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CC LECTURE
Exam
| Question | Answer |
|---|---|
| ● Refers to a collection of organic molecules of varying chemical composition - Are grouped together on the basis of their solubility in nonpolar solvents | Lipids |
| 4 main groups | ○ Fatty Acids (Saturated and Unsaturated) ○ Glycerides (Glycerol-containing Lipids) ○ Nonglyceride Lipids (Sphingolipids,Steroids,Wax) ○ Complex Lipids (Lipoproteins) |
| ★ When oxidized, each gram of fat releases 9 kcal of energy, or more than twice the energy released by oxidation of a gram of carbohydrate | ENERGY SOURCE |
| In the form of triglycerides (TAG) in adipocytes | ENERGY STORAGE |
| ★ Phosphoglycerides, sphingolipids, and steroids make up the basic structure of all cell membranes | CELL MEMBRANE STRUCTURAL COMPONENTS |
| Steroid Hormones | Hormones |
| Lipid-soluble vitamins (A, D, E, K) | Vitamins |
| Dietary fat serves as a carrier of the lipid-soluble vitamins | VITAMIN ABSORPTION |
| fats act as shock absorber | PROTECTION |
| subcutaneous fat | Insulation |
| ● Are long-chain monocarboxylic acids ● Generally contain an even number of carbon atoms | Fatty Acids |
| Less than 6 carbons | Short chain Fatty acids |
| 6-10 Carbons | Medium-Chain Fatty acids |
| Long-Chain Fatty Acids | LONG-CHAIN FATTY ACIDS |
| o Each C being “saturated” with H o General Formula: CH3(CH2)nCOOH | SATURATED FATTY ACIDS |
| ○ Composed of at least one carbon-to-carbon double bond ○ Are almost in the cis configuration | UNSATURATED FATTY ACIDS |
| Composed of one carbon-to-carbon double bond | Monosaturated Fatty Acids (MUFA) |
| Composed of more than one carbon-to-carbon double bond, ○ are identified by position of the double bond nearest the methyl end (CH3) of the carbon chain ;this is described as an omega number; | Polysaturated Fatty Acids (PUFA) |
| H’s on the same side of the double bond; fold into a U-like formation; naturally occurring. | cis-FATTY ACID |
| ○ H’s on the opposite side of the double bond; occur in partially hydrogenated food. | trans-FATTY ACID |
| Fatty acids react with alcohols to form esters and water | ESTERIFICATION |
| ● Producing fatty acids from esters ● Opposite of esterification | ACID HYDROLYSIS |
| ● Is the base-catalyzed hydrolysis of an ester ● the product of this reaction, an ionized salt, is a soap | SAPONIFICATION |
| ○ Used in the food industry to convert polyunsaturated vegetable oils into saturated solid fats | HYDROGENATION |
| ○ Carried out to add hydrogen to some, but not all, double bonds in polyunsaturated oils ○ In this way liquid vegetable oils are converted into solid form (Crisco and margarine) | PARTIAL HYDROGENATION |
| ● Are lipid esters that contain the glycerol molecule and fatty acids ● TWO CLASSES | Glycerides |
| nonionic and nonpolar | Neutral Glycerides |
| have polar region, the phosphoryl group, in addition to the nonpolar fatty acid tails | Phosphoglycerides |
| - Produced after the esterification of glycerol with a fatty acid | Neutral Glycerides |
| ● Esterification may occur at one, two, or all three positions, producing: | Monoglycerides, Diglycerides, Triglycerides - Most imporant and main storage form of lipids in a man (adipocytes) |
| ○ ○ ○ Are lipids that are not derived from glycerol Amphipathic and structural components of cellular membranes Derived from sphingosine (long chain, N-containing alcohol) | SPHINGOLIPIDS |
| ↪ is also an example of a phospholipid; the smallest sphingolipid in terms of molecular mass | Sphingomyelins |
| ■ Include the cerebrosides, sulfatides, and gangliosides ■ Are built on a ceramide backbone structure, which is a fatty acid amide derivative of sphingosine | Glycosphingolipids |
| ■ Located throughout the body, but are particularly important structural lipid components of nerve cell membranes ■ Found in abundance in the myelin sheath the surrounds and insulate cells of the CNS | SPHINGOMYELINS |
| Are characterized by the presence of a single monosaccharide head group | CEREBROSIDES |
| Found in the membranes of macrophages | Glucocerebroside |
| Found almost exclusively in the membranes of brain cells - Consists of ceramide jointed to the monosaccharide to galactose | Galactocerebroside |
| Contains the steroid nucleus (Steroid carbon skeleton) | Steroid |
| Example of steroid | Cholesterol |
| ○ Amphipathic ○ Involved in the regulation of the fluidity of the membrane as a result of the nonpolar fused ring ○ Hydroxyl group is polar ○ Perhydrocyclopentanophenanthrene ring | Cholesterol |
| Are amphipathic derivatives of cholesterol Synthesized in the liver and stored in the gallbladder ■ Cholate ↪ helps in fat digestion ■ Chenodeoxycholate | Balt Salts |
| whose polar hydroxyl groups interact with water and whose hydrophobic regions bind to lipids | Emulsifying Agent |
| STEROID HORMONES | ○ Testosterone ○ Progesterone ○ Estrone, Estrogen, and its derivatives ○ Cortisone and Cortisol ○ Aldosterone |
| Derived from many different sources and have a variety of chemical compositions, depending on the source | Waxes |
| Are bonded to other types of molecules | Complex Lipids |
| ● Consist of a core of hydrophobic lipids surrounded by amphipathic proteins, phospholipids, and cholesterol ● Typically spherical in shape and range in size 10 to 1200 nm | Lipoproteins |
| Composed of both lipids and proteins, | Apolipoproteins |
| CLASSIFICATION (BASED ON ULTRACENTRIFUGATION) | ○ Chylomicrons [chylos] ○ Very-low-density LPP [VLDL] ○ Low-density LPP [LDL] ○ High-density LPP [HDL] |
| ● Major protein on HDL ● Measure of anti-atherogenic HDL present in plasma | Apo A-I |
| Apo A-B ● Is a large protein with MW 500 kD ● Principal protein on LDL, VLDL, and Chylomicrons o Apo B-100 o Apo B-48 | Apo A-B |
| ● Is found on LDL and VLDL ● Ligand for the LDL receptor | Apo B-100 |
| ● Exclusively found in chylomicrons | Apo B-48 |
| ● Found in LDL, VLDL, and HDL ● Serves as a ligand for the LDL receptor and the chylomicron remnant receptor ● Apo E2, Apo E3, Apo E4 | Apo E |
| ● Contain apo B-48 ● Account for the turbidity of postprandial plasma ● Readily float to the top of stored plasma and form a creamy layer o chylous, turbid, milky, cloudy, lipemic plasma/serum ● Produced by the intestine | CHYLOMICRONS |
| Increased Chylomicrons | Cloudy Serum |
| Increased triglycerides | Cloudy Postprandial |
| ● Contain apo B-100, apo E, and apo C ● Produced by the liver ● Rich in TAG like chylomicrons ● Account for most of the turbidity observed in fasting hyperlipidemicplasma specimens but do not form a top, creamy layer | VLDL |
| ● Contains apo B-100 and apo E ● Primarily formed as a consequence of the lipolysis of VLDL ● Readily taken up by cells via the LDL receptor o Accounts for the reason that elevated LDL levels promote atherosclerosis | Low Density Lipoprotein |
| ● Smallest and the most dense ● Synthesized by both the liver and intestine ● Can exist either as disk-shaped or as spherical-shaped particles | High Density Lipoprotein |
| - Most active form in removing excess cholesterol from peripheral cells ▪ Also called as Nascent HDL | DISCOIDAL HDL |
| Accepts Cholesterol | Spherical HDL |
| ● Larger in size and richer in lipid than HDL3 ● May be more efficient in delivering lipids to the liver | HDL2 |
| The Four Pathways | 1. Absorption Pathway 2. Exogenous Pathway 3. Endogenous Pathway 4. Reverse Cholesterol Transport Pathway |
| Occurs in the Small Intestine Small Intestine absorbs food | Absorption Pathway |
| Chylomicrons are now secreted into bloodstream o Will interact with proteoglycans ▪ LPL (Lipoprotein Lipase) goes to Chylomicrons until they bind | Exogenous Pathway |
| Involves TAG o Endogenous TAG ▪ Packaged into VLDL | Endogenous Pathway |
| ● Excess cholesterol diffused out of peripheral cells o Will be carried to Nascent HDL by ABCA-1 transporter ▪ Encoded by ABCA-1 gene ● Nascent HDL receives Cholesterol o LCAT (Lecithin Cholesterol Acyltransferase) | REVERSE CHOLESTEROL TRANSPORT PATHWAY |
| Minor Lipoproteins | ● Intermediate Density Lipoprotein ● Lipoprotein (a) |
| ABNORMAL | ● LpX Lipoprotein ● ẞ-VLDL Lipoprotein or Floating ẞ Lipoprotein |
| Is an abnormal lipoprotein found in patients with obstructive biliary disease, and in patients with familial lecithin/cholesterol acyltransferase (LCAT) deficiency | LpX Lipoprotein |
| Is an abnormal lipoprotein that accumulates in type3 hyperlipoproteinemia | ẞ-VLDL Lipoprotein / Floating ẞ Lipoprotein |
| ● Genetic abnormalities ● Environmental/Lifestyle imbalances ● Develop secondarily, as a consequence of other diseases ● Associated with CHD or arteriosclerosis | DYSLIPIDEMIA |
| 2 Categories (Dyslipidemia) | o Hyperlipoproteinemias o Hypolipoproteinemias |
| ● Hypercholesterolemia ● Hypertriglyceridemia ● Combined Hyperlipidemia | HYPERLIPOPROTEINEMIA |
| ● Most closely linked to heart disease ● Increased in LDL cholesterol ● Genetic abnormalities | Hypercholesterolemia |
| ▪ Individuals synthesize intracellular cholesterol normally, but lack, or are deficient in,active LDL receptors ▪ Causes premature CAD | FAMILIAL HYPERCHOLESTEROLEMIA |
| - Cholesterol deposits on the backs of the hands, knuckles and the Achilles Tendon | Tendon xanthomas |
| Which are cholesterol deposits in the cornea | Arcus |
| ● Result of an imbalance between synthesis and clearance of VLDL in the circulation | Hypertriglyceridemia |
| Two types (Hypertriglyceridemia) | ● FAMILIAL HYPERTRIGLYCERIDEMIA ● SECONDARY HYPERTRIGLYCERIDEMIA |
| ● Presence of elevated levels of serum total cholesterol and triglycerides ● Considered at increased risk of CHD | Combined Hyperlipoproteinemia |
| ● Currently thought to confer increased risk ofCHD and CVD ● Can block plasminogen, forming clots along the arterial wall that will not be dissolved | Lp(a) Elevation |
| ● Are abnormalities marked by decreased lipoprotein concentrations o Hypoalphalipoproteinemia o Hypobetalipoproteinemia ▪ • Is a disorder consisting of low levels of LDLcholesterol or apolipoprotein B | Hypolipoproteinemia |
| ● Indicates an isolated decrease in circulating HDL ● Tangier Disease ● HDL concentrations as low as 1-2 mg/dL (0.03 – 0.05 mmol/L) | Hypoalphalipoproteinemia |
| - Is a disorder consisting of low levels of LDLcholesterol or apolipoprotein B | Hypobetalipoproteinemia |
| LCAT Deficiency 2 forms: | Complete (Homozygous - Corneal Clouding, Nephropathy, Hemolytic Anemia, HDL deficiency Mild (Heterozygous) - Fish eye |
| being at the outer region of your kidney, it will be the one containing your blood vessels which is connected to your nephrons. | Renal Cortex |
| being at the innermost, it contains the renal pyramid. Makes up about 8 to 12 renal pyramids, which contains about 1 million nephrons. | Renal Medulla |
| Functional unit of your kidney. | Nephrons |
| Loop of Henle, Collecting Ducts | Renal Medulla |
| Glomerulus, PCT, DCT | Renal Cortex |
| is a cluster or tuft of your capillaries | Glomerulus |
| single layer of epithelial cells. | Bowman Capsule |
| Cortical Nephron | 85% |
| Juxtamedullary Nephron | 15% |
| Glomerulus (Order) | Afferent arteriole→tuft of capillaries (glomerulus) → efferent arteriole |
| In men, the kidneys typically produce about | 180 liters per day. |
| The movement of substances out of the tubules, across the surrounding interstitial fluid | Reabsorption |
| So, the glomerular filtrate contains substances such | Water, Glucose, amino acids and inorganic ions. |
| Approximately how much percent of sodium ions are reabsobred here through various methods | 65% |
| Thin segments of the loop of Henle are lined with: | Squamous Epithelium |
| The study of how our human body works | Physiology |
| Can kidneys be considered an endocrine organ? | Yes |
| RAAS, the renin-angiotensin-aldosterone system. ▪ It helps control our blood pressure and it indirectly helps maintain the level of sodium and potassium. | Renin |
| Related to your erythrocytes or RBC ▪ Stimulates RBC production | Erythropoietin |
| Process on which unnecessary substances are being removed in our blood | Renal Blood Flow |
| Volume of blood filtered per minute | Glomerular Filtration Rate |
| What can pass through the glomerulus | Water, Electrolytes, Glucose, NPN's |
| Cannot pass through the glomerulus | Plasma proteins, Cellular elements, Protein-bound molecules |
| Happens about 90% in your proximal Convoluted tubule | Tubular Reabsorption |
| FACTORS THAT CAN HELP IN THE REABSORPTION OF THE DIFFERENT SUBSTANCES | 1. Osmosis 2. Diffusion 3. Passive Transport 4. Active Transport |
| The concentration of your substance in the blood above which the kidneys begin to remove it into the urine. | Renal Threshold |
| 160-180mg/dL | Glucose |
| Requires energy. From lower to a higher area. | Active Transport |
| Does not need energy. From higher to lower area | Passive Transport |
| Related to your aldosterone in which when a person has Conn Syndrome they are making too much aldosterone. | CONN SYNDROME |
| ● Not producing enough aldosterone. It is the opposite of Conn Syndrome | ADDISON’S DISEASE |
| ● Related to your antidiuretic hormone ● Increase antidiuretic hormone (ADH) ● Since there is increased antidiuretic hormone then there is increased water being reabsorbed. | SIADH |
| ● Related to your antidiuretic hormone ● Decrease antidiuretic hormone (ADH) ● Since there is decreased antidiuretic hormone then there is decreased water being reabsorbed. ● The role of your antidiuretic hormone (ADH) is that it controls your water. | DIABETES INSPIDUS |
| Two major functions of tubular secretion: | 1. Eliminating waste products not filtered by the glomerulus 2. Regulating the acid-base balance in the body through the secretion of hydrogen ions |
| The tests being performed here in order to check if the glomerulus is functioning well it's what we call your | Clearance Test |
| Readilyavailableinthebodybecauseitisan inhibitor of cysteine proteinase ▪ Produced by all nucleated cells ▪ Not affected by age, sex, and muscle mass | Cystatin C |
| Often the first function to be affected in renal diseases | Tubular Reabsorption |
| Tests performed in order to check if the kidney’s Tubular Reabsorption function is operating well | Concentration Tests |
| o Ability of the tubules to either concentrate or dilute the urine o Urine is concentrated or diluted in terms of the ▪ Number of substances present ▪ Amount of water being excreted | Concentration |
| number of osmos of solute in kilograms (kg) | Osmolality |
| number of osmos of solute in liters (L) | Osmolarity |
| Measures amount of solute-free water being excreted in the kidney | Free Water Clearance |
| Checking the specific gravity • “24-hr water deprivation” • Patient is deprived of fluid or water for 24 hours. After which, the specific gravity of urine is measured. | Fishberg Test |
| Checking the specific gravity • “Daytime vs Nighttime” • Compares the volume and specific gravity of the urine sample in the morning and evening to evaluate the concentrating ability of the kidney (or tubules) | Mosenthal test |
| Aka Para-aminohippuric test • Non-toxic substance • Not readily available in the body | PAH Test |
| Also known as NPN'S | Non-Protein Nitrogen Compounds |
| Where is urea formed? | Hepatocytes (Mitochondria) |
| in terms of the process done in order to measure acidity | Titratable |
| Carbon dioxide and Ammonia -> Carbomyl Phosphate (Enzyme responsible for the reaction?) | Carbomyl Phosphate Synthetase (CPS I) |
| Does CPS I require a allosteric activator? | Yes |
| a certain site in your enzyme where it is able to bind | Allosteric |
| The concentration of urea in the blood is affected by the | Protein content of the diet Rate of protein catabolism Renal function and perfusion |
| There is a elevation of the urea in the blood | Azotemia |
| Cause of thisis the reduction of renal blood | Prerenal |
| In the kidney | Renal |
| After the kidney | Postrenal |
| A combination of azotemia and renal failure | Uremia |
| Causes of Pre renal (Physiologic) | Increased protein catabolism, high protein diet: |
| Underlying problem of Pre renal : | Congestive Heart Failure |
| The problem is the kidney itself. There is decreased in renal Function | Renal |
| There is inflamation in your glomerulus. since the glomerulus is affected there is no proper filtration. Due to this, urea cannot be filtered | Glomerular Nephritis |
| in this condition the tubules cannot reabsorb or do its function properly due to necrosis | Tubular Necrosis |
| Urinary Tract Obstruction, thus increasing the amount of urine present within the body + concentration. | Post Renal |
| Decreased Concentration: | low protein intake, Severe vomiting and diarrhea, Liver disease and pregnancy |
| Normal BUN/CREA Ratio | 10-20:1 |
| Accounts to 75% of your NPN | BUN |
| Formed from creatine and creatine phosphate | Creatinine |
| What amino acids is creatinine synthesized from: | Arginine, Glycine, Methionine |
| Three amino acids undergo transamination -> forming _ | Guanidinoacetic acid |
| What is the process of conversion for said : Guanidinoacetic acid | Methylation |
| Clinical Application of Creatinine Measurement | ● Determine the sufficiency of kidney function ● Determine the severity of kidney damage ● Monitor the progression of the kidney disease |
| How is uric acid formed | Purine Breakdown |
| Process in which Uric acid is safely excreted from the body | Uric acid -> Blood ->Sodium Urate -> kidneys -> Urine |
| Enzyme responsible for the breakdown of uric acid | Xanthine Oxidase |
| A drug commonly used for gout: Inhibitor of Xanthine Oxidase | Allopurinol |
| Most uric acid in the plasma is in the form of: | Monosodium Urate |
| Gout | Found primarily in men (30-50 years old) |
| Reference range for possible gout | 6mg/dL > |
| Normal Range for Men and Women: | 3.4, 2.4 |
| Produced from the breakdown of Amino acids and protein metabolism | Ammonia |
| It is an acute metabolic disorder in the liver. A child’s sugar level would typically drop while the level of ammonia and the acidity will increase. level of ammonia and the acidity will increase. | Reye Syndrome |
| What causes Hepatic encephalopathy | This ammonia will accumulate in the blood, there is a tendency that ammonia in the bloodstream will reach the brain and it would temporarily or sometimes (if there is no treatment), it can permanently affect our brain functions. |
| Weighs 1.2 - 1.5 kg | Liver |
| Connects the two sides of the Liver | Falciform Ligament |
| Two main blood vessels found in the Liver | Hepatic Artery and Portal Vein |
| Portal Vein | Nutrient Rich Deoxygenated Blood 75% |
| Hepatic Artery | Blood is oxygen rich 25% |
| Liver macrophages | Kupffer Cells |
| Functional Unit | Lobule |
| Portal triad composed of | Hepatic Portal Vein Hepatic Artery Hepatic Portal Duct |
| ● Has the capacity to regenerate through: | o Cell division o Hypertrophy |
| - Secrete bile acid and waste products. | Hepatocytes |
| Liver Functions | ● Synthetic Function ● Conjugation Function ● Detoxification and Drug Metabolism ● Excretory and Secretory Function ● Storage Function |
| ● Once phagocytized, it has the ff. breakdown products: | ○ Heme ○ Globin |
| ➔ A protein. ➔ When further metabolized, it becomes amino acids. ➔ It will be put into the amino acid pool to be reused for protein synthesis. | Globin |
| ➔ Is the iron carrier portion of the blood. ➔ Consists of an iron and a porphyrin ring | Heme |
| ◆ The heme is oxidized by the enzyme heme oxygenase, producing biliverdin. ◆ Biliverdin is reduced by biliverdin reductase, producing unconjugated bilirubin. | Prophyrin Ring Portion |
| Storage form of iron | Ferritin |
| Transport form of iron | Transferrin (Carrier Protein) |
| Unconjugated | Indirect bilirubin, nonpolar bilirubin, water insoluble, |
| Conjugated | Direct, Polar, Water Soluble |
| Unconjugated needs a tranpsort protein: what protein is that | Albumin |
| Process within the intestine (Conjugation of bilirubin) | B2 -> Mesobilirubin -> Mesonbilirubinogen -> Urobilinogen |
| Urobilinogen is divided into two: | Stercobilin - Feces Systemic Circulation, Extrahepatic circulation |
| Urobilinogen is then oxidized to form -> | Urobilin |
| Third fraction of bilirubin | Delta bilirubin |
| When does Delta bilirubin form: | Usually when patient has liver problems |
| ● Detoxify Ammonia ● Protects body from potentially harmful substances absorbed from GIT and toxic by-products of metabolism | DETOXIFICATION AND DRUG METABOLISM |
| Excretion of Bile Bile acids or salts, pigments, cholesterol | Excretory and Secretory Function |
| Bile acids are conjugated with amino acids Glycine and Taurine forming bile acids | o Cholate o Chenodeoxycholate |
| Storage Function | ● All fat-soluble vitamins ● Water-soluble vitamins ● Glycogen |
| ● Comes from the French word “Jaune” which means yellow ● Characterized by yellow discoloration of the skin, mucous membrane, and sclera most often because of bilirubin o Icterus-yellowserumorplasma | Jaundice |
| (Turbid)-HighChylo/VLDL | Chylous |
| yellowserumorplasma ▪ Icteric samples have effects on test results ▪ It is an indication of High Bilirubin levels | Icterus |
| Has 3 phases: | Pre Hepatic Hepatic Post Hepatic |
| ● Excessive amount of bilirubin is presented to the liver for metabolism increase in B1 | Prehepatic Jaundice |
| Results from impaired cellular uptake, defective conjugation, or abnormal secretion of bilirubin by the liver (intrinsic liver defect) | Hepatic |
| Types of unconjugated hyperbilirubinemias | Gilbert Crigler-Najjar Syndrome (GC) |
| Conjugated Hyperbilirubinemia | Rotors syndrome, Dubin-Johnson (RJ) |
| Benign Autosomal Recessive Hereditary disorder (UGT1A1)(Malformation of UDGPT) | Gilbert Syndrome |
| More serious than Gilbert Syndrome, Characterized by deficiency of the enzyme UDGPT | Crigler-Najjar Syndrome |
| ● Complete absence of UDPGT ● Lifeexpectancy<1yr | Type 1 |
| ● Severe/partialdeficiencyofUDPGT ● Can still use phototherapy | Type 2 |
| AccumulatedBilirubin ● Neuronal degeneration brought about by accumulation of bilirubin ● Brain has yellow spots , or whole brain | Kernicterus (Brain damage) |
| Autosomal recessive disease which presents shortly after birth with an increase of conjugated bilirubin without elevation of liver enzymes (ALT, AST) | Dubin-Johnson Syndrome |
| Liver granules are not pigmented (LiverBiopsy) ▪ No liver granules under the microscope | Rotor Syndrome |
| o Bilirubin-conjugation inhibition o Aka. Transient Familial Neonatal Hyper bilirubinemia o Circulating inhibitor of bilirubin conjugation o Transient | LUCEY-DRISCOLL SYNDROME |
| Impaired bilirubin excretion, o Biliary obstructive diseases o Gallstones, Tumor | POSTHEPATIC JAUNDICE |
| o Not enough B2 to convert to Stercobilin | ● Stool Color: Gray/Dark White |
| ○ Formation of tumors ○ Occur due to mutation of growth factors and oncogenes | Turmorigenesis |
| Spreading of tumors | Metastasis |
| ○ Expressed during the development of the fetus, then re-expressed in tumors ○ Found in fetuses but are found in adults with certain kinds of cancer | ● Oncofetal antigens |
| ○ The likelihood that given the presence of the disease, an abnormal test result predicts the disease ○ No false negatives | Sensitivity |
| ○ The likelihood that given the absence of disease, a normal test result excludes diseases ○ No false positives | Specificity |
| Development of new blood vessels to supply oxygen and nutrients to cells | Angiogenesis |
| Programmed cell death | Apoptosis |
| Phases of cell activity divided into G, S, and M (growth, DNA synthesis, and mitosis, respectively) | Cell Cycle |
| ○ Synonymous with "tumor," it refers to uncontrolled tissue growth; it may be cancerous (malignant) or non-cancerous (benign). ○ Derived from Greek meaning "new formation" | Neoplasm |
| ○ Encodes a protein, that, when mutated, promotes uncontrolled cell growth | Oncogene |
| ○ Encodes a protein involved in protecting cells from unregulated growth | Tumor suppressor gene |
| ● Refers to the uncontrolled growth of cells that can develop into a solid mass or tumor and spread to other areas of the body | Cancer |
| 2 main types of tumor | Benign, Malignant |
| ● Non-cancerous ● Does not spread towards other parts of the body ● Grows slowly ● Localized → remain in one place | Benign |
| ● Cancerous ● Have the ability to invade nearby tissues and spread to other parts of | Cancerous/Malignant |
| Are all tumors cancer? | No |
| Type of cellular growth that occurs in response to normal physiological demands or hormonal stimulation.Type of cellular growth that occurs in response to normal physiological demands or hormonal stimulation. | Physiologic Hyperplasia |
| Tumor Markers Tumorigenesis | 1. NORMAL CELL 2. STAGE I: INITIATION 3. STAGE II: PROMOTION 4. STAGE III: PROGRESSION 5. STAGE IV: METASTASIS 6. DEATH |
| ● Initial genetic alteration in a normal cell that makes it susceptible to becoming a cancer cell ● Alterations → caused by chromosomal rearrangements or epigenetic changes | Initiation |
| During this stage, the initiated cell undergoes further changes that promote its growth and division. Exposure to certain chemicals, hormones, or chronic inflammation can contribute to the promotion of cancer cells. | Promotion |
| The promoted cells acquire additional genetic alterations that can enhance their ability to invade nearby tissues and spread to distant sites in the body. | Progression |
| The process by which cancer cells spread from the primary tumor to other parts of the body through the bloodstream or the lymphatic system. | Metastasis |
| Necrosis | Death. |
| MULTIPLE FACTORS CONTRIBUTING TO TUMORIGENESIS | Genetic predisposition Exposure to carcinogens, Chronic Inflammation, Viral Infections, Lifestyle, Tumor microenvironment |
| Cancer Staging and Progression up to what stage? | Stage 1 -> 4 |
| Stage 1 | Localized Primary Tumor |
| Stage 2 | Invasion of primary tumor through epithelium and into blood vessels |
| Stage 3 | Migration of tumor into regional lymph nodes |
| Stage 4 | Metastasis and invasion of tumor to distant tissues |
| Numerous factors are used in combination to define cancer stages, these include | Tumor size, Extent of Invasion, Lymph node, Involvement, Metastasis, Histologic Assessments |
| Are substances found in increased amounts in the blood, other body fluids and tissues that may suggest the presence of cancer | Tumor markers |
| Used in (Tumor Markers) | Cancer diagnosis, Monitoring and treatment response, Detecting cancer recurrence, Assessing prognosis |
| TUMOR MARKERS ARE DETECTED IN: | Solid Tumor, Circulating tumor cells in peripheral blood, Serum, Lymph Nodes, Bone Marrow, Other bodily fluids |
| most commonly used method to detect certain tumor markers in the bloodstream. | Blood tests |
| Involves the removal of a small sample of the tissue from the tumor or suspected cancer site. | Biopsy and Tissue Analysis |
| Testing certain tumor markers such as protein or metabolites can be detected in the urine. | Urine Test |
| A tumor marker should be: | Highly Specific Highly Sensitive |
| Tumor markers can provide a valuable prognostic information and help assess the risk of disease progression | Prognosis and Risk Assessment |
| Tumor markers are frequently used to monitor the response to cancer treatment and serial measurements of tumor marker levels during and after treatment can help assess the effectiveness of therapy. | Treatment Monitoring |
| Tumor markers can be valuable in detecting cancer recurrence after treatment. | Detection of Cancer Recurrence |
| Tumor markers can be used as a screening tool to detect cancer at an early stage or identify individuals at high risk of developing cancer | Cancer screening for Early Detection |
| Often used to aid in the diagnosis of tumors | Endocrine hormone metabolic markers |
| Methods used to measure tumor markers | Immunoassays, HPLC, Immunohistochemistry, Enzyme Assays |
| Biochemical test that measures the presence or concentration of a macromolecule or a small molecule in a solution through the use of a antigen | Immunoassays |
| Example of IA | Mini Vidas Machine |
| Principle of Mini Vidas System | utilizes an enzyme linked fluorescent assay or the alpha technology which combines an enzyme linked technology which combines an enzyme immunoassay principle with fluoresence detection |
| Most widely used methodology to detect catecholamines and their metabolites in plasma and urine. Commonly used for the detection of small molecules such as endocrine metabolites | HPLC |
| Detection directly within a solid tissue, Special Staining process performed on a fresh or frozen breast cancer tissue removed during biopsy. | Immunohistochemistry |
| These are laboratory measurements used to measure the activity, concentration or kinetics of an enzymes. Enzymes are biological molecule that catalyze specific chemical reactions in a living organism. | Enzyme Assays |
| Types of Tumor Markers | Antigen, Hormones, Enzymes, Receptors (AHER;P) |
| Tumor Antigen , Monoclonal defined antigens are directly identified from human tumor extracts and it is useful in monitoring the treatment of tumors. | Carbohydrate/Cancer Antigen |
| These are proteins transiently expressed during embryogenesis or fetal development and they are turned on again during tumor formation. | Oncofetal Antigens |
| Substances produced by endocrine tumors, Used in the diagnosis, monitoringm and management of endocrine tumors. | Endocrine Tumor Markers |
| What saple is being utilized during endocrine tumor markers | Serum. Except for Catecholamines and its metabolites - HVA and VMA and metanephrines. |
| Serum M protein Serum free light chains B2-Microglobulin | Serum protein Markers |
| Proteins expressed on the surface or within the cells that lay a crucial role in cell signaling and response to a virus stimuli, Used in diagnostic, prognostic and therapeutic application to identify the specific receptors and evaluate their expression . | Receptor Tumor Markers |
| Is a receptor protein that is expressed in breast cells and involved in the response to estrogen receptor hormones | Estrogen Receptor |
| Similar to the estrogen receptor which is expressed in the breast cells and has a role in hormonal signaling, Evaluated along the ER status to guide the treatment decisions in breast cancer | Progesterone Receptor |
| Overtly expressed in some breasts and other types of cancers, Essential in identifying the patients who may benefit from the targeted therapies like herceptin or Lapatinib therapy | Human Epidermal Growth Factors 2 (HR-2/neu) |
| Regulates the cell growth and diffusion - An over expression or mutations EGF or are found in various cancers such as lungs, colorectal head and neck cancers, can guide the treatment decisions for the targeted therapies like Gefirnib and Cetuximab | Epidermal growth factor receptor (EGFR) |
| Refers to a specific enzymes that are produced or released by tumor cells. | Enzyme Tumor Markers |
| Enzyme Produced by the prostate gland Elevated levels of PSA in the blood are associated with prostate cancer PSA testing is commonly used for prostate cancer screening, | PSA (Prostate Specific Antigen) |
| ● Can observed in various cancers including lymphoma, leukemia, and germ cell tumors ● This enzymes is often used as marker for tumor burden and treatment response | LDH (Lactate Dehydrogenase) |
| ● Amylase and Lipase ● involved in the digestion of the carbohydrates and fats respectively ○ Elevated levels of these enzymes can be observed in pancreatic cancer and certain gastrointestinal cancers | AMS (Amylase), LPS (Lipase), Trypsin and Ribonuclease (RNAse) |
| ● Are found in immature influences (??) to detect prognosis and responsiveness of a drugs to leukemia | 5'Nucleotidase and Terminal Deoxynucleotidyl Transferase (TdT) |
| ● Collagenase ● Enzymes that break the peptide once in the collagen ● It assists in destroying extracellular structures in the pathogenesis of bacteria such as clostridium | Collagenase |
| Bacteriolytic enzyme that if found in some hematopoietic cells, it is primarily present in the granular sets monocytes and histiocytes that are used for monitoring of the monocytic and myeloma monocyttic leukemias | Muramidase (Lysozyme) |
| Hepatoma | AFP |
| Ovarian CA | CA-125 |
| Breast | CA15-3 CEA Her-2/neu Estrogen and Progesterone |
| Cancer of the pancreas | CA 19-9 CEA |
| Pheochromocytoma | Vanillylmandelic Acid (VMA) in urine |
| Nonseminomatous testicular cancer | AFP, B-hCG, CEA |
| Vesicular mole and Choriocarcinoma | B-hCG |
| Prostate Cancer | PSA |
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