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| Question | Answer |
|---|---|
| define metabolism | sum total of all the biochemical |
| what is catabolism | breaking of complex molecules into simple molecules. Releases energy |
| define anabolism | construction of complex molecules from simple molecules. Requires energy |
| where is the energy for anabolism produced | it is produced from catabolism |
| what is the difference between ATP & ADP | ADP holds less energy than ATP |
| what are metabolic pathways | hundreds of specific chemical changes that must occur in a particular sequence. the rate is controlled by enzymes |
| How is energy released from ATP | it's released in a hydrolysis reaction that breaks off the terminal phosphate group |
| where is energy held in ATP | it is locked up in the phosphate bonds |
| what are nutrients | chemical constituents of food necessary to sustain the normal functions of the body |
| define a balanced diet | contains all the ingredients necessary to maintain homeostasis |
| what are the symptoms of kwashiorkor disease | oedema, skin lesions, de-pigmented hair, anorexia, enlarged fatty liver, decreased plasma albumin, "plump belly" appearance |
| what causes Kwashiorkor disease | an inadequate intake of proteins in the presence of adequate intake of calories |
| what is marasmus | chronic deficiency in calories even in the presence of adequate levels of protein intake |
| when does marasmus occur | typically in children under one year when breast milk is supplemented with thin watery gruels of cereals |
| what are the symptoms of marasmus | arrested growth, extreme muscle wasting, weakness & anaemia |
| what can occur from calcium & phosphorus imbalances | Osteoporosis, ricketts |
| what can occur from sodium & potassium imbalances | hypertension/stroke |
| what can deficiency of vit. B1 cause | is important in nervous system. Causes beriberi. Leads to tachycardia, vomiting, convulsions & death |
| wernickle-koraskoff syndrome occurs in | chronic alcoholism |
| what does vit. B3 (niacin) deficiency cause | pellagra. affects skin digestive system & N.S |
| what does vit. c deficiency cause | scurvy spongy gum, loose teeth, fragile blood vessels & swollen joints |
| what does vit. A deficiency cause | night blindness dryness of conjunctiva & cornea if untreated corneal ulceration leads to formation of scar tissue-blindness |
| where does energy from catabolism go | heat energy 60% ("waste", temp. homeostasis) chemical energy 40% (cells) |
| what are the 3 categories of energy transfer within the cell? | performance of mechanical work active transport of molecules & ions the synthesis of new biological molecules |
| what is metabolic rate | total energy expenditure of a persons body within a given period of time |
| what factors influence metabolic rate | muscle activity (increases) food-induced thermogenesis (increases) epinephrine (increases) other factors |
| what is metabolic rate | the metabolic rate of a person at rest in a room at a comfortable temperature, and who has not eaten for at least 12 hours |
| what is the concept of energy balance | energy intake - energy expenditure = change in body mass/energy stores. if intake is greater than output then results in positive energy balance & vice versa |
| fate of glucose depends on body's needs at time. Name the types of metabolism that can occur | cellular respiration storage of glycogen storage as TAG in adipose tissue production of amino acids. |
| what are the steps in cellular resp | glycolysis formation of Co-A Krebs cycle electron transport chain |
| what does glycolysis do to glucose | 10 steps. 6 c glucose split into two 3 C pyruvic acid |
| what happens in anaerobic glycolysis | pyruvic acid is reduced by NADH to lactic acid |
| what steps in glycolysis involve adding 2 ATP | steps 1+3 are converted into ADP in the process |
| what occurs in step 7+10 of glycolysis | 4 ATP molecules are produced. leading to a NET GAIN OF 2 ATP |
| how do low energy NAD, NADP, FAD & FMN turn into high energy | by receiving high energy H atoms & electrons produced in catabolic reactions becoming chemically "reduced" |
| why is anaerobic glycolysis important | it permits continued production of ATP in cells than lack mitochondria or tissues deprived of O2 supply |
| what is the Cori Cycle | when lactic acid diffuses into blood & is processed back into glucose which may enter the muscle to feul anaerobic glycolysis |
| What occurs in the formation of acetyl co-a | pyruvic acid prepared for krebs cycle by removing Co2 to make a 2 C fragment |
| what is an acetyl group & how does it for acetyl co-a | its a 2 C fragment from pyruvic acid. it attaches to co enzyme A to form acetyl co enzyme a |
| T or F | formation of Co a needs to occur in an aerobic condition |
| what is the krebs cycle | 9 reactions that break the co a into ATP |
| why is the krebs cycle AKA citric cycle | co a delivers acetyl to the start, 2 C acetyl combines with 4 C oxaloacetic acid to form 6 C citric acid |
| How does Krebs cycle produce ATP | citric acid is manipulated by enzymes back into 4 c oxaloacetic acid which can pick up another co a. manipulation allows capture of released energy by ATP |
| how many ATPs are released from each acetyl group entering the krebs cycle | 1 molecule |
| where does electron transport chain occur | upon inner mitochondrial membrane |
| how does the electron transport chain release energy | as electron move down they loose free energy which is captured by ATP |
| OIL RIG | Oxidation Is Losing Reduction Is Gaining |
| what occurs in the kreb cycle | enzymatically catalysed reactions which release energy. occurs by transfer of electrons thru a chain of carrier molecules that are oxidise & reduce |
| how many ATPs are made from the electron transport chain | 11 ATP from processing of each NADH + FADH2 of each acetyl group |
| what is occurs in the final step of the ETC | combination of O2 + H to form water (produces metabolic water-300ml/day) if O2 absence, cannot take place & ETC grinds to a hault. stops ATP pathway |
| name a site specific inhibitor if the ETC | hydrogen cyanide inhibits enzyme cytochrome oxidase which is responsible for the last step. Hence can kill like O2 deprivation |
| define gluconeogenesis | when glucose molecules can be made from lactic acid, pyruvic acid , A.A & glycerol during fasting |
| what hormone is responsible for gluconeogenesis | Glucagon from pancreas cortisol stimulates break down of protein into A.A |
| define glycogenesis | when glycogen stores are made from glucose when acess is high. occurs by insulin |
| what is the function for muscle gycogen | fuel reserve for the synthesis of ATP during muscle contraction |
| what is the function of glycogen in the liver | to maintain BGL |
| there is 500g of glycogen stores in the body, where is it? | 400g in skeletal muscle 100g in the liver [20g of free glucose in body fluids] |
| what is glycogenolysis | release of individual glucose molecules from polymer glycogen. stimulated by glucagon & epinephrine |
| what are the essential fatty acids | lineleic & linolenic acid cannot be synthesised arachidonic acid becomes essential if insuffecient amount of linoleic acid |
| what are the essential fatty acids needed for | fluidity of membrane structure. deficiency leads to 'scaly dermatitis' |
| how are fatty acids stored | as TAG in adipose tissue |
| what is lipolysis | mobilisation of stored fats. first step in lipid catabolism. Lipase splits TAG which are processed along different pathways |
| what is the fate of glycerol after lipolysis | contains 5% of energy of TAG cant be metabolised by adipocytes, instead in liver. incorporated into new TAG Gluconeogenesis Glycolysis & into Krebs cycle |
| what is the fate of fatty acids after lipolysis | contain 95% of energy from TAG bind with albumins & transported to other tissues where they undergo 'beta oxidation' for ATP |
| what is beta oxidation | catabolism of fatty acids occurs in the mitochondria |
| how does beta oxidation occur | 2 c acetyl groups are removed from the long HC tail of the fatty acid & linked to co-a & fed into krebs cycle |
| what are prostaglandins | modification of fatty acid & elict pain, inflam, fever, nausea, vomiting ect. |
| why are prostaglandins hard to study | have short life produced in small quantities produced locally, not transported are not stored |
| how do anti inflammatory's work | they inhibit prostaglandin synthesis |
| what are the forms of catabolism of glycerol | obtained from TAG breakdown, can be converted to glucose (gluconeogenesis) Can enter glycolysis by convertion of pyruvic acid & into krebs cycle |
| what is lipogenisis | anabolism of lipids. excess dietary intake of carbs & proteins are converted to TAG |
| how are carbs & proteins involved in lipogenisis | A.A -> acetyl co a -> TAG glucose -> glyceraldehyde-3-phosphate -> glycerol glucose -> acetyl co a -> fatty acid |
| TAG can be converted into what? | lipoproteins, phospholips & cholesterol |
| how are ketone bodies formed | liver mitochondria diverts excess acetyl co-a from fatty acid oxidation or pyruvate oxidation into ketone bodies |
| what are the 3 ketone bodies that can be formed | acetoacetic acid 3-hydroxybutyric acid acetone (a dead end product which can be metabolised further) |
| what are ketone bodies used for | they are transported in blood to peripheral tissues where they can be reconverted to acetyl co-a & enter the Krebs cycle |
| what are the reasons for the liver producing ketone bodies | are soluble so don't require transport. produced when amount of acetyl co-a exceeds the oxidative capacity of liver are utilized by nonliver tissues CNS can use in prolonged fasting |
| what is the down side of excessive ketone bodies | when amount is greater than utilization, blood levels rise ->ketonemia & urine levels ->ketonuria |
| what is a problem of accumulation of ketone bodies | the organic types (acetoacetic & 3-hydroxybutyric) can effect blood pH leading to ketoacidosis |
| what are the type of protein metabolism that can occur | A.A used to synthesis new proteins for growth A.A may be processed for Kreb cycle Excess dietary A.A are converted into glucose or TAG |
| in protein metabolism, what occurs when A.A are processed for the kreb's cycle | the amino functional group is removed (de-amination). The NH2 is converted to ammonia NH3 which is transformed by liver into urea CO(NH2)2 which is excreted in urine. Ammonia is very toxic |
| what is the amino acid pool | A.A released by hydrolysis of dietary/tissue proteins mix with other free A.A distributed throughout the body make up the 'amino acid pool' |
| how big is the A.A pool | small, 100g in a 70kg adult compared to amount of protein (about 12kg) |
| what is protein turnover | when proteins are constantly being synthesied and degraded. 300-400g protein/day |
| why is ammonia toxic | because ammonia deplets a-ketoglutarate in the equation, which is an essential component of the Kreb's cycle. Thus ammonia causes depressed cellular resp & reduced ATP |
| what are pyrimadines & purines | of the 5 nucleotides that make up nucleic acid, 3 are small & called pyramidines (T,C & U) the remaining 2 are large & called purines (A & G) |
| T or F | dietary nucleic acids are not used for the production of human nucleic acids. Nucleotides can be synthesised from simple molecules within the cell |
| what is the metabolism of pyramidines & purines | pyramidines are broken into ammonia -> urea Purines are catabolised to uric acid & also lost in urine |
| what is a complication of the metabolism of nucleic acids | Gout |
| what causes gout | a metabolic defect that causes the over productive of uric acid. Insoluble sodium urate crystals are deposited in the joints of extremities causing severe inflammation & excuciating pain |
| what can gout cause | can lead to kidney diseas |
| what is the process of breaking down haem | iron is removed from RBC leaving haem residue called biliverdin, converted to bilirubin & concentrated in the liver & excreted in the bile & then transformed by intestinal bacteria to stercibilin - makes poo brown |
| what are the different causes of jaundice | increased destruction of RBC (haemolytic jaundice) Liver disease (hepatitis/cirrohsis) obstruction of bile ducts causing accumulation of bile that 'spills over' into blood (surgical jaundice) |
| what does 'pivot point' of metabolic pathways mean | that certain key molecules act as pivot points allowing one original category of molecule to be sent down one of several different pathways |
| what are the hormones that control maintenance of BGL | insulin glucagon epinephrine sympathetic nerves to liver & adipose tissue |
| what are the kinds of disturbances to metabolism that can occur | hormonal enzymatic other |
| what is under the 'other' class of disturbances to metabolism | dietary stress (starvation, obesity ect) extrinsic influences on enzymes (disease, toxins) Trauma high intensity exercise |
| what are hormonal disturbances on metabolism | diabetes (insipidus & mellitus( cretinism, myoxedema, graves disease, osteitis fibrosis cystica, tetany, addisons disease, cushings, aldosteronism, hyperinsulinism, congenital adrenal hyperplasia |
| what are enzymatic disturbances | deficiency or non-functional enzyme may cause significant interferance with a metabolic pathway. primary cause is usually genetic |
| what happens if there is an enzymatic disturbance of metabolism | the outward signs of this interferance may be due to the lack of an essential end product of metabolism or the accumulation of unused reactants |
| define cancer | a malignant tumor that has the ability to metastasize or invade into surrounding tissues |
| define tumor | a general term for an uncontrolled growth of cells that becomes progressively worse with time. can be benign or malignant |
| Define neoplasm | same as tumor |
| define neoplasia | the growth of new tissue with abnormal & unregulated cellular proliferation |
| define benign tumor | a tumor that does not metastasize or invade surrounding tissue |
| define malignant tumor | a tumor that has the ability to metastasize or invade into surrounding tissues (cancer) |
| Define metastasis | ability to establish secondary tumor growth at a new location away from original site |
| define carcinogenesis | the production of a carcinoma (epithelial cancer). sometimes carcinogenesis is used as a general term for production of any type of tumore |
| what is the classification of tumor names | cells or tissues of origin whether benign or malignant |
| what are the 2 major categories tumours fall into | carcinoma sarcoma |
| define carcinoma | malignant tumour arising in epithelium most common form. usually spread in lymph |
| define sarcoma | malignant tumour arising in connective or muscle tissue usually spread by blood frequently metastasizes to lung |
| what does 'oma' refer to in terms of tumor classifications (carcinoma) | indicates a swelling or tissue enlargment |
| what are the 4 types of damage that can occur to cells that try to repair themselves from toxicity | may completely repair & return to normal incompletely repair but able to function with reduced capacity death or complete loss of tissue neoplasm or cancers may result |
| what are the 2 type of reversible cell damage | cellular swelling fatty change |
| what are the 2 typer of irreversible cell damage | necrosis apoptosis |
| in terms of tissue repair what is labile cells | cells that routinely divide & replace cells that have a limited lifespan ( epithelial cell of skin, GI, gonands & stem cells) |
| what are stable cells in terms of tissue repair | cells that usually have a long lifespan with normally a low rate of division, but capable of rapid division on demand |
| what are permanent cells in terms of tissue repair | cells that never divide in the adult body & don't have the ability for replication even when stressed or some cells die |
| what is the term used that describes when permanent cells die they are not replaced but instead connective tissue (fibrosis) occupies the damaged area | it is a form of metaplasia. Cirrhosis of liver Cardiac infarcts pulmonary fibrosis |
| what are tumours composed of | all tumours are composed of cells with genetic alterations that make them perform differently from their progenitor (parent) cells |
| how big must a tumour get before it can be detected | must attain a size of at least one cubic cm |
| what are the 3 main phases in cancer development | initiation promotion/conversion progression |
| what is the initiation phase in cancer | an irreversible alteration of DNA. is distinguishable from other cells in same tissue. Can consist of a single exposure to a carcinogenic agent or may be an inherited genetic defect. may remain dormant for years or never develop into cancer |
| what is the promotion/ conversion phase in cancer | enhance the further development of initiated cells. interacts with DNA furthering mutuation and progresses further thru carcinogenesis process. [benign tumour] |
| what is the progression phase of cancer | portion of benign tumour cells may be converted into malignant form. individual cells can metastasis and start new clones else where |
| what are the 3 genetic involvements in cancer | regulatory genes are involved: proto-oncogenes oncogenes suppressor genes |
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