Section II - Hairston

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Section II - Hairston
2013-03-24 21:37:14
bio 122 hairston

Section II - Bio 122 Hairston
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  1. Catabolism
    breaks down complex organic molecules into simpler ones (exergonic). 

    glucose --> CO2 and H2O --> ENERGY (ATP)
  2. anabolism
    combining simple structures and making them complex. (endergonic). this process requires ATP

    (AA)n -- ATP --> structural and globular proteins
  3. specific dynamic action (SDA)
    energy expenditure necessary to get ingested material to a useable form of ATP. 

    SDA begins at mastication/salvation

    • CHOs = 6 cal/100c ingested (94% efficient)
    • PROTEINS = 30 cal/100c ingested (70% efficient)
    • LIPIDS = 4 cal/100 cal ingested (96% efficient)
  4. BMR
    basal metabolic rate

    -measures metabolism under standard conditions

    • Average BMR for humans:
    • 1) 70c/hr
    • 2) 40c/hr/m2 x Surface Area
    • 3) 4.8 cal/liter of O2
  5. g/cal (Calorie) Values
    CHOs = 4.1 c/g

    Proteins = 4.1 c/g

    Lipids = 9.3 c/g
  6. CHOs - Glucose

    (glu)n Liver ---glycogenesis---> glycogen (500g) Anything over 500g of glycogen = Lipogenesis 

    (lipogenesis is the process by which acetyl CoA is converted to fats)
  7. Where is most glycogen stored?
    Where it is most needed. 80% of glycogen is stored in skeletal muscles (NOT IN THE LIVER)
  8. Can you get energy directly from glycogen?
    NO - needs to be brought back to a catabolic reaction to use it as glucose.
  9. Glycogenolysis
    Catabolic reaction --> going from glycogen back to glucose
  10. McArdle's 
    a metabolic disorder in children where they are missing the 5th step to perform glycogenolysis

    Exclude all carbohydrates from the diet for cure.
  11. Glycolysis
    glucose splitting

    glucose --- 10 step program to get 2 three-carbon molecules = pyruvic acid + 2 ATP

    NAD ---->> NADH2

    NAD = a coenzyme that carries hydrogen atoms

    Nets: 2 ATP, 2 NADH, 2 pyruvic acid

  12. Aerobic & Anaerobic
    O2 comes into the picture allowing pyruvate acid to take glucose directly into the cells into the cristae. O2 allows pyruvate acid into the mitochondrial matrix. 

    Anaerobic - lack of O2 and the cells will change pyruvic acid to lactic acid - this is a holding molecule waiting for O2 to become available.

  13. Mitochondria Matrix
    transitional reaction

    • (decraboxylation takes place here)
  14. Decarboxylation
    takes the COOH off of lactic acid --> diffuses out of the mitochondria and into the cell = waste product CO2
  15. Krebs Cycle
    Follows Glycolysis

    • 9 steps
    • 2 ATP (NAD --> NADH)

    FAD --> FADH2e ---> Cristae = Electron transport system (ETS)
  16. Lipids - Triglycerides
    Fatty Acids and Monoglycerides
  17. Gluconeogenesis
    Non-CHOs giving you glucose
  18. Fatty Acids
    16 carbons on average

    Fatty acids gets diffused into our cells in the cytoplasm and waiting for it in the cytoplasm to get it into the matrix is CARNITINE.

    Carnitine groups with FAs in the cytoplasm to assist its movement from the cytoplasm to the mitochondria matrix.
  19. What tissue has the highest level of carnitine?
    Cardiac muscle
  20. Beta Oxidation
    the process by which fatty acid molecules are broken down in the mitochondria to generate acetyl-coA. 

    Acetyl Group = CoA waiting ---> Krebs cycle
  21. Proteins
    Amino Acids - 20
  22. NAD (NADH)
    strictly made to carry hydrogen so it doesn't jump to oxygen (this is why vitamins are important - B3 is perfectly structured to hold hydrogen). Hydrogen links with NAD to become NADH.
  23. ETS
    Electron Transport System
  24. Deamination
    remove the amide groups from a molecule
  25. Transamination
    shift amide groups to carriers (called ketos)

    (the reversible exchange of amino groups between different amino acids.)
  26. Essential Proteins
    body cannot make these

    (12 of these)
  27. Nonessential Proteins
    body can make these - although some you can't make enough of and still need to supplement

    (8 of these)
  28. What are the essential amino acids?

    • Threonine
    • Valine
    • Tryptophan
    • Isoleucine
    • Leucine
    • Lysine
    • Phenylalanine
    • Methionine

  29. Hypervitaminosis
    Fat Soluble Vitamins = A, D, E, K
  30. What controls the volume and composition of the blood?
    Cortical Nephrons - 85%

    Juxtamedullar Nephrons - 15%
  31. What two tubules are there?
    Uriniferous Tubule (urine is called filtrate if it is in the tubule, it is only urine when it's ready to be excreted) 

    Vasculature Tubule
  32. EC Membrane
    endothelium capsular membrane (podocytes)

  33. Glomerluar Capillary 
    has 100 nanometers openings/gaps

    Protocytes are found on the outer rim of the glomerular cappillaries are Podia

    Pedicels - give us filtration slits (the gap between the rungs in the latter)
  34. Renal Vasculature
    • Renal Arteries = 85mmHg/1.5 Lit/min
    • (volume 25% coming out of the left ventricle of the heart)

    Renal Fraction (% of blood that goes to the kidneys from the heart) = 25% of cardiac output

    a) segmentals - subdividing before penetrating into the kidneys (still large pore arteries)

    b) interlobar artery

    c) arcuate artery

    d) interlobulars - extensions going up into the cortex - 45mmHG

  35. What is the difference between interlobar and interlobular arteries?

    Interlobar arteries pass between the renal pyramids.

    Interlobular Arteries pass between renal lobules.
  36. Juxtaglomerular Apparatus
    association of structures called the JGA

    Function is to control pressure and flow
  37. JG cells
    baroreceptors (BP sensor) 
  38. Renin
    an enzyme produced by the JG cells designed to counter low blood pressure and flow

  39. Can RBCs fit into Bowman's capsule?
    NO - filtration slits are only 8 nanometers - much too small (RBC are 2 micrometers). Seeing blood would be pathological.
  40. Can H2O fit into Bowman's Capsule
    YES - H2O is 1 nm and can fit into filtration slits.
  41. Peff
    blood hydrocartic pressure (aka BHP) pressure going from glomerulus into bowman's capsule --> push out 45mmHg
  42. Blood Osmotic Pressure - BOP
    works against BHP (hold back is 25mmHg)
  43. Capsular Hydrostat Pressure - CHP
    works against BHP --> push back 10mmHg
  44. What are two things that work against BHP?
    Blood Osmotic Pressure (BOP) and Capsular Hydrostat Pressure (CHP)
  45. What three things do you need for Peff?
    Peff, BOP, CHP

    (average Peff is 10mmHg--> if the number is positive you will have flow in your bowman's capsule, if zero there's no flow and the number will not go negative. If Peff = 0mmHg = Renal Suppression)
  46. E-C Membrane Dynamic
    some forces will work for filtration and some will work against filtration
  47. Kf
    Filtration coefficient (how porous is the membrane of filtration)
  48. GFR
    Glomerular Filtration Rate - the amount of filtrate formed in all the renal corpuscles of both kidneys each minute

    Peff x Kf = standard of nephron EC function--> GFR

    perfect # for GFR is 180Liters/day aka 48 gallons/day

    Formula = Uconc x Uvol/Plasma Tag
  49. What tags are in GFR?
    GFR --> (a) Plasma Tag (inulin IN--> PIN) will flow freely through e-c membrane, remains unchanged ---> urine (.25% Plasma) (b) Urine tag 31.25mg --> (c) urine per volume (standard is 1ml/min)
  50. Creatinine Study 
    Cr - a waste product of muscle metabolism

    • 1) Pcr = average is 1mg% of Cr
    • 2) Urine = 1ml/min
    • 3) 130mg% in urine

    *will be a little higher and clinicians compensate for built in error because it's light*
  51. Tubular Reabsorption
    filtrates into the blood

    H2O (constant)
  52. obligatory reabsorption
    Pts (transports sodium), by shifting salt you can pull 38 gallons of water into your bloodstream

    (part of tubular reabsorption)
  53. Glomerulo Nephritis
    aka Bright's Disease --> autoimmune disease, thinks EC membranes are foreign tissue causing scarring (loses Kf, causes GFR to go down). Strep can produce a toxin that can trigger this autoimmune attack.
  54. Pyelonephritis
    Kidney Infection -

    Once a patient has this their biggest complaint is often dysuria (pain while urinating, can be a lifelong problem). E-coli is the prime culprit in kidney infections. Once E-coli is in your kidneys it knocks out CCM.
  55. Diabetes Insipidus
    aka DI. 3 gallons of urine, massive loss of fluid because of a dysfunction of ADH (they don't have enough of it or are too sensitive to it). GFR is unaffected since it doesn't affect the EC Membranes. Symptom is drinking all the time.
  56. Polycystic Kidneys (PKD)
    most inherited (1/800), chronic and slow progressing. Incomplete urineferous tubules. Pressure Atrophy - little bubbles put pressure on the other nephrons causing damage and compromising them.
  57. Hydronephrosis
    water on the kidneys - urinary pathway blockage, widened calyses
  58. Osmotic Diuresis
    can be clinical or induced with mannitol (has 2 more hydrogens so it won't be reabsorbed). Defined as the presence of any solute that should not be in the filtrate of the CDs. Patients complain of polyuria (they have too much sugar in the blood and can't absorb it, so its in their CDs holding water - causes frequent urination). Or can cause swelling on brain stem and that will cause it to snap. Mannitol will absorb the water decreasing the swelling near the brain.
  59. What two requirements are necessary for facultative reabsorption?
    Force (CCM) and Modulator (ADH)
  60. Describe what happens in the Loop of Henle. Include Facultative Reabsorption.

    1) As you ascend you actively transport chloride out into the tissue

    2) Ascending limb has a special property relative to water (it's impermeable)

    3) Sodium chloride is pumped out of tissues and the filtrate will follow the solute out into the tissue. The wall blocks the water.

    4) Exchanger Effective - Vasa Recta --> looping capillaries parallaling will complement the multiplier by having blood descend and pick up the increasing solute concentration going into the vessel. Diffusion can also drop solute concentration off. Now solutes are deep in medulllary tissues (recycling them). 

    5) Modulator - ADH (anti-diuretic hormone) is invoked. When circulating it has one function - open the walls of the collecting ducts to water to create aquaphorine channels. (if ADH is up, urine output will be decreased and vice versa)

    Alcohol blocks your ADH - making your collecting ducts closed causing dehydration.
  61. CCM
    counter current mechanism - a current going down and a current going back.

    vasculature paralleles the loops deep down into the medela resulting in a countercurrent flow. 

    ultimate objective = multiplier effect (generate osmotic force as a fucntion of the loops --> 1200 is force deep down in pyramids)

    *this is part of tubular reabsorption*
  62. Solutes (threshold)
    Threshold (spill over). When the first solute shows up in your urine (creatnine dumped out in urine very quickly).

    If glucose is present indicates a problem because it has a high threshold --> means you're losing a needed substance.

    Solute rings the toxins out of the blood. 
  63. Tm
    Tubular Max --> maximum rate that you can reabsorb any particular solute
  64. Tubular Secretion
    Opposite of Tubular Re-absorption (blood --> filtrate after GFR). Has nothing to do with water.

  65. What is something that undergoes tubular secretion?
    Antibiotics (Penicillin) - this is why you have to take high doses frequently because your body is trying to rid itself of the substance.
  66. What would cause the body to produce more Renin?
    JGA - JG cells + Macula Densa DT (Filtrate Flow) --> if either or both of these drop than your body will produce more Renin.
  67. RAAS
    Renin Angiotensin Aldosterone System

    Angiotensinogen is constantly produced in the liver (constantly in blood, a proenzyme). Angiotensinogen I does nothing. 

    Lungs activate Angiotensin Converting Enzyme (ACE) -- becoming Angiotensin II (most intense vasoconstrictor known to human physiology)

    Increases Blood Pressure

    Angiotensin II circulates to adrenal glands (lasts years), particularly to the cortex (Glomerulosa) = Aldosterone (shifts from enzyme to hormone).

    Aldosterone is circulated back to the kidneys (DT's now increase reabsorption of sodium) Cl- follows INCREASING BLOOD VOLUME and increasing BP.

  68. What do ACE inhibitors do?
    They make it so Angio I doesn't covert as much to Angio II.
  69. Goldblatt's Hypertension (Renal)
    Renal Artery Atherosclerosis --> compressed blockage of renal artery resulting in a drop of BP going to kidneys causing high BP
  70. Hypoxic Effect (hypoxia)
    EC membranes double as a filter but as O2 sensors, Low O2 to kidneys will now produce REF (Renal Eythroporetic Factor) --> Results in Plasma Protein (Liver)

    Erythropoietin --> Red Marrow = increased RBC