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