinemia
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Lipoprotein lipase deficiency
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Once chylomicrons/VLDLs are recognized, lipoprotein lipase typically breaks apart triglycerides into fatty acids to be absorbed. Deficiency in enzyme results in hyperlipoproteinemia.
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Familial hypercholesterolemia
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Liver doesnt recognize LDL particles in blood, therefore cant take them up
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LDL receptor defect
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Liver will not recognize LDLs due to defective receptor on the liver. LDL's are high in cholesterol and will stay in the blood --> familial hypercholesterolemia
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Apo B defect
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Liver will not recognize LDLs due to defective ApoB marker proteins on the LDL particles. LDL's are high in cholesterol and will stay in the blood --> familial hypercholesterolemia
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MCAD
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single base substitution of Glu->Lys, produces unstable MEDIUM chain acyl CoA dehydrogenase. Excrete dicarboxylic acids, formed from omega oxidation of fatty acids, into the urine.
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LCAD
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Similar to MCAD but with long chains?
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B12 deficiency
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Used as a coenzyme to convert L-Methylmalyonyl-CoA to Succinyl-CoA. Important for oxidation of ODD numbered fatty acids (increase in L-Methylmalyonyl-CoA if deficient)
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Biotin deficiency
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Inability to carboxylase... lots of problems. Oxidation of ODD chain fatty acids relys on carboxylation of propionyl-CoA to D-Methylmalonyl-CoA. Build up of odd chain fatty acids
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Methylmalonyl CoA mutase deficiency
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Converts L-Methylmalonyl-CoA to Succinyl-CoA during oxidation of ODD numbered fatty acids - rare disease - destroys kidneys
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Zellweger syndrome
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defect in peroxisomal enzymes (flavoprotein dehydrogenase). Problems metabolizing hydrogen peroxide leading to oxidative stress. A high fat diet would result in an increased production of peroxizomal enzymes and peroxide and hydroxyl radicals
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Ketoacidosis
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Build up of ketone bodies. Can be acidic...
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Antacids
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Chemically neutralize acid in the stomach
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Histamine (H2) blockers
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Intervate/block nerves in the stomach that stimulate acid production. Also use for immune system.
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Proton Pump inhibitors
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Block hyrogen/potassium channels. Blocks acid production.
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Encapsulated pancreatic enzymes
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Come in pills that people with cystic fibrosis take
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Benzoic acid
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Drug used to remove glycine & ammonia (treats urea cycle defects)
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Phenylbutyrate
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Drug used to remove glutamine & ammonia (treats urea cycle defects)
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Gastric reflux
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Stomach acid going up the espohagus and forming lesions (aka: acid reflux -- USE PPI, H2 Blockers & Antacids to treat)
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Ulcers
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People with O blood are most at risk. Cause by bacteria (H.pylori). Treat it with antibiotics.
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Cystic fibrosis
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Defective chloride ion pump. Causes thick mucas in the GI, causing problems for pancreatic juice release… destroying the pancreas. Leads to type 1 diabetes.
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Kwashiorkor
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general protein deficiency; essential amino acid deficiency
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Pancreatitis
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From obstruction of pancreatic duct. Zymogens slowley activate in pancreas and noms on itself.
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Hartnup disease
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Defect in neutral AA transport. Typically non essential AA, but tryptophan has trouble. Tryptophan is needed for NADH production. Pallegra like symptoms
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Cystinuria
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Defect in Cysteine, Lysine, Ornithine, and Arginine uptake/transfer. Also can't reuptake from kidneys. Can cause kidney stones from S-S bonds of cystine being insoluble in water.
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Celiac Disease
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The lining of the intestines contains areas called villi, which help absorb nutrients. When people with celiac disease eat foods or use products that contain gluten, their immune system reacts by damaging these vill
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Ammonia toxicity
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Can lead to tremors, slurring of spleech, blurring of vision (possible coma/death). acquired through liver problems (alcoholism/hepatitis/biliary obscruction) or heraditary through effects in enzymes (can lead to future mental retardation within a week of birth if not addressed)
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Urea cycle defects
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All urea cycle enzyme defects will result in an accumulation of ammonia in the body.
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Liver function tests
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Alanine aminotransferase and Aspartate aminotransferase assay used for blood. These enzymes in blood indicate leakage from liver due to inflamation.
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Albinism
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Defective melanin synthesis from Tyrosine (L-Dopa) via defective enzyme. Lack of pigmentatin, whitehair and pink skin.
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Alcaptonuria
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Defective tyrosine degredation via defective enzyme. Causes dark pigment in the urine and late developing arthrtis
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Homocystinuria
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Defective methionine degradation via defective enzyme. Faulty bone development, mental retardation.
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Maple Syrup Urine disease
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Defective degradation of Ile, Leu, and Val (branched chain AA) due to defective "brancehd-chain alpha-ket acid dehydrogenase complex. Vomiting, convulsions, mental retardation.
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Urea cycle defects
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Build up of ammonia in the body.. cant be converted to urea to be excreted. Defects at all of the urea cycle enzymes will have this effect. some will have a build up of intermediates (which ones?)
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Tyrosinemia I
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Defect of metabolism of tyrosine furthr along metabolism.
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Tyrosinemia II
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Defective tyrosine metabolism via tryrosine aminotransferase. Cant degrade tyrosine. Makes too much melanin. Cause pigmentation in palms.
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PKU
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Defective conversion of phenyl-alanine to tyrosine. Defect in phenylalaine hydroxylase. Neonatal vomiting and mental retardation
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Methylmalonic acidemia
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Defective conversion of propionyl-CoA to succinyl-CoA via defective methylmalonyl-CoA mutase. Problems with ODD chain fatty acids. Vomiting, convulsions, mental retardation, and early death.
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