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Renal Physiology Study Notes for the medical student focusing for the exam.
|3 parts of fetal kidney and fate?||1. Pronephros – degenerate @ week 4|
2. Mesenephros – 1st trimester kidney then form male internal genitalia, ureteric bud extends into metenephros to form Collecting Duct, Renal Calyces, Renal Pelvis, Ureter.
3. Metenephros – permanent kidney – forms glomerulus through the distal tubule.
|Which kidney is harvested for transplant and why?||1. Left Kidney because it has a longer renal vein|
|How much of TBW is intracellular vs. extracellular?||1. 1/3 is extracellular|
-> 25% is plasma volume
-> 75% is interstitial volume
2. 2/3 is intracellular
|What is the 60-40-20 rule?||1. TBW = 60% of Total Body Weight|
2. ICF = 40% of total body weight
3. ECF = 20% of total body weight
|What is measured to determine plasma volume?||1. Radiolabeled albumin – look at distribution|
|What is used to measure extracellular fluid volume?||1. Inulin – can distribute to plasma compartment and interstitial volume but not into the cells|
|How do you calculate the intracellular fluid volume?||1. Total body water – (ECFV via inulin)|
|What happens to GFR, RPF and the filtration fraction if blood plasma protein concentration increases?||1. RPF does not change|
2. GFR decreases
3. Filtration fraction decreases
|What happens to RPF, GFR, and the filtration fraction if blood plasma protein concentration decreases?||1. RPF no change|
2. GFR increases
3. Filtration fraction increases
|What happens if there is constriction of the ureter to RPF, GFR, FF?||1. RPF NC|
2. GFR decrease
3. FF decrease
|How do you calculate reabsorption and secretion amounts for a given filtered substance?|| 1. Filtered Load = GFR(Px)|
2. Excreted Load = Ux(V)
Reabsorbed = GFR(Px) – Ux(V) (if positive reabsorbed if negative then secreted).
Secrete Load = (Ux)(V) – GFR(Px)
|When does glycosuria begin?||1. @ 160mg/dL, Na/Glucose cotransporters in the proximal tubule become saturated @ 350mg/dL (plateau of the reabsorption rate).|
|Why might there be glycosuria and aminoaciduria in pregnancy?||1. Decreased reabsorption of glucose and amino acids at the level of the proximal tubule.|
|What 3 things increase renin secretion from the JGA?|| 1. B1 receptor activation on the JGA|
2. Decreased Na delivery to the MD in the distal convoluted tubule
3. Decreased BP sensed @ the JGA
|Why does decreased Na delivery to MD cause an increase in renin secretion?||1. Decreased Na delivery means more Na is being reabsorbed proximally in response to lower fluid volume, thus need to increase volume (renin secretion)|
|What are the 5 primary actions of ATII?|| 1. ATI receptors in vasculature = vasoconstriction|
2. Increased Aldosterone secretion
3. Increased Na/H exchanger activity in PCT to increase Na, HCO3, and H20 reabsorption
4. Increased ADH from posterior pituitary (supraoptic nucleus via neurophysins)
5. Increased thirst (hypothalamus)
|Where is Angiotensin Converting Enzyme located?||1. Lungs and Kidney –> Remember it is important for the degredation of bradykinin, inhibition can potentially lead to angioedema.|
|What does ADH primarily respond to?What does ADH primarily respond to?||1. Decreases in osmolarity (remember this is sensed by the osmoregulator fenestrated areas in the brain)|
– At very low volume, ADH will be secreted
|What does Aldosterone mostly respond to?||1. Decreases in blood volume|
|How does ANP regulate volume?|| 1. Leads to vasodilation via release of cGMP and then NO|
2. Increases the GFR and increases Na excretion without increases in proximal tubule Na reabsorption. to net volume loss and Na loss
–> This is why in hyperaldosteronism you will have normal fluid volume with hyponatremia, hypernatremia, and increased bicarbonate.
|What substances/changes will shift potassium out of the cell?|| DO Insulin LAbs:|
Lysis of Cells
Beta Antagonists (anti catabolic)
|What substances/changes shift potassium into cells? (4)|| 1. Insulin|
4. Beta Adrenergic Agonists (increased Na/K ATPase)
|What are the causes of anion gap metabolic acidosis?|| MUD PILES CAT|
|What are the causes of normal anion gap metabolic acidosis?|| HARD ASS|
Renal Tubular Acidosis
| 1. What is Type 1 renal tubular acidosis?|
2. What kidney stones is a person with type 1 RTA at risk for developing?
| 1. Defect in collecting tubule’s ability to excrete H+ ions -> Resulting in hypokalemia, acidosis,|
2. Increased risk of calcium phosphate kidney stones because increased pH or urine (>5.5)
| 1. What is Type 2 renal tubular acidosis?|
2. What is the effect on potassium levels and what disease state is it associated with?
3. What is urine pH?
|1. Defect in PCT ability to reabsorb HCO3- resulting in hypokalemia (at the distal collecting tubule/duct)|
2. Fanconi’s Syndrome
3. Urine pH is <5.5 (Collecting duct and distal tubule can still secrete H+)
| 1. What is Type 3 renal tubular acidosis?|
2. What happens to urine pH in type 3 RTA?
| 1. Hypoaldostronism – decreased collecting tubule response to aldosterone resulting in hyperkalemia|
2. Urine pH will decrease because hyperkalemia messes up ammoniagenesis and thus NH3 buffering capacity