All diseases and conditions discussed in lectures for exam 1
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| Reducing Sugar Test | If reducing sugar test is positive, then sugar is present in the urine. Reducing sugar test does not specify which sugar. There are specific tests for Glucose and Galactose using glucose oxidase and galactose oxidase.
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| Amyloidosis | characterized by the formation of amyloid fibers. These fibers come from proteins that have become insoluble, often due to a conformational change such as partial folding, misfolding, or cleavage.
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| HbA | Normal hemoglobin, 2 alpha and 2 beta chains
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| HbA2 | Acts as normal hemoglobin, 2 alpha and 2 delta chains
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| HbS | Glu to Val substitution, poor oxygen binding, where 2,3 BPG worsens Sickle Cell.
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| HbF | Higher affinity for Oxygen, 2 alpha and 2 gamma chains. 2,3 BPG binding is reduced.
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| HbM | A mutation that makes Hb resistant to reduction by NADH, which is involved in the conversion of Hb-Fe3+ back to Hb-Fe2+. The prior cannot carry oxygen and results in methemoglobinemia (blue people of Kentucky).
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| Deficiency in Methemoglobin Reductase | Causes HbM
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| Carboxyhemoglobin Test | High levels of carboxyhemoglobin indicate carbon monoxide poisoning
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| HbA1c Test | Tests for non-specific glycosylatoin
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| Creatine Kinase Test Result of MM | Skeletal Muscle Injury
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| Creatine Kinase Test Result of BB | Brain Injury
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| Creatine Kinase Test Result of MB | Cardiac Muscle Injury
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| HbC | Glu to Lys substitution, pushes water out of the cell, Oxygen won't bind.
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| Sickle Cell Disease | Polymerization is due to the presence of a hydrophobic protrusion and a complimentary hydrophobic pocket. Low oxygen concentration causes more Hb to go into the deoxy form and results in more sickling.
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| Carcinoma | Tumor derived from epithelial tissue
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| Jaundice | Increased bilirubin levels
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| Serum Bilirubin Test | Levels of indirect or direct bilirubin are measured
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| Cholestasis | A possible reason for jaundice due to a blockage in the bile
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| TIBC | Total Iron Binding Capacity, determines the amount of transferrin unbound to iron. This can show defficiency in iron.
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| Porphyias | Genetic disorders that result in deficiency in certain enzymes in heme synthesis
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| Lead Poisoning | Inhibits first and last steps of heme synthesis, causing build of intermediates.
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| Niacin | Needed for NAD
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| Riboflavin | Needed for FAD
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| Thiamine | Needed for TPP
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| Pantothenate | Needed for CoA
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| Biotin | Needed for Biotin
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| Tetrahydrofolate | Needed for Folic Acid
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| Pyridoxine | Needed for Pyridoxal phosphate
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| Ischemia | Decreased blood flow to specific cells only; can cause lactate build up
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| Hypoxia | Decreased oxygen supply body wide; leads to acidosis and increased anaerobic metabolism
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| Acidosis | Caused by carbonic acid or lactic acid; low oxygen or high carbon dioxide in tissues
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| Alanine and Asparate Aminotransferase Test (ALT and ASP) | Used to test for liver function, as they are present at high levels in the liver and can leak out of damaged liver cells. This means ALT and AST would be high if a liver is damaged.
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| Alkaline Phosphotase (ALP) | Found at high concentrations in the cells that line the biliary tract. Disorders affecting the bile duct can result in elevated serum levels of ALP.
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| Serum Albumin test | d. As albumin is synthesized by the liver, patients with suboptimal liver function would show low serum albumin.
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| Prothrombin Time (PTT or PTT) | Prolonged in patients where one of the following liver products is in a reduced amount: Factor I, II, V, X, VII. Extrinsic and Common Pathways
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| Activated Prothrombin Time (aPTT) | Activated Prothromboplastin Time (aPTT) is increased when one or more of the following liver products is in a reduced amount: Factor I, II, V, X, VII, IX, XI, or XII. Intrinsic and Common Pathways.
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| Ischemia | Decreased blood flow to specific cells only, increased lactate build up.
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| Hypoxia | Decreased oxygen supply body wide, leads to acidosis.
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| Acidosis | Lower pH in cells, can be caused by lowered oxygen levels or elevated carbon dioxide levels. Caused by build up of lactic acid or carbonic acid.
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| Scurvy | Caused by a vitamin C deficiency, which is required as a cofactor in the hydroxylation of proline and lysine, which contributes to the non-covalent bonding of collagen.
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| Vitamin K Inhibition | Aspirin is a Vitamin K inhibitor. Vitamin K serves as a cofactor for Factors II, VII, X, IX, and protein C/S. Vitamin K deficiency can be found in diet, Tb infection, antibiotic use, and klling of bacteria in gut.
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| Marfan Syndrome | Occurs due to lack of fibrillin, which helps maintain structure of elastin fibers.
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| Anaphylaxis | Causes vessels to dilate and become more permeable due to release of histamine from mast cells.
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| Scars and Keloids | Results when too much connective tissue builds up after wound healing.
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| Cirrhosis | Results due to damaged reticular fibers in liver, collagen fibers replace reticular fibers. Collagen fibers are thicker, liver organization is messed up so filter and blood flow gets impeded.
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| Basal Cell Carcinoma | Tumor of epithelial tissue, where there is an overgrowth of cells from the stratum basale. Keratinocytes are growing out of control.
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| Squamous Cell Carcinoma | Tumor of epithelial tissue, most common.
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| Melanoma | Assymetrical, irregular boarders, change in color, or diameter .
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| Albinism | Genetic defect in the enzyme tyrosinase, melanocytes are present but cannot produce melanin.
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| Hemophilia A | Deficiency in factor VIII, X link disorder, symptoms include joint and muscle hemorrhage, easy bruising and prolonged bleeding from wounds.
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| Hemophilia B | Deficiency in factor IX, prevalence 1/10 of that in hemophilia A, sx include prolonged coagulation times and decreased factor IX clotting activity.
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| D-Dimer Test | Measures Fiber Degradation to test for
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| Factor XIII Deficiency | Leads to neonatal umbilical cord bleeding, intracranial hemorrhage, and soft tissue hematomas.
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| Von Willebrand Disease | Inherited deficiency in vWF. Most common inheribited bleeding disorder.
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| Factor XI Deficiency | Leads to increased bleeding.
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| ATIII Deficiency (anti-thrombin) | Shows DVT and PE.
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| Bernard-Soulier Syndrome | Caused by a deficiency in the GPIIb protein which disrupts platelet adhesion to subendothelial collagen.
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| Glanzmann's Thrombasthenia | Bleeding disorder caused by a decrease in the functional platelet membrane protein GPIIb. If you recall, GPIIb is responsible for platelet aggregation.
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| Lactose intolerance | A condition of pain, nausea, and flatulence following ingestion of foods containing lactose. This can be caused by low levels of lactase, or intestinal (injury of intestinal villi that absorb) injury (caused by gastroenteritis, colitis, etc.).
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| Fructose Malabsorption (intolerance) | Adolase B deficiency, which blocks fructose 1-Phosphate conversion to glyceraldehyde or DHAP. Symptoms include vomiting, intestinal discomfort, hypoglycemia, hepatomegaly, fructose detected in urine, and can lead to hepatic and renal failure.
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| Glycemic Index | An indication of how quickly blood glucose levels rise following a food’s ingestion.
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| GLUT 1 | Found in RBC and has a low Km for glucose, not insulin dependent.
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| GLUT 2 | Found in the Liver and has a high Km for glucose.
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| GLUT 3 | Found in the Brain and has a low Km for glucose, not insulin dependent
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| GLUT 4 | Insulin Dependent, found in Adipose and Muscle, high Km for glucose.
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| G6PD Deficiency | Causes a lack of NADPH, which would result in sensitivity to oxidative species.
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| Essential Fructoseuria | Involves a deficiency in fructokinase, which will block fructose from being converted to fructose 1-phosphate. Sx include benign, fructose buildup that is secreted in urine.
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| Classical Galactosemia | Deficiency in Galactose 1-phosphate transferase, converting galactose 1-phosphate to glucose 1-phosphate. Sx include vomitting, diarrhea, jaundice, liver failure, cataracts, fatal if not tx. Tx includes elimination of galactose from diet
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| Nonclassical Galactosemia | § Galactokinase deficiency which blocks conversion of galactose to galactose 1-phosphate. Sx include galactose in blood and urine, cataracts. Tx includes elimination of galactose from diet.
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| Uncoupling Ox Phos | The process whereby protons leak back into the matrix without going through the ATP synthase pore, dissipating the electrochemical gradient across the membrane without generating ATP.
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| Kearnes-Sayre Syndrome | Deletion of segments of tRNA. Onset before age 20 characterized by ophthalmoplegia (other eye defects) and cardiac conduct defects.
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| Pearson Syndrome | Deletion of contiguous segments of tRNA and OxPhos polypeptides. Affects bone marrow due to disorder of OxPhos.
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| Myoclonic epilepsy and ragged red fiber disease (MERRF) | Mutated tRNA (lysine). Symptoms include myoclonic epilepsy, ragged red fibers, progressive dementia.
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| Mitochondrial myopathy encephalopathy lactic acidosis and stroke like episodes (MELAS) | Mutated tRNA (leucine). Neurodegeneration characterized by strokelike episodes.
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| Leigh disease | Mutations in subunits of ATP synthase and causes optic atrophy, ophthalmoplegia.
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| Leber hereditary optic neuropathy (LHON) | Mutation in NADH dehydrogenase. Late onset, acute optic atrophy.
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| Parkinson's Disease | Rotenone impedes complex 1 activity and leads to reduction in dopaminergic neurons which produce dopamine.
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| Reprofusion Injury | Myocardial infarct leads to loss of aerobic respiration (ox phos). Increase in ROS Opening of mitochondrial permeability transition pore (MPTP). Opening allows cytochrome C to leak out of mitochondria (Apoptosis), which ultimately leads to cell death.
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| Rotenone | Impedes Complex I
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| Malonate | Impedes Complex II
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| Antimycin A | Impedes Complex III
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| Cyanide | Impedes Complex IV
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| Carbon Monoxide | Impedes Complex IV
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| Oligomycin | Impedes Complex V
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| Microcytic | Small Red Cells
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| Macrocytic | Large Red Cells
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| Hemolytic | Breakdown of Red Blood Cells
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| Alpha Thalassemia | Arise from complete gene deletions, reducing size and Hb concentration of RBC. Less alpha.
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| Beta Thalassemia | Arise from heterogenous genetic disease and deletions, promoter mutations, and splice junction mutations. Homo is worse.
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| Methemoglobinemia | Can be aquired or congenital (cytochrome b5 reductase deficiency). Oxygen can't bind to heme because of Ferric state.
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| Osteoporosis | Bone is broken down by osteoclasts faster than osteoblasts are able to build.
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| Paget's Disease | Bone becomes thicker, as it is being built/repaired quicker than it is being broken down.
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| Auricular Hematomas | Caused by repeated trauma. Hematomas between the perichondrium and the cartilage, which prevents nutrition. Underlying cartilage dies and is replaced by dense irregular connective tissue.
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| Meniscal Tears | Menisci stabilize and cushion the knee, stressed often so tears are common; Tears on the outside are not as bad because blood vessels are available to help repair;Inner meniscus is often removed if damaged because it is avascular and doesn't repair.
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| Place these in order of largest to smallest: Myofiber, Myofibril, Cell, and Muscle | Cell > Myofibril > Myofiber > Muscle
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| Achondroplasia | Problems with the zone of proliferation; Skulls continue to grow because it is intramembranous ossification; Long bones however quit lengthening
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| Osteoarthritis | Age, repetitive use, trauma cause chondroblasts to start overproliferating; Too much water, too many cells makes the cartilage start to fall apart; Pieces of floating cartilage (joint mice) cause problems for the joint surface; Usually isolated problem
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| Rhuematoid Arthritis | Autoimmune disease, cause unknown; Joint coverings thicken and capsular blood increases causing the joint to warm; Formation of pannus (extra cells, specifically white blood cells, accumulate in joint reducing viscosity); Tends to be bilateral;
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