Section II - Hairston

breaks down complex organic molecules into simpler ones (exergonic). 

glucose --> CO2 and H2O --> ENERGY (ATP)

combining simple structures and making them complex. (endergonic). this process requires ATP

(AA)n -- ATP --> structural and globular proteins

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)

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

CHOs = 4.1 c/g

Proteins = 4.1 c/g

Lipids = 9.3 c/g

Anabolic 

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

(lipogenesis is the process by which acetyl CoA is converted to fats)

Where it is most needed. 80% of glycogen is stored in skeletal muscles (NOT IN THE LIVER)

NO - needs to be brought back to a catabolic reaction to use it as glucose.

Catabolic reaction --> going from glycogen back to glucose

a metabolic disorder in children where they are missing the 5th step to perform glycogenolysis. 

Exclude all carbohydrates from the diet for cure.

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

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.

transitional reaction

• 
• (decraboxylation takes place here)

takes the COOH off of lactic acid --> diffuses out of the mitochondria and into the cell = waste product CO²

Follows Glycolysis

• 9 steps
• 2 ATP (NAD --> NADH)

FAD --> FADH₂^e ---> Cristae = Electron transport system (ETS)

Fatty Acids and Monoglycerides

Non-CHOs giving you glucose

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.

Cardiac muscle

the process by which fatty acid molecules are broken down in the mitochondria to generate acetyl-coA. 

Acetyl Group = CoA waiting ---> Krebs cycle

Amino Acids - 20

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.

Electron Transport System

remove the amide groups from a molecule

shift amide groups to carriers (called ketos)

(the reversible exchange of amino groups between different amino acids.)

body cannot make these

(12 of these)

body can make these - although some you can't make enough of and still need to supplement

(8 of these)

TVTILLPM

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

Fat Soluble Vitamins = A, D, E, K

Cortical Nephrons - 85%

Juxtamedullar Nephrons - 15%

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

endothelium capsular membrane (podocytes)

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)

• 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

Interlobar arteries pass between the renal pyramids.



Interlobular Arteries pass between renal lobules.

association of structures called the JGA

Function is to control pressure and flow

baroreceptors (BP sensor) 

an enzyme produced by the JG cells designed to counter low blood pressure and flow

Angiotensinogenase

NO - filtration slits are only 8 nanometers - much too small (RBC are 2 micrometers). Seeing blood would be pathological.

YES - H₂O is 1 nm and can fit into filtration slits.

blood hydrocartic pressure (aka BHP) pressure going from glomerulus into bowman's capsule --> push out 45mmHg

works against BHP (hold back is 25mmHg)

works against BHP --> push back 10mmHg

Blood Osmotic Pressure (BOP) and Capsular Hydrostat Pressure (CHP)

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)

some forces will work for filtration and some will work against filtration

Filtration coefficient (how porous is the membrane of filtration)

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

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)

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*

filtrates into the blood

H₂O (constant)

Pts (transports sodium), by shifting salt you can pull 38 gallons of water into your bloodstream

(part of tubular reabsorption)

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.

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.

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.

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.

water on the kidneys - urinary pathway blockage, widened calyses

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.

Force (CCM) and Modulator (ADH)

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.

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*

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. 

Tubular Max --> maximum rate that you can reabsorb any particular solute

Opposite of Tubular Re-absorption (blood --> filtrate after GFR). Has nothing to do with water.

Antibiotics (Penicillin) - this is why you have to take high doses frequently because your body is trying to rid itself of the substance.

JGA - JG cells + Macula Densa DT (Filtrate Flow) --> if either or both of these drop than your body will produce more Renin.

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.

They make it so Angio I doesn't covert as much to Angio II.

Renal Artery Atherosclerosis --> compressed blockage of renal artery resulting in a drop of BP going to kidneys causing high BP

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